| By Author | [ A B C D E F G H I J K L M N O P Q R S T U V W X Y Z | Other Symbols ] |
| By Title | [ A B C D E F G H I J K L M N O P Q R S T U V W X Y Z | Other Symbols ] |
| By Language |
|
Download this book: [ ASCII ] Look for this book on Amazon Tweet |
Title: Influenza : An epidemiologic study
Author: Vaughan, Warren T. (Warren Taylor)
Language: English
As this book started as an ASCII text book there are no pictures available.
*** Start of this LibraryBlog Digital Book "Influenza : An epidemiologic study" ***
INFLUENZA
An Epidemiologic Study
BY
WARREN T. VAUGHAN, M.D.
BALTIMORE, MD.
THE AMERICAN JOURNAL OF HYGIENE
Monographic Series No. 1
1921
COPYRIGHT, 1921, BY
THE AMERICAN JOURNAL OF HYGIENE
BALTIMORE, MD.
PRESS OF
THE NEW ERA PRINTING COMPANY,
LANCASTER, PA.
PREFACE.
Following every widespread epidemic or pandemic of influenza, the
contemporary literature becomes virtually flooded with reports of
scientific studies on the etiology and the epidemiology of the disease.
By the time that recrudescences have ceased, interest has usually lagged
and eventually research in this subject has practically ceased, only to
be revived with the development of the next extensive epidemic.
To one who has had occasion to review the extensive literature of the
last pandemic, it becomes apparent that many of the recent writers are
uninformed, or at best only partially informed, regarding the rather
extensive information accumulated during the 1889 epidemic. The longer
one studies the observations made in 1889–93 the more firmly convinced
one becomes that the recent pandemic was identical with the former in
practically all of its manifestations.
It is desirable that, following each epidemic prevalence some individual
or individuals review the literature of the preceding epidemics,
acquaint himself with what has been written regarding influenza in the
intervening time up to the epidemic prevalence and correlate the work
done in these two periods with the various reports regarding the latest
epidemic.
The following pages constitute an attempt to correlate the epidemiologic
observations of the epidemic thirty years ago with those of the 1918–20
epidemic, and with the observations made during the intervening years.
The house census in the City of Boston and the preparation of this
monograph were made possible by the financial assistance of the
Metropolitan Life Insurance Company. This organization has devoted a
considerable sum of money to the study of influenza in its various
phases.
The author is indebted to his chief, Dr. Milton J. Rosenau, for helpful
advice and criticism and for the inspiration to carry on this
investigation. Dr. W. H. Frost has made many valuable suggestions.
Appreciation is also due Mr. Edwin M. Knights, who is responsible for
all of the charts, and to Mrs. V. K. Davis, who aided in the tabulation
of results of the Boston investigation.
The house-to-house census was carried out with the co-operation and
assistance of the Federated Jewish Charities in Boston and individual
members of the social service departments of the Massachusetts General
Hospital and the Peter Bent Brigham Hospital.
THE AUTHOR.
Department of Preventive Medicine and Hygiene,
Harvard Medical School, Boston,
_September 17, 1920_.
This monograph is one of a series of studies carried out under the
supervision of the Influenza Commission of the Metropolitan Life
Insurance Company. The Influenza Commission is investigating the
etiology and prevention of the acute respiratory diseases, and the work
is being carried on in Boston, New York City, Chicago, and Washington.
The members of the Commission are Dr. M. J. Rosenau, Chairman, Dr. G. W.
McCoy, Dr. L. K. Frankel, Dr. A. S. Knight, Dr. E. O. Jordan, Dr. W. H.
Frost and Dr. W. H. Park, Secretary.
INFLUENZA.
AN EPIDEMIOLOGIC STUDY.[1]
BY WARREN T. VAUGHAN, M. D.
(Received for publication April 6th, 1921.)
CONTENTS
SECTION I.
PAGE
GENERAL EPIDEMIOLOGIC CONSIDERATIONS 1
Historical 2
Clinical and epidemiologic identification 13
General characteristics of early epidemic outbreaks 14
Symptoms in former epidemics 19
Manner of spread 20
Human intercourse 23
Crowd gatherings 26
Mass attack 27
Healthy carriers and convalescents 30
General manner of spread in individual localities 31
Primary type of epidemic 31
Secondary type of epidemic 33
Mortality curves 36
Duration of explosive outbreak 37
Morbidity curves in 1920 recurrences 41
Spread in countries and continents 42
Spread in primary waves 42
Spread in recurrences 44
SECTION II.
INFLUENZA EPIDEMICS SINCE 1893 47
Occurrence since 1893 47
Period from 1893–1918 47
Increase in 1900–1901 49
Period from 1901–1915 51
Influenza in 1915–1916 55
Influenza between 1916 and 1918 58
The pandemic of 1918 59
Date of first increased prevalence in various localities 65
Influenza in China 80
Autumn spread in the United States 81
Recrudescences 87
Recurrences in the winter of 1919–1920 89
The winter of 1920 90
Incubation period 95
Predisposing causes 96
Periodicity 97
Virulence enhancement 108
Meteorologic conditions 113
Secondary invaders 114
Origin of the 1918 pandemic 116
SECTION III.
AN INVESTIGATION OF INFLUENZA IN BOSTON (WINTER OF 1920.) 127
Diagnostic standards for the 1918 epidemic 134
Standards for 1920 134
Morbidity 137
Relation of sex to morbidity 143
Relation of sex to severity 145
Morbidity by age 145
Relationship of occupation to morbidity 150
Effect of race stock 155
Mortality 156
Mortality by sex 165
Relationship to age 167
Relationship of occupation 170
Density of population 170
Race stock and mortality 173
SECTION IV.
AN INTENSIVE STUDY OF THE SPREAD OF INFLUENZA IN SMALL GROUPS OF
CLOSELY ASSOCIATED INDIVIDUALS 175
Effect of overcrowding 179
Domestic cleanliness 187
Economic status 189
Distribution of the disease through the household 191
The first case in the family 194
Intimacy of family contact 197
Recurrent cases 198
SECTION V.
IMMUNITY 199
SECTION VI.
INFLUENZA AND OTHER DISEASES 212
Influenza and tuberculosis 212
Other infectious diseases 220
Encephalitis lethargica 222
SECTION VII.
COMPARISON OF INFLUENZA WITH OTHER EPIDEMIC DISEASES 224
Epizootics 224
Asiatic cholera 228
Epidemic meningitis 228
Plague 229
Measles 231
SECTION VIII.
THE PREVENTION AND CONTROL OF INFLUENZA 234
Anticipatory or preventive measures 236
Organization of health services 237
Palliative measures in the presence of an epidemic 239
Problems for the future. Constructive research 241
Bibliography 245
Footnote 1:
From the Department of Preventive Medicine and Hygiene, Harvard
Medical School, Boston, Mass.
INFLUENZA.
AN EPIDEMIOLOGIC STUDY.
SECTION I.
_General Epidemiologic Considerations._
Those who seek to find in a study of the epidemiology of epidemic
influenza the secret of the causation of the disease, and its ultimate
eradication, are probably predestined to at least partial failure. We
must call upon the bacteriologist for information as to the causative
organism, and in time he may be able to furnish us with satisfactory
prophylactic measures, particularly with a successful vaccine.
But while pure epidemiologic studies will not demonstrate the ultimate
factor in the etiology, nevertheless these studies do subserve several
most important functions. The bacteriologist, the immunologist, the
serologist have accumulated a wealth of information since the 1918
pandemic, but as far as definite conclusions concerning the causative
agent of the disease are concerned we are no nearer to the truth than we
were at the time when Pfeiffer made his original observations. There is
no incontrovertible evidence by which one may say that the influenza
bacillus is or is not the cause of the disease. We must therefore await
further studies and future discoveries. But we cannot await idly in the
knowledge that new epidemics of the dread disease will surely come,
probably mild ones in the next few years, and certainly severe ones
again within a few decades. We must amass all of the available
information concerning the mode of action of the disease, its manner of
spread, its degree of infectivity, its distribution and the mode of its
recurrences, and try to formulate from a study of the available facts
some means of protecting ourselves against the epidemic, if not of
preventing it entirely.
In short, in the present state of the bacteriologic knowledge of the
disease, we may say that the epidemiologic features are the only facts
upon which we have to build in planning our defense. Today, the
practical work in the eradication of influenza must depend chiefly, if
not solely, on the general methods of preventive medicine.
Many valuable monographs have been written on the subject, particularly
following the pandemic of 1889–1893, but these have all emphasized
features and phases of the disease which seemed at that time to be
particularly important. Facts which seemed of extreme importance to the
earlier writers are today in some instances considered relatively
unimportant, while other phenomena which were but touched upon by the
former investigators today have assumed deep significance. For this
reason it is worth while to reproduce here the observations made in
previous epidemics, and to correlate them with the facts developed in
the abundant literature of the last few years, and to draw therefrom
inferences as to the life and habits of the influenza virus, and
conclusions as to the means of interrupting its progress.
HISTORICAL.
The history of influenza can justly be divided into two phases, the
first ancient, and the second modern. The latter period begins with the
1889 pandemic. By that time the science of bacteriology had altered our
concepts of the etiology of disease and epidemiologists had begun to
avail themselves of statistical methods of analysis. For the purposes of
this paper, therefore, consideration will be given chiefly to the
epidemic of 1889, and a summary of earlier epidemics will be made merely
to refresh our minds concerning the antiquity of the disease and the
periods of its occurrence. References to the earlier epidemics will be
made more particularly in the special discussions later, where points of
similarity or difference will be brought out. Further than that it is
unnecessary to go in the history of the disease, for the several
excellent monographs of 1890 to 1900 tell the historical story in a
manner that could scarcely be improved upon.
The great antiquity of epidemic influenza is a fact which I think may be
admitted in spite of some who hesitate to accept it because of lack of
convincing descriptive evidence. Some believe that the epidemic of the
year 412 B.C., described by Hippocrates and by Livy, was an epidemic of
influenza. Some have suggested that the epidemic described by Thucydides
was the same disease. Parkes remarks that the epidemic pervading the
Athenian Army in Sicily in 415 B.C., recorded by Diodorus Siculus, has
been supposed to have been influenza. Finkler, in referring to a report
by Diodorus of a pestilence occurring in 395 B.C., which broke out in
the Greek Army at the siege of Syracuse, and which killed off the
soldiers murderously, says that this could not have been influenza. He
regards as sufficient argument the fact that the mortality was high.
After the epidemic of 1918, one is more inclined to believe that the
epidemic in Sicily may well have been true influenza. We must remember
that previous to the last few pandemics the stories have been
fragmentary in character and were told, not by physicians, but chiefly
by the historians of the time, men who have desired to impress their
readers with some idea of the horrible ravages of the disease, and who
have doubtless in some instances transmitted the impression of monstrous
mortality rates. The early historians were much given to figures of
speech, many of which were very telling in conveying the impression
desired. Finally, the writers of the middle ages and of earlier times
had little or no statistical material on which to base their
conclusions. I have no doubt that a historian who during the 1918
epidemic of influenza might have limited his observations entirely to
the disease as it occurred at Camp Sherman, Ohio, and who saw 125 robust
soldiers dying each day, would have truly written that the disease
killed off the soldiers murderously. A further statistical argument in
favor of considering the epidemic among the Greek soldiers as quite
possibly influenza is the fact that as shown by present day findings
these men were all of the age in which the mortality is highest, and
were living under sanitary conditions which predispose to high incidence
and high mortality.
According to Parkes, in 827 A.D., an attack of “cough” which spread like
the plague was recorded. In 876, Italy and later the whole of Europe was
attacked, and the army of Charlemagne, returning from Italy, suffered
greatly. “Dogs and birds were attacked at this time.” In 976 the whole
of France and Germany was attacked by a fever whose principal symptom
was cough. There is also record of diseases which may have been
influenza which were seen in Germany and France in 927 and in England in
996 and 997. All of these records are indefinite and from their nature
unconvincing to a critical student. Several investigators have gone over
these past records up to 1889 with the idea of determining definitely
what plagues were, and which were not, true influenza. The criteria used
by the various investigators have differed slightly in some instances.
For instance, one chooses to use the record of low mortality in
widespread epidemics as the chief characteristic of pandemic influenza,
while another emphasizes principally the complications.
The experience of recent years has amply demonstrated that influenza may
be characterized by a high mortality or a low mortality; that pneumonia
may be prevalent or relatively rare during an epidemic. These features
are not truly characteristic of influenza itself. They are phenomena
which depend chiefly for their existence on secondary invasion with
organisms other than the causative agent of influenza. It may be that
the influenza virus itself is capable of producing pneumonia, but it is
generally accepted that an overwhelming majority of the complicating
pneumonias are due to secondary infections. One perusing the former
literature today would hesitate to state that an ancient epidemic was
not influenza merely because it was accompanied by high mortality, nor
would he wish to say that it was not this disease because there was no
mention of a high incidence of pneumonia. We have had both types within
the last few years, as in March and April, 1918, when the disease
appears to have been accompanied by a very low mortality and a low
incidence of pneumonia, and in October of the same year when the
pneumonia incidence and the death rate were both relatively much higher.
Attention should be called to a certain inaccuracy which has appeared in
the literature and which has resulted in some instances in a
misunderstanding of the entire history of influenza. Finkler says:
“According to August Hirsch the first influenza epidemic occurred in
1173 and he places it in his work as the first out of eighty.” This has
given the impression to some that influenza was unknown previous to that
date. Leichtenstern has quoted Hirsch more accurately and thereby given
an entirely different meaning to the statement. “August Hirsch says that
the first epidemic that can be definitely said to be influenza occurred
in 1173.” Jordan also conveys the latter impression. He remarks that the
first extensive, well described epidemic of influenza occurred in 1510.
Hirsch places the first authoritative influenza epidemic in the year
1173; Zeviani in 1293; Gluge in 1323; Schweich, Biermer and Ripperger in
1387; while Saillant, Thompson, Zuelzer and Leichtenstern accept nothing
prior to the first pandemic of 1510 as being unquestionably influenza.
It should be remarked here that opinion is not unanimous in every case
as to the identity of all epidemics following 1510.
Hirsch concluded that there have been about eighty epidemics since that
of 1173. Parkes states that in the fourteenth century there were six
epidemics, in the fifteenth seven, in the sixteenth eleven, in the
seventeenth sixteen, in the eighteenth eighteen, while in the first half
of the nineteenth ten epidemics are on record.
Table I shows in brief review the occurrence of the more important
epidemics since the year 1173. Like all similar summaries given in
tabular form it possesses the disadvantage of telling only parts of the
entire story, and those in only a very general way, but it will suffice
as a resumé and for the emphasis of certain phenomena to which attention
will be later directed.
Concerning the epidemic of 1889, it is usually stated that it had its
origin in Bokhara in May of that year. As will be seen from the table
influenza was present also in Greenland and the Hudson Bay territory in
the spring of 1889. The possibility of simultaneous origin in at least
two localities in that year will be discussed later. The epidemic
remained in Bokhara until August of the same year, after which time it
slowly traveled to Siberia where at Tomsk traces of the disease were
observed with certainty in October. At that time it was also observed in
the Caucasus and in European Russia. It appeared in Petrograd in
October, 1889, and remained epidemic until December of that year. The
spread of this epidemic throughout the world is indicated in the
following table adopted from Leichtenstern:
_Spread of Influenza in 1889–90._
═══════════════════════════════════════════════════════════════════════
Month. 1889–90.
───────────────────────────────────────────────────────────────────────
First (October) St. Petersburg, Moscow, Courland, Livonia, Finland.
Second Berlin, Paris, Vienna, Sweden, Denmark.
Third London, Holland, Belgium, Balkan States, North America.
Fourth Capetown, Egypt, Honolulu, Mexico, Japan, Hong Kong.
Fifth San Francisco, Buenos Ayres, India, Sierra Leone,
Scilly Islands.
Sixth Chili, Kamerun, Zanzibar, Basutoland, Tasmania.
Seventh British Bechuanaland, Barbados.
Eighth Gold Cost, Natal.
Ninth Trinidad.
Tenth Iceland, Madagascar, China, Senegal.
Eleventh Kashmir, Katunga.
───────────────────────────────────────────────────────────────────────
Between the years 1889 and 1893 according to Leichtenstern there was no
period altogether free from influenza. Here and there individual cases
or small epidemics sharply localized were observed. In 1893 another
epidemic appeared in many places and became quite widespread. There was
not, according to this author, the definite geographic progression that
had been observed in 1889. This was but a recrudescence, a lighting up
from endemic foci remaining after the first wide spread. In the first
half of 1893 there was a light spring epidemic, and in November of the
same year a larger epidemic swept over the whole of Europe. The height
of the latter was reached chiefly in December.
The influenza incidence subsequent to 1893 will be discussed later.
TABLE I.
_Influenza epidemics previous to 1889._
═════╤══════════════╤═════════════╤══════════════╤═══════════════╤══════════════
Date.│ General │ Site of │ Direction of │ Localities │ Rapidity of
│ features. │ origin. │ spread. │ affected. │ spread.
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1173│Rather meagre │Unknown. │ │Described in │Not known.
│description. │ │ │Italy, Germany,│
│ │ │ │England. │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1239│Described by │Described in │ │Invaded all of │
1311│Zeviani. │France. │ │France. │
│Records not │ │ │ │
│definite. Not │ │ │ │
│generally │ │ │ │
│accepted. │ │ │ │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1323│Mentioned by │ │ │ │
│Hirsch, Gluge │ │ │ │
│and Zeviani. │ │ │ │
│Most believes │ │ │ │
│it was a │ │ │ │
│typhoid │ │ │ │
│epidemic. │ │ │ │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1327│Mentioned by │ │ │Described in │
│Zeviani, │ │ │Italy. │
│Hirsch and │ │ │ │
│Gluge. Rather │ │ │ │
│doubtful. │ │ │ │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1358│Described by │ │ │Savoy, Germany,│
│Zeviani. Not │ │ │France, │
│generally │ │ │Catalonia. │
│accepted. │ │ │ │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1387│(Zeviani, │Italy. │ │Italy, France, │
│Schweich, │ │ │Strasbourg, │
│Gluge, Hirsch │ │ │Southern │
│and │ │ │Germany. │
│Ripperger.) │ │ │ │
│Characteristic│ │ │ │
│description. │ │ │ │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1403│A very short │France. │ │Described in │
│epidemic. │ │ │France. In 1404│
│(Gluge, │ │ │it invaded │
│Ripperger, │ │ │Flanders and │
│Pasquier.) │ │ │Germany │
│ │ │ │(Hirsch). │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1411│Described only│Described │ │Described by │
│in Paris. │only in │ │Pasquier as in │
│Extent │Paris. │ │Paris. │
│unknown. │ │ │ │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1414│Characteristic│ │ │In Italy and │
│description. │ │ │France in │
│ │ │ │February and │
│ │ │ │March. In the │
│ │ │ │Danube district│
│ │ │ │between January│
│ │ │ │and April. │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1427│Very │ │ │Described in │
│characteristic│ │ │France. │
│description. │ │ │ │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1438│Cited only by │ │ │Described in │
│Zeviani. │ │ │Italy. │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1482│Very limited │ │ │ │
│description by│ │ │ │
│Mezeray. │ │ │ │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1510│Widespread │Malta (?) │Generally, │Malta, Sicily, │
│over all of │(Webster and │from South to │Spain and │
│Europe. │Hancock │North. │Portugal, │
│ │report that │ │Italy, France, │
│ │it began in │ │Hungary, │
│ │Africa). │ │Germany, │
│ │ │ │Holland, │
│ │ │ │England, │
│ │ │ │Norway. │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1557│All of Europe.│Conflicting │General │Asia, │4 months from
│ │information │direction from│Constantinople,│Italy to
│ │(Asia?). │South to North│Sicily, Italy, │Netherlands.
│ │ │in Europe. │Spain, │Sicily in
│ │ │ │Dalmatia, │June. Nimes in
│ │ │ │Switzerland, │July. Italy in
│ │ │ │France, │August. Madrid
│ │ │ │Netherlands, │in August.
│ │ │ │England. │Dalmatia in
│ │ │ │ │September.
│ │ │ │ │Netherlands in
│ │ │ │ │October.
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1562│Uncertain │ │Only small │ │
1563│information. │ │epidemics at │ │
│ │ │most. │ │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1580│True pandemic │Orient │From Asia to │Orient, North │France in May.
│covering the │(Hirsch) │Constantinople│Africa, │Germany and
│Orient, Africa│Africa and │and in Europe │Constantinople,│Hungary in
│and Europe. │Malta │from South to │Malta, Venice, │August.
│ │(Pechlin). │North. │Sicily, Italy, │England and
│ │ │ │Spain, Hungary │Rhine Valley
│ │ │ │and Germany to │in September.
│ │ │ │the Baltic, │Saxony in
│ │ │ │Bohemia, │October.
│ │ │ │France, │
│ │ │ │Belgium, │
│ │ │ │England, │
│ │ │ │Denmark, │
│ │ │ │Sweden. │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1587│Apparently │ │ │Described in │
│quite │ │ │Italy and │
│localized. │ │ │Germany. │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1591│High │ │ │ │
│mortality. │ │ │ │
│Indefinite │ │ │ │
│information. │ │ │ │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1593│Spread over a │Said to have │Uncertain. │ │
│wide area in │commenced in │ │ │
│Europe. │Belgium, │ │ │
│ │“following a │ │ │
│ │violent │ │ │
│ │earthquake,” │ │ │
│ │and gradually│ │ │
│ │extended over│ │ │
│ │all the │ │ │
│ │cities of │ │ │
│ │Europe. │ │ │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1626│Local. │ │ │Described in │
│ │ │ │Italy. │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1627│In America. │ │Spread from │ │
│ │ │North America │ │
│ │ │to West Indies│ │
│ │ │and Chili. │ │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1647│In America │ │ │ │
│(Webster). │ │ │ │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1658│Local. │England (?). │ │Described in │
│ │ │ │England and in │
│ │ │ │Treptow near │
│ │ │ │Stettin. │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1675│Over Western │Germany (?). │ │Germany, │Germany in
│Europe. │ │ │Hungary, │September,
│ │ │ │England, │England and
│ │ │ │France. │France in
│ │ │ │ │October and
│ │ │ │ │November.
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1688│Apparently │England(?). │ │Described only │
│localized in │ │ │in England and │
│Great Britain │ │ │Ireland. │
│and Ireland. │ │ │ │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1693│England and │Dublin(?). │ │Dublin, Oxford,│One month from
│the adjacent │ │ │London, │Dublin to
│continent. │ │ │Holland, │London.
│ │ │ │Flanders. │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1709│A period of │In 1712, │1712, spread │Italy, France, │Six months
1712│extensive │onset in │from Germany │Belgium, │from Germany
│endemics. │Germany. │to Holland and│Germany, │to Italy.
│ │ │Italy. │Denmark. │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1729│First epidemic│Usually │Russia through│Moscow, Sweden,│Moscow in
│said to have │designated as│Sweden, │Poland, │April, 1729.
│originated in │Russia │Poland, │Silesia, │Sweden in
│Russia and │(Moscow). F. │Germany, etc. │Austria, │September,
│first │Hoffman │to Italy and │Hungary, │England in
│described as │claimed to │perhaps North │England, │November.
│entering │have seen the│America. │Switzerland, │Paris in
│Europe from │epidemic in │ │France, Italy, │December. Rome
│the Northeast │Halle in │ │Iceland. │in February,
│rather than │February, │ │ │1730.
│the Southeast.│1729. │ │ │
│First spread. │ │ │ │
│Pandemic │ │ │ │
│period. │ │ │ │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1732│Second spread.│ │Over Europe │ │Germany in
│Pandemic │ │and America. │ │November.
│period. │ │According to │ │France in
│ │ │Pelargus it │ │January, 1733.
│ │ │again followed│ │Spain and
│ │ │the route from│ │Italy in
│ │ │Russia through│ │February.
│ │ │the North of │ │
│ │ │Europe and │ │
│ │ │then South. │ │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1737│Not generally │ │ │England, North │
│recognized. │ │ │America, │
│ │ │ │Barbados, │
│ │ │ │France. │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1742│Slow spread │Began either │Occurred in │Germany, │Germany in
1743│from Germany. │on the shores│Germany in │Switzerland, │January, 1742.
│Recurrences in│of the Baltic│Jan. and Feb.,│Italy, France, │England in
│Germany up │Sea or in │1742, and then│Holland, │April, 1743.
│until 1745. │single cities│disappeared to│Belgium, │
│ │in Germany. │reappear in │England. │
│ │ │Switzerland in│ │
│ │ │the spring. │ │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1757│A period of │Began either │France, │Barbados, │Villalba
1758│related │first in │Scotland, │Germany, │states that
1761│epidemics with│North America│America, │Austria, │the epidemic
1762│complicated │and spread │Finkler states│Hungary, │in 1767 had
1767│geographic │thence to │that in 1762 │Denmark, │traveled over
│pictures and │Europe or │influenza │England, │the whole of
│without clear │else began │first started │Ireland, │Europe in a
│cut direction │spontaneously│in Germany and│Alsace. │period of two
│of spread. │in both │spread thence │ │months.
│ │hemispheres. │in a very │ │
│ │ │irregular way │ │
│ │ │over Western │ │
│ │ │Europe. Gluge │ │
│ │ │and Hirsch │ │
│ │ │state that in │ │
│ │ │1767 the │ │
│ │ │disease │ │
│ │ │appeared │ │
│ │ │simultaneously│ │
│ │ │in Europe and │ │
│ │ │North America.│ │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1775│Slow spread │First │First spread │Germany, Italy,│Invaded Vienna
1776│through │appearances │to Vienna, and│Austria, │in June. Made
│Western │in Autumn of │after a │England, │appearance in
│Europe. │1775 in │quiescence │Ireland, │Italy in
│ │village of │broke out in │France. │September. In
│ │Clausthal in │France and │ │England and
│ │the Harz │England and │ │France in
│ │mountains. │possibly │ │October,
│ │ │spread to │ │November and
│ │ │America and │ │December.
│ │ │China. │ │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1780│Western Europe│January, 1780│Spread to │ │Three months
1781│and possibly │in France. │Alsace, │ │from France to
│Brazil and │ │Germany and │ │Brazil.
│China. │ │Italy, and in │ │
│ │ │March reported│ │
│ │ │in Rio de │ │
│ │ │Janiero. │ │
│ │ │Appeared in │ │
│ │ │Sept. 1780 on │ │
│ │ │Southern coast│ │
│ │ │of China. │ │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1781│One of the │China and │Through │China, India, │Moscow,
1782│most │perhaps India│Siberia and │America, │January, 1782.
│widespread │in Autumn of │Russia to │Russia, Riga, │Riga,
│pandemics. │1781 │Petrograd, │Germany, │February.
│Abundant │(Hirsch). │Finland, Riga,│England, │Germany,
│literature. │English │Germany, etc. │Scotland, │March.
│ │writers │ │Netherlands, │England,
│ │connect onset│ │Ireland, │April.
│ │with │ │France, Italy, │Scotland, May.
│ │occurrence of│ │Spain. │Ireland,
│ │influenza in │ │ │France and
│ │the British │ │ │Italy, June.
│ │Army in │ │ │Spain, August.
│ │India, Nov., │ │ │
│ │1781. Wittwer│ │ │
│ │and others │ │ │
│ │begin its │ │ │
│ │history in │ │ │
│ │Petrograd in │ │ │
│ │January, │ │ │
│ │1782. │ │ │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1788│Throughout all│Russia, in │West and │Russia, │Seven months
1789│of Europe. One│March, 1788. │South. Spread │Germany, │required to
│year later in │“Apparently │in America in │Hungary, │cover this
│America. │independent │1789 │Denmark, │territory.
│ │origin in │throughout │England, │
│ │America in │United States │Scotland, │
│ │Sept., 1789.”│from New York │France, Italy, │
│ │ │North and │Switzerland. │
│ │ │South and │ │
│ │ │finally │ │
│ │ │touching the │ │
│ │ │West Indies, │ │
│ │ │South America │ │
│ │ │and Nova │ │
│ │ │Scotia. │ │
│ │ │Recurrences in│ │
│ │ │single cities │ │
│ │ │of U. S. in │ │
│ │ │1790. │ │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1799│Local epidemic│Origin in │Spread West │Russia, │
1800│confined to │Russia. │and South. │Galicia, │
│Northeastern │ │ │Poland, │
│Europe. │ │ │Germany, │
│ │ │ │Denmark. │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1802│Local endemic │First │No clear cut │France, │
1803│outbreaks │reported in │direction. │Germany, Italy,│
│covering │France. │Recurrences │England, │
│considerable │ │until 1805–08.│Switzerland, │
│territory │ │General │Central Europe.│
│which follow │ │dissemination │ │
│the last │ │throughout │ │
│period by a │ │North America │ │
│quiescence of │ │in 1807. │ │
│five months. │ │ │ │
│There appears │ │ │ │
│to have been │ │ │ │
│an │ │ │ │
│unassociated │ │ │ │
│epidemic early│ │ │ │
│in 1800 in │ │ │ │
│China and one │ │ │ │
│in Brazil. │ │ │ │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1811│Several │1807, onset │Usually from │North and South│1815, one
1815│epidemics in │in │New England │America. │month from
1816│North America │Massachusetts│West and │ │Boston to New
1824│and to some │in February. │South. │ │York, and five
1826│extent in │1815, onset │ │ │months to
│South America.│in Boston in │ │ │South Carolina
│ │September. │ │ │and Brazil.
│ │1824, onset │ │ │1824, three
│ │in Boston in │ │ │months from
│ │October. │ │ │Boston to
│ │ │ │ │Georgia.
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1827│Widespread │ │ │ │
│epidemics │ │ │ │
│throughout │ │ │ │
│Eastern Russia│ │ │ │
│and Siberia. │ │ │ │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1830│Extensive │China in │To Manila in │Entire earth. │Ten months
1833│influenza │January, │September, │ │from China to
│period made up│1830. │1830. Later to│ │Russia. Four
│of two or │ │South Sea │ │months from
│three pandemic│ │Islands and │ │Russia to
│periods. │ │India. │ │Germany. Two
│ │ │Appearance in │ │additional
│ │ │Russia in │ │months through
│ │ │October, 1830,│ │France,
│ │ │with │ │England,
│ │ │subsequent │ │Scotland,
│ │ │spread West │ │Sweden,
│ │ │and South and │ │Belgium,
│ │ │on to North │ │Switzerland.
│ │ │America (Feb.,│ │Six months
│ │ │1832). │ │from Germany
│ │ │ │ │to Italy.
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1833│Second │Probably │After an │Europe. │Petrograd in
│pandemic in │Asia. │interval of │(America │January.
│above period. │ │one year │appears to have│Berlin and
│ │ │Europe was │escaped this │Constantinople
│ │ │again visited │second │in March.
│ │ │with an │epidemic.) │Denmark and
│ │ │extensive │ │Sweden, France
│ │ │plague which │ │and Great
│ │ │attacked the │ │Britain in
│ │ │same countries│ │April, Italy
│ │ │in about the │ │in May.
│ │ │same order. │ │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1836│Third spread │Origin rather│West and South│Europe, Faroe │Almost
1837│in above │obscure, │as previously.│Islands, │simultaneous
│period. │possibly in │ │Mexico,(?) │invasion at
│ │Russia. │ │India, Java. │Petrograd,
│ │ │ │ │Sweden,
│ │ │ │ │Denmark,
│ │ │ │ │Germany and
│ │ │ │ │England;
│ │ │ │ │Egypt, Syria,
│ │ │ │ │France,
│ │ │ │ │Ireland,
│ │ │ │ │Holland, and
│ │ │ │ │Switzerland
│ │ │ │ │one month
│ │ │ │ │later. Italy,
│ │ │ │ │Spain and
│ │ │ │ │Portugal yet
│ │ │ │ │another month
│ │ │ │ │later.
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1838│Every year in │ │ │1838, February;│
1847│this period │ │ │Island of │
│with the │ │ │Bourbon and │
│exception of │ │ │Iceland. │
│1840 showed, │ │ │1838, November;│
│according to │ │ │Australia and │
│Hirsch, some │ │ │New Zealand. │
│local │ │ │1839, │
│epidemic. │ │ │Abyssinia. │
│ │ │ │1841, Germany, │
│ │ │ │Hungary, │
│ │ │ │Ireland. │
│ │ │ │1842, Belgium, │
│ │ │ │England, │
│ │ │ │France, Egypt, │
│ │ │ │Chili. │
│ │ │ │1843, Germany, │
│ │ │ │England, │
│ │ │ │Iceland, │
│ │ │ │France, │
│ │ │ │Siberia, the │
│ │ │ │United States. │
│ │ │ │1844, Germany, │
│ │ │ │England, │
│ │ │ │Switzerland, │
│ │ │ │Cayenne. │
│ │ │ │1845, Germany │
│ │ │ │and │
│ │ │ │Switzerland. │
│ │ │ │1846–1847, │
│ │ │ │France, Russia,│
│ │ │ │Constantinople,│
│ │ │ │Brazil, │
│ │ │ │England, │
│ │ │ │Denmark, │
│ │ │ │Belgium, │
│ │ │ │Switzerland. │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1847│Epidemic │Origin │Spread not │All of the │
1848│period │uncertain. │definite, │countries of │
│throughout │ │North America │Western Europe,│
│Europe without│ │in 1848. │West Indies, │
│clear cut │ │ │New Zealand, │
│direction of │ │ │Newfoundland, │
│spread. │ │ │Sandwich │
│ │ │ │Islands, Egypt,│
│ │ │ │Algiers, West │
│ │ │ │Coast of │
│ │ │ │Africa. │
─────┼──────────────┼─────────────┼──────────────┼───────────────┼──────────────
1850│Epidemics │ │1857, began in│1850–51, │1855, only one
1889│covering │ │August in │particularly │month between
│larger or │ │Panama and │throughout the │Petrograd and
│smaller │ │spread to West│whole Western │Italy.
│territory │ │Indies and up │coast of South │
│every year, │ │and down the │America with │
│but none to │ │Pacific Coast.│later spread to│
│compare in │ │Prevailed in │California & │
│intensity with│ │Europe in │Europe. │
│those of 1831,│ │December. │1852, │
│1833, 1836 and│ │ │Australia, │
│1847. │ │ │Tasmania, South│
│ │ │ │America. │
│ │ │ │1853, Faroe │
│ │ │ │Islands. │
│ │ │ │1854, Bavaria. │
│ │ │ │1855, Europe, │
│ │ │ │spreading │
│ │ │ │rapidly West │
│ │ │ │and South from │
│ │ │ │Petrograd. │
│ │ │ │Later in same │
│ │ │ │year, Brazil. │
│ │ │ │1857–58, │
│ │ │ │widespread │
│ │ │ │epidemic in │
│ │ │ │both │
│ │ │ │hemispheres. │
│ │ │ │1860–70, very │
│ │ │ │irregular │
│ │ │ │appearances in │
│ │ │ │Australia, │
│ │ │ │Tasmania, │
│ │ │ │Philadelphia, │
│ │ │ │the Bermudas, │
│ │ │ │Holland, │
│ │ │ │California, │
│ │ │ │France, │
│ │ │ │Switzerland, │
│ │ │ │Africa, │
│ │ │ │Germany, │
│ │ │ │Belgium, │
│ │ │ │Russia, │
│ │ │ │Denmark, Sweden│
│ │ │ │and Turkey. │
│ │ │ │1874–75, │
│ │ │ │Extensive │
│ │ │ │spread in │
│ │ │ │America, │
│ │ │ │Germany and │
│ │ │ │France, with │
│ │ │ │recurrence one │
│ │ │ │year later in │
│ │ │ │eleven areas of│
│ │ │ │the United │
│ │ │ │States. │
│ │ │ │1879, America. │
│ │ │ │1885–88, │
│ │ │ │Re-appeared │
│ │ │ │each year in │
│ │ │ │Petrograd. │
│ │ │ │1889, (Spring) │
│ │ │ │Greenland and │
│ │ │ │Hudson Bay │
│ │ │ │territory. │
│ │ │ │(May) Bokhara │
│ │ │ │in Turkestan │
│ │ │ │from where the │
│ │ │ │great pandemic │
│ │ │ │of 1889–90 is │
│ │ │ │usually said to│
│ │ │ │have taken its │
│ │ │ │origin. │
─────┴──────────────┴─────────────┴──────────────┴───────────────┴──────────────
Table I shows that prior to 1510 the information was so limited as to be
not entirely conclusive. We must rely upon the fragmentary descriptions
of writers located usually in or near the intellectual centers who
described the disease as they saw it in their city or country. We have
no way of ascertaining what other countries were invaded, and we possess
no method by which we may enumerate the “silent areas,” countries which
in the absence of a chronicler have not been able to transmit their
story.
There have been fourteen very widespread epidemics since 1510, all of
which might appropriately be designated as pandemics. They are those of
1510, 1557, 1580, 1593, 1729, 1732, 1762, 1782, 1788, 1830, 1833, 1836,
1847, 1889 and 1918. Some of these have spread farther than others
according to the records, but in nearly all we have reports of influenza
being present in practically every country provided with a historian. We
may find from the table another group in which there have been more or
less extensive epidemics, apparently related, but without any general
direction of spread. Such are the epidemics of 1709–12, 1757–67,
1802–03, 1838–47 and the period 1850–59. Finally, there are at least ten
periods during which relatively small areas have been affected with
epidemic influenza. Such for instance is the year 1688 when the disease
was apparently localized in Great Britain and Ireland; in the year 1693
when England and the adjacent continent were involved, with little
spread elsewhere; and again in 1742, when there was a slow spread
through Germany into adjacent countries with recurrences in the former
up until 1745.
In England the following epidemics have been recorded, some of them in
great detail: 1510 and 1557, described by Thomas Short; 1658 by Willis;
1675, by Sydenham; 1729–1743 by Huxham; 1732–33 by Arbuthnot; 1758 by
Whytt; 1762 by Baker and Rutty; 1767 by Heberden; 1775 by Fothergill,
who collected observations from many physicians; in 1782 by Gray,
Haygath and Carmichael Smith; 1803 by Pearson and Falconer, and a great
number of others; 1833 by Hingeston and others; 1837 by Streeten,
Graves, and Bryson, etc.; 1847 by Peacock, Laycock and many others; also
those of 1855 and 1889–93.
According to Stallybrass, epidemic crests have been reached in England
in 1789–90, 1802–03, 1830–32, 1840–41, 1848–51, 1854, 1869–70, 1879,
1890–91, 1898 and 1918 to 1920. The periodicity in multiples of ten
years in this latter group is remarkable.
The disease appears to have visited North America in the years 1627,
1647, 1729, 1732, 1737, 1762, 1782, 1789, 1811, 1832, 1850, 1857, 1860,
1874, 1879, 1889, 1900, 1915–1916 and 1918–20. Abbott speaks
particularly of the years 1647, 1655 and 1697–98, 1732, 1762 and 1782
and 1889 as being years of especial epidemic prevalence in this country.
CLINICAL AND EPIDEMIOLOGIC IDENTIFICATION.
Up to the present time we have discovered no one characteristic by which
we may say that a case or an epidemic is positively influenza. We have
had to rely on the general symptomatology, which indeed is sufficiently
characteristic, although so nearly like the symptoms of certain other
diseases as to make us hesitate to make an absolute diagnosis, and on
the epidemic characteristics. The necessity of an absolute criterion in
the clinical diagnosis is particularly felt in the presence of an
isolated interepidemic case, or a small endemic outbreak. It is at this
point that the opinions of epidemiologists diverge, a divergence which
results in two schools of thought in the explanation of the endemic
source of epidemic influenza. Are the interepidemic cases and the small
localized epidemics due to the virus which causes the great pandemics;
are they _influenza vera_, or are they entirely different diseases with
similar symptomatology, caused by some other microorganism and should
they be designated by some other name? Thus Leichtenstern remarks: “When
we go over the records of the years 1173 to 1875, and particularly those
of the last century, when the information has been more extensive and
more accurate, we find that scarcely a year has passed without news of
the epidemic occurrence of influenza at some point or other of the
earth. Some of these local and territorial epidemics are merely endemic
recurrences of the great pandemics which have left the germ deposited in
the various localities. Others of these small epidemics probably have
nothing to do with _influenza vera_, but are local outbreaks of
_catarrhal fever_.”
Contrary to the usual belief, influenza is a disease of quite definite
and distinct characteristics, both clinical and epidemiological. The
symptoms are clear cut, with sudden onset, severe prostration out of all
proportion to the clinical symptoms and to the fever, headache and pain
in the back, general body pains, and fever of greater or less degree.
There is usually a lack of leucocytosis or a true leucopenia. In
uncomplicated influenza there are as a rule no localizing symptoms.
There may be a slight soreness of the throat, or a slight cough, but
these are at best mild. The fever lasts from three to five days and
disappears, while at the same time all of the symptoms clear up with the
exception of the profound prostration, which as a rule continues for
some time, rendering convalescence surprisingly slow. The pain in the
back may remain for a week or so. This is the description of
uncomplicated influenza.
The manner of spread of epidemic influenza is constant in a primary
epidemic and the epidemic as a whole has certain features which render
it characteristic. The sporadic case has as a rule the same quite clear
cut clinical symptomatology, but it fails to manifest the one feature
most characteristic of epidemic influenza—a high degree of
contagiousness. Further, although the symptoms in themselves are
characteristic, there is no one pathognomonic sign by which one may say,
“this is a case of influenza,” and, finally other disease conditions
such as tonsillitis, frequently resemble it so much as to cause error in
diagnosis.
This becomes, then, one of the problems in the study of influenza
epidemiology. It is a matter of first importance to determine once and
for all whether true influenza is with us always, or whether it appears
only at the time of the great pandemics. Upon the answer to this
question more than upon any other one thing rests our choice of methods
of eradication. Any procedures of preventive medicine that may be
undertaken on the assumption that the source of pandemic influenza is to
be found in one or a few endemic foci, such as the one supposed to exist
in Turkestan, would fail utterly should the true condition be that of a
universal distribution of a relatively avirulent virus which from time
to time from some unknown cause assumes a highly increased virulence.
Before becoming involved in this very complicated question, let us
familiarize ourselves completely with the characteristics of the
pandemic and epidemic variety of the disease.
GENERAL CHARACTERISTICS OF EARLY EPIDEMIC OUTBREAKS.
We have described the symptomatology of uncomplicated influenza. It is
rare that this clinical picture is seen alone during the height of an
epidemic. Complications, chiefly of the respiratory tract, as a rule
occur in such a large proportion of individuals that they very nearly
dominate the picture. Although caused by various microorganisms, all of
which appear to be secondary factors the results are so characteristic
that in the past, descriptions of influenza epidemics have usually been
descriptions of the complications of epidemic influenza. Most influenza
epidemics are complicated. But we do know from the experience of recent
years as well as from history that relatively uncomplicated epidemics of
influenza have occurred, and that when they do so occur a predominant
characteristic has been the extreme mildness.
It is a fundamental characteristic of pandemic influenza that early
cases in widespread epidemics, as well as in “pre-epidemic increases”
are very mild, with a minimum of respiratory complications and with
exceedingly low mortality. It is because we are better acquainted with
the more severe variety that, when these mild precursors appear we are
always in doubt for a time as to their true identity.
In spite of our 20th century erudition, the influenza when it first
appeared in mild form in the American Expeditionary Forces in 1918, for
a lack of better knowledge as to its cause was called “three-day fever.”
In Italy in the same year the designation of the disease progressed from
pappataci fever through “Spanish grip” and “summer influenza,” until
finally it was designated influenza, pure and simple. Sampietro in Italy
particularly discussed the possibility of the disease being pappataci
fever.
Belogu and Saccone, who wrote in May of 1918, decided that the epidemic
was not influenza in spite of the manifest clinical similarity, chiefly
because of the absence of signs of secondary invasion, such as nervous
symptoms, gastro-intestinal symptoms, and pneumonia, and especially
because of the rapid recovery after defervescence. They also considered
the possibility of pappataci fever and dengue, and ruled out both. They
discussed calling the condition “influenza nostras,” but reached no
definite conclusion. Trench fever was also considered by some. United
States Public Health Reports for 1918 record that dengue was reported
prevalent at Chefoo, China, during the two weeks ended June 15th, 1918.
One week later there was a paragraph stating, “Prevalence of a disease
resembling dengue and affecting about fifty per cent. of the population
was reported at Shanghai, China, June 15, 1918.” It is not impossible
that this was influenza.
Zinsser reminds us that Hayfelder, when he saw the influenza as it
spread in Petrograd in November of 1889, remarked its close clinical
similarity to the description of an epidemic of dengue which had
prevailed in Constantinople during the preceding September. Hayfelder,
in studying the 1889 epidemic at its onset in Russia and the East, wrote
of “Sibirisches Fieber” which was first looked upon as malaria owing to
the apparently complete absence of the complicating lesions habitually
associated in our minds with influenza.
The same difficulty in early identification was experienced in this
country in 1918. At the end of March of that year the author who was
stationed at Camp Sevier, South Carolina, was one of a Board of Officers
appointed to investigate a disease which had broken out among troops
stationed at that camp. At that time the line troops consisted of three
infantry regiments and three machine gun battalions. On the day
following a parade in the city of Greenville a considerable number of
men in three out of the six organizations suddenly took ill. There were
a few isolated cases in other organizations, but in the one infantry
regiment and two machine gun battalions the regimental infirmaries were
filled, and some cases were sent to the base hospital. Nearly all were
very mildly ill and exhibited the symptoms of pure uncomplicated
influenza as described above. The onset was sudden, there were the usual
pains and aches, the bowels were regular, there was a feeling of
discomfort in the pit of the stomach in many instances, and there were
no sore throats and very little cough. Recovery was as a rule very
rapid, although about a dozen of the entire number developed pneumonia
and some of these died. Physical examination of those only mildly ill
and who remained in the regimental infirmary showed as a rule nothing,
but in some instances scattered fine moist rales near the hilus of the
lungs. In some of the organizations the disease was definitely spread
down rows of company tents. Careful bacteriologic examination was made
at the time and the predominating organisms were found to be a
gram-negative coccus resembling micrococcus catarrhalis, and a
non-hemolytic streptococcus. This was in uncomplicated cases.
The Board decided that the disease should be called influenza, but our
only basis for such decision were the clinical symptoms and the
contagious character. At that time none of us dreamed of any possible
connection with a severe epidemic to occur later, and laboratory search
for influenza bacilli which was carefully made in view of the clinical
diagnosis showed none of these organisms to be present.
At about the same time a similar epidemic was being experienced at Fort
Oglethorpe, Ga. V. C. Vaughan, in describing this epidemic, remarks: “A
disease strongly resembling influenza became prevalent in the Oglethorpe
Camp about March 18, 1918. It soon assumed pandemic proportions. Within
two weeks every organization in Camp Forrest and the Reserve Officers
Training Camp was affected.
“The symptoms were as follows: Headache, pain in the bones and muscles,
especially the muscles of the back, marked prostration, fever, sometimes
as high as 104 degrees. Sometimes there was conjunctivitis, coryza, a
rash and possibly nausea, recovery taking place in a few days.
“In all organizations the epidemic was first located in companies before
it became general.
“The incubation period was short, not over one or two days.
“Some organizations suffered more than others for no apparent reason.
“It is probable that the epidemic disease was recently brought to these
camps. If it is genuine influenza, and the epidemiological features no
less than the leading symptoms seem to point to that disease, there is
here offered the most reasonable explanation of the outbreak which is
now possible. No other disease spreads so fast or is so prostrating,
considering its symptoms.”
We will quote at some length from the report of Zinsser of the Chaumont
epidemic in France in 1918, because of the excellence of the
description, and particularly because Zinsser has followed three
successive epidemics with successive increases in the complications and
corresponding transformations in the clinical picture. It is worthy of
special note that he has remarked that the influenza, as first seen at
Chaumont, showed nothing in the symptoms that would suggest a
predominant respiratory tract infection.
“It will be useful to discuss briefly the early cases as we saw them
during the Chaumont epidemic, not because the observations made there
add much that is new from a clinical point of view, but because they
will remove any possible ambiguity concerning our conception of
influenza in its pure uncomplicated form.
“As far as we can judge the little outbreak at headquarters was typical
of the first advent of epidemic influenza in many places. The population
of the town, at the time, consisted of a large office personnel attached
to the military administration, scattered as to billets and places of
work; of military units living in barracks and eating at common messes;
and of the townspeople. The epidemic descended upon individual military
units with the suddenness of a storm, striking a considerable percentage
of the men, perhaps most of the susceptible material, within less than a
week, and ending almost as abruptly, with only a few isolated cases
trailing behind. Among the more scattered office workers and among the
townspeople it was disseminated more gradually and trailed along for a
longer period.
“These early cases were clinically so uniform that a diagnosis could be
made from the history alone. The onset was almost uniformly abrupt.
Typical cases would become ill suddenly during the night or at a given
hour in the day. A patient who had been perfectly well on going to bed,
would suddenly awake with a severe headache, chilliness, malaise and
fever. Others would arise feeling perfectly well in the morning, and at
some time during the day would become aware of headache and pains in the
somatic muscles.
“The typical course of these cases may be exemplified by that of J. T.
W., a draftsman attached to the 29th Engineers. He was perfectly well
until May 20th, working regularly, his bowels and appetite normal,
considering himself healthy. On May 21st, at 4:30 A.M. he awoke with a
severe headache. He arose, forced himself to eat breakfast and tried to
go to work. He began to feel feverish and chilly. At the same time his
headache became worse, with pains in the back, and burning in the eye
balls. At 2 P.M. he reported sick, and was taken to the hospital with a
temperature of 102.8 degrees. At midnight his temperature dropped to
101.6 degrees, and came down to normal by noon of the 22d. As he
recovered he developed a slight sore throat, great soreness of the legs
and a very slight cough. He recovered completely within a few days.
“These cases with a few exceptions developed no rashes. One or two of
them had blotchy red eruptions which we felt incompetent to characterize
dermatologically. The leucocyte counts ranged from 5,000 to 9,000. A
very few went above this. Sometimes there was a relative increase of
lymphocytes, but this was by no means regular. The few spinal fluids
that were examined were normal. As to enlargement of the spleen, we can
say nothing definitely.
“Soon after this we observed the disease in a Division, the 42d, then
holding a part of the line in front of Baccarat. Here it had already
developed a somewhat different nature, due, we believe, to the fact that
the men of this Division were not, as were those at Chaumont, living in
a rest area, but were actively engaged in military operations, working,
sleeping, and eating under conditions that involved greater fatigue,
less protection against weather, and greater crowding in sleeping
quarters. The Baccarat cases were much more frequently catarrhal; sore
throats, coughs and more serious respiratory complications were more
common. However, they were usually coupled unmistakably with an
underlying typical influenzal attack, sudden onset, pains and short
lived fever. Moreover, there were a great many of the entirely
uncomplicated cases interspersed with the others.
“Still later, in September, October and November, respiratory
complications were so frequent and severe, came on so early in the
disease, and the pneumonia mortality became so high, that the
fundamental identity of these later cases with the early three-day fever
might easily have been lost sight of by observers who had not followed
the gradual transformation.
“In consideration of these facts, it is apparent that etiological or
other investigations can throw no light upon the problems of influenza
unless they are carried out with clearer understanding of the
differentiation between the complications and the basic disease.
“The serious respiratory infections of the bronchi and lungs we can set
down with reasonable certainty as complications due, certainly in the
overwhelming majority of cases, to secondary bacterial invaders. It is a
matter of considerable difficulty, however, to know exactly where the
basic disease stops and the complications begin; and whether we must
regard the mild sore throat and conjunctival injection which so often
accompany the simple cases as a part of this basic clinical picture, or
as the simplest variety of complication. This is much more than an
academic question, since, as we shall see, the bacteriological analyses
of such lesions have played an important role in etiological
investigations.”
SYMPTOMS IN FORMER EPIDEMICS.
The difficulty in making a decision in the presence of an epidemic is
very similar to that of deciding whether the epidemics of former times
were in each case influenza. Some few have been recorded in which the
description has corresponded fairly well to that of primary
uncomplicated influenza. Thus, concerning the epidemic of 1557 in Spain,
Thomas Short wrote as follows: “At Mantua Carpentaria, three miles from
Madrid, the epidemic began in August.... There it began with a roughness
of the jaws, small cough, then a strong fever with a pain of the head,
back, and legs. Some felt as though they were corded over the breast and
had a weight at the stomach, all of which continued to the third day at
furthest. Then the fever went off, with a sweat or bleeding at the nose.
In some few, it turned to a pleurisy or fatal peripneumony.”
Most of the descriptions, however, have been of a general character and
include descriptions of the complicated periods of the epidemic. One of
the more complete of the early descriptions was that by Lobineau in
1414, who wrote: “C’était une espèce de rhume, qui causa un tel
enrouement que les chastelets furent obligez d’interrompre leurs
séances; on dormoit peu et l’on souffroit de grandes douleurs à la
teste, aux reins et par tout le reste du corps; mais le mal ne fut
mortel que pour les vieilles gens de toute condition.”
With this exception we possess no very good or complete description of
influenza prior to the epidemic of 1510. After that time they have as a
rule been detailed enough to enable identification. Hirsch bases his
conclusions concerning the year 1173 chiefly on the following quotation:
“Sub hisdem diebus universus orbus infectus ex aeris nebulosa
corruptione, stomacho catarrhum causante generalem tussim, ad singulorum
perniciem, ad mortem etiam plurimorum immissam vehementer expavite.”
Nearly all that we have to go on in this description is the widespread
incidence of the disease and the presence of respiratory symptoms,
particularly cough. In 1323 the description emphasizes only the high
morbidity. Thus, Pietro Buoninsegni writes: “In questo anno e d’Agosto
fu un vento pestilenzia le per lo quale amalò di freddo e di febbre per
alcuni dì quasi tutte le persone in Firenze e questo madesimo fu quais
per tutta Italia.” The same author describes the epidemic of 1327,
emphasizing again the high morbidity and in addition the low death rate:
“In detto anno e mese fu quasi per tutto Italia corruzione di febbre per
freddo; ma pochi ne morirono.” Again in 1387, he emphasizes the same two
features.
Pasquier, in writing of the epidemic of 1403 in France, says: “En
Registres de Parlement on trouve que le vingt-sixième jour d’avril 1403
y eut une maladie de teste et de toux, qui courut universellement si
grande, que ce jour-là le Greffier ne pût rien enrégistrer et fut-on
contraint d’abandonner le plaidoyé.” Here the high morbidity and the
symptoms, particularly cough and pain, are emphasized. In 1414,
Baliolanus describes again the high morbidity and symptoms, particularly
cough and hoarseness: “Eoque frigore humanis corporibus concepto ...
tussis maxima atque raucitas orta unde nullus pene ordo, aetas et sexus
liber evasit.” In 1411, Pasquier writes the following: “En 1411 y eut
une autre sorte de maladie dont une infinité de personnes furent
touchez, par laquelle l’on perdoit le boire, le manger et le dormir ...
toujours trembloit et avec le estoit si las et rompu que l’on ne l’osoit
toucher en quelques parts. Sans qu’aucune personne en mourut.”
Subsequent to 1510 descriptions have been as a rule more definite. There
are, however, exceptions to this statement and these fall in the
epidemics concerning which there is some dispute.
MANNER OF SPREAD.
More characteristic and more important from an epidemiologic standpoint
than the symptomatology in general, as we have discussed it, is the mode
of development of the epidemic as a whole.
_Human intercourse._—Before the days of bacteriology the contagiousness
of the disease was little discussed. Its infectiveness was in fact not
universally established until the epidemic of 1889–1890. One of the
first writers who attempted to see in the influenza a contagious disease
was Ch. Calenus who wrote in 1579: “Contagiosum dico morbum, quia etsi
quidem ab occulta quadam coeli influentia, principaliter eum profisci
haud dubium est ... eo in loco quo jam grassabatur inter homines citius
eos invadabat, qui cum affectis frequenter conversabantur, quam eos, qui
a consuetudine affectorum studiose abstinebant.” This keen observer saw
that those who carelessly exposed themselves to close contact with cases
of influenza were more likely to develop the disease than those who
protected themselves in every way possible. The “contagious” school
first developed in England, where Haygarth, Hamilton, Gray, Hull,
Duggard, Bardsley, and others, in 1775–1803 described the disease as
being not in the air, but in a specific contagion. Others who considered
influenza a contagious disease were Simonin, Lombard, Petit de Corbeil
(1837), Blanc (1860), and Bertholle (1876).
Watson (1847) quotes Cullen as saying that this species of catarrh
proceeds from contagion. He, himself, is not convinced of this fact. He
says the visitation is too sudden and too widely spread to be capable of
explanation in that way. “There are facts in the history of influenza
which furnish a strong presumption that the exciting cause of the
disorder is material, not a mere quality of the atmosphere; and that it
is at least _portable_. The instances are very numerous, too numerous to
be attributed to mere chance, in which the complaint has first broken
out in those particular houses of a town at which travelers have
recently arrived from infected places.... What I wish to point out now
is the fact that the influenza pervades large tracts of country in a
manner much too sudden and simultaneous to be consistent with the notion
that its prevalence depends exclusively upon any contagious properties
that it may possess.”
Parkes, writing in Reynolds’ System of Medicine in 1876, views the
subject more as we see it today: “The rapidity of the spread would seem
at once to negative any connection between human intercourse and the
propagation of the disease; yet there is some affirmative evidence. It
does not appear to follow the great lines of commerce; but when it has
entered towns and villages in which the investigation can be carried on,
it is curious how frequently the first cases have been introduced, and
how often the townspeople nearest the invalids have been first affected.
In this country especially, Haygarth in 1775 and 1782, and Falconer in
1802, collected so many instances of this that they became convinced
that its propagation was due entirely to human intercourse. So also,
when it passes through a house, it occasionally attacks one person after
another. But if it is introduced in this way it afterwards develops with
marvelous rapidity, for we cannot discredit the accounts of many
thousands of persons being attacked within a day or two, which is quite
different from the comparatively slow spread of the contagious diseases.
This _sudden_ invasion of a community makes it, to many persons, appear
highly improbable that any effluvia passing off from the sick should
thus so rapidly contaminate the atmosphere of a whole town.
“Still, we must remember how singularly, of late years, the knowledge of
the introduction of cholera by persons coming from infected districts
has increased, and how very striking are the instances of this kind
already recorded in several works on influenza.
“In some cases, again, isolation or seclusion of a community, as in
prisons, has given immunity; or at least that community has not been
attacked.”
The great rapidity of spread has caused even in 1918 some temporary
doubt as to the contagiousness of the disease. Thus, Zinsser wrote:
“The opinion of direct and indirect transmission from man to man is also
well supported by a detailed study of the epidemiology of individual
outbreaks. In our own experience with epidemics such as those at
Chaumont, Baccarat and other places, the suddenness with which the
malady attacked large numbers of people at almost one and the same time,
caused me at first to be exceedingly skeptical of accepting transmission
by contact as the only means of conveyance. We considered food and
insect transmission as possibilities, and tried our best to find grounds
for involving such agencies. But in every case we were forced to return
to the conclusion that direct and indirect contact between men came
nearest to doing justice to all observed facts.”
There have been many examples reported from personal experience to show
that influenza is transmitted from man to man. Two objections, however,
have had to be met, before this view was generally accepted. First, it
has been claimed by some that the disease spread more rapidly from an
assumed focus than individuals could travel, and second, that instances
were on record of cases occurring spontaneously in isolated communities.
Yet a third argument formerly raised against the contagious character of
the disease was the claim that it broke out in mass attacks, that large
numbers became ill on the same day without the occurrence of isolated
antecedent cases. The splendid work of epidemiologists following the
1889 epidemic appears to have answered all of these objections. Many,
such as Leichtenstern, have gone into great detail on this subject. In
fact, at that time this was the question of greatest importance. Today
we assume the correctness of the hypothesis, and pass on to
consideration of other subjects of more recent development. We will,
therefore, review very hurriedly some of the evidence quoted to prove
that influenza is transmitted only from man to man and only by human
intercourse.
_Isolated places._—Has it ever been shown that individuals completely
isolated from communication with communities where influenza is present
have, during an epidemic, developed the disease? Leichtenstern, after a
comprehensive review, concludes as follows: “We have not a single
example on record where influenza has attacked individuals in completely
isolated localities, as on mountain tops and mountain passes. Study of
this has been undertaken in Switzerland by F. Schmid. The same has been
true of ships at sea, as has been shown chiefly from the English Marine
Reports. There have been reports of influenza occurring in mid-ocean and
particularly in the earlier epidemics, but the information has been
insufficient.”
Parkes at even an earlier period observed: “I cannot but consider that
we require better evidence of ships being attacked in mid-ocean. In some
of the quoted instances the ships had been at a port either known to be
infected or in which influenza was really present, although it had not
become epidemic. As we are ignorant of the exact period of incubation
some men may have been infected before sailing.”
Critical investigation into stories of spontaneous infection in isolated
localities such as ships at sea and island lighthouses will quite
invariably demonstrate that these popular reports have been distortions
of the actual facts. One or two examples will suffice. Abbott records an
example: “An impression having gained some credence that influenza had
appeared on board the squadron of naval vessels which sailed from Boston
in December, 1889, while on their course across the Atlantic and before
their arrival in Europe, a letter was addressed by the writer to the
Bureau of Medicine and Surgery of the United States Navy for information
upon this point, to which a reply was received, as follows:
“The ‘Chicago,’ ‘Boston,’ ‘Atlanta’ and ‘Yorktown’ left Boston December
7, 1889, for Lisbon, Portugal. The first three arrived at Lisbon on
December 21st without having touched at any port _en route_. The
‘Yorktown’ arrived at that port December 23d, having, stopped about
twenty-four hours at Fayal, Azores.... Influenza first appeared on the
‘Chicago’ December 23d, on the ‘Boston’ December 28th, on the ‘Atlanta’
December 30th and on the ‘Yorktown’ December 28th.
“Influenza was prevailing in Lisbon at the date of arrival of the
squadron.”
In March, 1920, the author was notified of a somewhat similar story
which he undertook to trace. The results show well the inaccuracy of
verbal transmission through several individuals. A letter was first sent
to the Quarantine Officer at Portland, Maine: “It has been reported to
us that in a lighthouse just outside of Portland, Maine, there has been
a rather interesting prank played by influenza. We are told that three
men and one woman live in the lighthouse; that during the 1918 influenza
epidemic the woman contracted the disease while none of the men became
sick, and that in the present epidemic all three of the men became sick
with the disease and the woman remained well. It was claimed that they
had had no communication with the mainland for some time before the men
became ill,” etc.
The reply was as follows: “I have inquired of the Light House
Inspector’s office in Portland and they know of no stations to which the
terms of your inquiry would apply.
“At the Boon Island station, there are three keepers with families. At
the Half Way Rock station, there are three keepers but no woman. The
Inspector does not seem to know of any station where there are three men
and one woman.”
A second letter, sent to the Inspector of Lighthouses at Portland
brought corroborative information:
“The Boon Island Light Station was stricken by this epidemic in the
following manner: The keeper, his wife and five children were all
stricken, the keeper himself having had the hardest battle, having
apparently been subject to same while ashore in Portsmouth, N. H. after
provisions, supplies, etc. The 2d assistant’s wife and two children were
also stricken, but the 2d assistant, himself, and the 1st assistant
keeper did not contract the malady in spite of the fact that they were
all confined on a small island working together at the station.
“During the year 1920 none of the keepers or their families, consisting
of thirteen in number, were affected. The Halfway Rock Light Station
where three keepers are employed did not contract this malady either in
the years 1918 or 1920.
“For your information I might add that during the inspection trip in the
months of January, February and March, 1920, all of the light stations
in this district were visited, and it was found that they were all
enjoying good health and had not been visited by the epidemic, with the
possible exception of three stations which are located either on the
mainland or close to where the keeper or his family were able to visit
the nearby cities or towns.”
Although it has not been shown that completely isolated places have been
visited by the disease, there is abundant evidence that such places have
remained influenza free as long as the isolation has remained complete.
Islands and lighthouses, which have not been in communication with the
mainland, individuals living isolated on mountain tops, and ships at sea
remained free from influenza even in the presence of a pandemic, as long
as they did not come into communication with individuals sick with the
disease. The following places remained free from influenza throughout
the 1889 epidemic: the Isle of Man, several of the islands of the West
Indies, particularly the Bahamas, Granada and St. Lucia, also the
British Honduras, British Guiana, and the Seychelle Islands.
Even in 1918, when the paths of commerce reached nearly every portion of
the world, we have examples of relative immunity of isolated places.
Thus we know that the Esquimaux were attacked late in the course of the
pandemic, and we have the statement of Barthélemy who traveled in 1919
to some of the oasis towns of the Sahara Desert, and there discovered
that there had not only been no influenza up to that time, but also that
they had not even heard of the pandemic.
Another type of isolated place is the closed institution. As early as
1709, Lancisi remarked that the prisons of the Inquisition in Rome
remained free from influenza. Twenty-one prisons in Germany in 1889–90
remained entirely free from the disease. This was true of 39 prisons in
England, some of which were in cities where the epidemic was most
extensive. Linroth, who observed this same phenomenon in Sweden, makes
the wise remark that, “the influenza conquers more easily the space of
500 to 1,000 kilometers than it does the small barrier made by a prison
wall.” A convent in Charlottenburg housing one hundred women remained
entirely free during the 1889–90 epidemic.
As a rule institutions of this sort have been unable to maintain a
complete quarantine throughout the period of an epidemic, and the
relative immunity has been demonstrated more in late invasions, at a
time when the restrictions have become somewhat lax. Thus, in 1918,
Winslow and Rogers, report that in an orphan asylum in New Haven,
Connecticut, which had completely escaped during the month of October
when the epidemic was at its height, one of the Sisters and the priest
in charge came down with influenza about December 15th. By the 27th of
December 127 cases had occurred in the institution within twenty-four
hours, and by January 7th there had been 424 cases, with seven deaths
out of a total population of 464. The probable source of the sudden
outbreak of December 27th seems to have been the Sister first affected
who, when convalescent, resumed her duties in the kitchen, which
included the inspection and handling of the milk given out to the
children.
_Crowd gatherings._—Yet another phenomenon which would lead us to
conclude that human intercourse is the most potent factor in the
transmission of influenza is the fact that there is frequently a high
increase in the influenza rate following crowd gatherings. Parkes
observed long ago that persons in overcrowded habitations, particularly
in some epidemics, suffered especially, and several instances are on
record of a large school or a barracks being first attacked and the
disease prevailing there for some days, before it became prevalent in
the towns around.
In England, the weekly market played an important role in the spread of
the disease in 1889. One frequently saw such reports as that: “The first
case of influenza was a man who went to London daily.” Or, “All the
earliest cases were men going to London daily, while their wives and
families were later affected.”
In the epidemics at San Quentin Prison, it was noted that apices of
incidence usually occurred on Tuesday and Wednesday. During the first
epidemic it was these days of the second and third weeks. Stanley sees a
direct connection between this fact and the fact that every Sunday
morning large groups of the men were crowded together in a comparatively
small auditorium where they saw moving pictures. On Sunday, October
20th, they sought to eliminate this source of spread by having a band
concert in the open air, but the prisoners crowded around the band and
were loud in their cheers, and on the following day there was a large
increase in hospital admissions.
On November 24th after the second epidemic had apparently ceased the
picture shows were again started after having been closed for over six
weeks. The following Tuesday and Wednesday twenty-four well defined new
cases were admitted to the hospital. On Thanksgiving Day there was a
field meet between the various departments of the prison. About 200
prisoners took active part, while 1,600 prisoners were spectators. The
meet was held in the open air, but the prisoners were closely packed and
they cheered and yelled. For the three days following this celebration
there were 9, 5 and 8 patients admitted respectively.
In discussing the recrudescence of influenza in Boston in November and
December, Woodward remarks as follows:
“Whether or not it may be more than a succession of coincidences it is
certainly of interest to note that the November outbreak of influenza
showed itself three days after the Peace Day celebration on November
12th, when the streets, eating places and public conveyances were jammed
with crowds; that the December epidemic began to manifest itself after
the Thanksgiving holiday, with its family re-unions and visiting; and
that reported cases mounted rapidly during the period of Christmas
shopping, reaching a maximum a week after the holiday.” That this may
have been a coincidence is indicated by the fact that, according to
reports by Pearl and others this was not consistently true in other
large cities.
Dr. Meredith Davies records the case of a hostel in Wales accommodating
200 students. Infection was introduced on October 19th on the occasion
of a dance attended by some students from an infected institution in the
neighborhood. Four cases occurred on the 20th and within the short space
of five days seventy-nine students out of the 200 were attacked.
Parsons found numerous similar examples in the epidemic of 1889. In 1918
it was frequently observed that among American Soldiers in France, those
troops quartered in barracks suffered a much more rapid spread of the
disease than those billetted out among the houses of the towns.
_Mass attack._—Another argument formerly raised against the contagious
character was the claim that it broke out in mass attack, and large
numbers became ill on the same day without the occurrence of isolated
antecedent cases. The first cases of such epidemic diseases as the
plague and small pox became a matter of record because of the
accompanying high mortality, while in influenza, with its relatively low
death rate the record usually begins only after a comparatively large
mass of individuals have been attacked.
Watson in 1847 observed as follows: “Although the general descent of the
malady is, as I have said, very sudden and diffused, scattered cases of
it, like the first droppings of a thunder shower, have usually been
remembered as having preceded it. The disorder is most violent at the
commencement of the visitation; then its severity abates; and the
epidemic is mostly over in about six weeks. Yet the morbific influence
would seem to have a longer duration. In a given place nearly all the
inhabitants who are susceptible of the distemper suffer it within that
period, or become proof against its power. But strangers, who, after
that period, arrive from uninfected places have not, apparently, the
same immunity.”
Parkes in 1876 observed that, “When the disease enters a town it has
occasionally attacked numbers of the inhabitants almost simultaneously.
But more frequently its course is somewhat slower; it attacks a few
families first and then in a few days rapidly spreads; the accounts of
thousands of persons being at once attacked at the onset of the disease
are chiefly taken from the older records, in which the suddenness of the
outbreak is exaggerated. Frequently, perhaps always, in a great city the
outbreak is made up by a number of localized attacks, certain streets or
districts being more affected than others, or being for a time solely
affected, and in this way it successively passes to different parts of
the city. It has generally occurred in a great city before appearing in
the smaller towns and villages round it and sometimes these towns,
though in the neighborhood, have not been invaded for some weeks.
“In some cases and perhaps a large number, it breaks out after persons
ill with influenza have arrived from infected places.
“The decline in any great town is less rapid than its rise, and usually
occupies from four to six weeks, or sometimes longer.”
Detailed studies of the Munich epidemic of 1889 and numerous similar
studies of the recent epidemic, which will be referred to later, have
shown a period of two or three weeks of steadily increasing numbers of
cases before the height of the epidemic was reached.
_Droplet infection and spread through inanimate objects._—The actual
mode of spread of the virus of influenza from one individual to another
is unknown. The more generally accepted explanation is that the
infecting agent leaves the body through the respiratory tract, usually
in the spray of coughing or talking; contagion is by droplet infection,
as is sometimes the case in other respiratory infections. Thorne and
others have called attention to the capillary congestion of the
conjunctivae very early in the disease. They suggest that possibly the
mucous membrane of the eye is the site of infection.
There has recently been considerable discussion concerning the spread of
influenza through inanimate objects.
Leichtenstern reviews the reports of 1889–93 in which influenza was
supposed to have been transmitted through wares, merchandise and other
inanimate objects. He concluded that the evidence in all of the cases
cited was insufficient for conclusive proof. Such an example was the
supposed importation of the disease in goods sent from Russia to the
Grands Magazins du Louvre at Paris. In one day 100 people became ill and
in a few more 500 were sick with influenza. The explanation was that the
germs had been imported in goods sent from Russia to the store. Detailed
investigation showed that this could not have been the case because no
goods had been received from Russia for a period of three years. Another
example is that of one of the two winter caretakers at the St. Gothard
Hospice. One of the two men went down into the valley where he purchased
supplies. Ten days after his return the man who had remained in the
Hospice fell ill with influenza while his comrade remained well. It was
stated that influenza was introduced into Basel by goods shipped to that
place from the Magazins du Louvre in Paris. The first case occurred in a
man who had been working at unpacking these goods.
Lynch and Cumming believe that droplet infection plays but a minor role
in the spread of sputum-borne diseases, but that insanitary methods of
washing dishes and eating utensils was the chief cause for the high
rates of “sputum-borne” infections both in army and civilian life in
1918. They found that among 31,000 troops eating from tableware which
was cleaned by kitchen police, the influenza rate was 51 per 1,000,
while among 35,000 eating from mess kits which each individual washed
himself the rate was 252 per 1,000. “Eighty-four per cent. of the cases
occurred among those whose hands were contaminated by washing their own
eating utensils.”
Among 17,236 employees of hotels, restaurants and department stores, who
ate from machine washed dishes, there occurred 349 cases of influenza,
while among 4,175 who ate from hand washed dishes there were 429 cases.
The rate was but 20 per 1,000 in the former, while in the latter group
it reached 103 per 1,000. Here again the chances of infection between
the two groups were as one is to five.
These authors have records covering 252,186 individuals in scattered
institutions in the United States. Among those eating from machine
washed dishes the rate was 108 per 1,000 while those eating from hand
washed dishes suffered at the rate of 324 per 1,000. The ratio was 1 to
3 between the two groups. Seventy-five per cent. of the cases occurred
in that group which ate from dishes not disinfected with boiling water.
They do not state the number of individuals in each of the two groups.
Lynch and Cumming claim that in the act of coughing only a few organisms
are expelled from the mouth, rarely over 1,500, and conclude that
transmission by direct contact through the air route but rarely, if
ever, takes place. While about 1,500 organisms are expelled onto the
floor by an act of coughing, a sterile glove wiped across the lips may
pick up nearly 2,000,000 organisms. Such organisms may be readily
transferred to inanimate objects which are handled by many people.
Hemolytic streptococci and pneumococci may be isolated with great
regularity from the hands of carriers or patients, from table ware,
inanimate objects touched by these patients, and from floor dust.
Diphtheria and tubercle bacilli have been isolated from the hands and
eating utensils of patients. The average count of a large number of
restaurant dishwater specimens was 4,000,000 bacteria per c.c. The
temperature of this water averaged 43° C. and the dishes were
practically never scalded. The water was often so highly polluted, “that
the dishes are more highly contaminated after they are washed than
before washing begins. The spoon or fork is often freer from organisms
just after being used by the restaurant patron than when taken from the
restaurant’s polluted dish water.”
Major John S. Billings, epidemiologist at Camp Custer, reported that one
of the larger organizations did not properly observe the regulation
requiring that all mess kits and table equipment be properly sterilized.
The disease appeared early and spread unusually rapidly in this
particular organization.
In summarizing the subject of transmission through utensils, we may say
that the evidence is suggestive but inconclusive. It is possible, even
probable, that this is one mode of transmission. That it is the most
important has not been proved. Lynch and Cumming do not take into
consideration that the regiments with more sanitary methods of cleansing
the dishes are apt to be those regiments with more sanitary habits
throughout their daily routine. Those restaurants using mechanical dish
washers are usually the cleaner restaurants.
Pontano in Italy is quoted by the Office International d’Hygiène
Publique as having observed in his epidemiological study that there was
a constant connection between the living conditions and the severity of
the complications. Notable differences were observed in neighboring
houses according to the hygienic conditions of the various households.
_Healthy carriers and convalescents._—Leichtenstern, who apparently
accepted the Pfeiffer bacillus as the cause of influenza, did not
believe that the disease could be transmitted by healthy carriers. He
based this assumption on the statement, made by Pfeiffer, that the
influenza bacillus was only found in acute influenza cases. In the past
few years it has been abundantly shown, however, that the influenza
bacillus can and does exist on the mucous membranes of healthy
individuals.
The outbreak in an orphan asylum in New Haven has been previously
described. There the probable source of the sharp outbreak of December
27th seemed to be the sister who, on convalescence, resumed her duties
in the kitchen. There she inspected and handled the milk served to the
children. This suggests the possibility of infection being propagated by
convalescents and by food.
At present we do not know whether or not a patient remains infectious
after the acute symptoms have subsided; we are ignorant as to whether a
convalescent patient can transmit the disease; and we are not certain
whether the organism found in healthy carriers is virulent or not. The
information at hand strongly indicates that apparently healthy
individuals may transmit the infection, but the wide distribution of the
disease, with multiple possible sources of infection for each
individual, and the relative insusceptibility of experimentally exposed
individuals has made it impossible so far to answer these questions
satisfactorily.
GENERAL MANNER OF SPREAD IN INDIVIDUAL LOCALITIES.
Having discussed the mode of propagation of influenza among individuals
we will follow the disease as it attacks one person after another in a
community and study the epidemiologic picture, drawn no longer with the
individual as a unit, but with the community as the unit.
We must here distinguish between a primary epidemic, the first wave of a
progressing pandemic, and the secondary type in which may be grouped
those large or small recurrences which light up for a period of one to
three or more years after the primary wave.
_Primary type of epidemic._—One of the first important statistical
studies on this subject was that of P. Friedrich who charted the
influenza morbidity in Munich between the months of December, 1889, and
February, 1890. Similar observations have been made by Parsons, Raats,
Linroth, and H. Schmid, following the 1889 epidemic.
Between the occurrence of the first known case of influenza and the time
of the first very definite increase in influenza incidence in a
community, which interval may be termed the invasion period, there is as
a rule two weeks. During this period, of course, more and more cases are
occurring, but remain usually sufficiently isolated to attract no public
notice. From this point the epidemic develops very rapidly and reaches
its peak, usually within two or at most three weeks. In another two or
three weeks the incidence has fallen away nearly to normal. The epidemic
period comprises from four to six weeks, or, including the invasion
period, an entire duration of six to eight weeks. This is the picture
produced in a community by a primary uncomplicated epidemic of
influenza. Greenwood well describes the salient features of a primary
epidemic as “first a rapid and quasi-symmetrical evolution, and second,
a frequency closely concentrated around the maximum.” In other words the
duration is short, the rise to a peak rapid, and the subsequent fall
equally rapid. He showed that in the July and August, 1918 epidemic in
Great Britain nearly 80 per cent. of the total incidence in the
localities studied was grouped within three weeks time. His curve
corresponds so well with that of the Munich epidemic that he is able to
superimpose them (Chart I). The rapid rise to a peak, almost explosive
in character, more characteristic of this disease than of any other, is
to be explained by the high degree of invasiveness of the organism, by
the short period of incubation, by the fact that many of the sick
continue at their work, thus spreading the disease, and by the
non-immunity of large masses of people, together with the fact that the
transmission of a respiratory infection is accomplished much more easily
than is any other type of infection.
The author holds that the infrequency of immunity is a most important
factor in the production of this type of outbreak. The mode of
transmission of influenza is the same as that of other respiratory
diseases. The infectivity is probably no greater than that of measles,
although that indeed is relatively great. The means of transmission are
presumably the same in each. Were we able to develop an immunity for
influenza of as high degree and permanence as we possess against
measles, pandemics of influenza would disappear. We wish to emphasize
that the primary type of curve is a phenomenon not peculiar to
influenza, but that under certain circumstances it may be found in other
infectious diseases, and that it would be found more frequently in the
other diseases if the immunity developed against them was of as short
duration as it appears to be against influenza. If, for example, measles
were to break out in a large group of individuals, none of whom had had
the disease, the type of curve would be the same. We will produce
evidence supporting our theory under another subject. Of course, other
factors such as short incubation period and unusual opportunities for
spread through mildly ill individuals play a not unimportant role.
CHART I.
[Illustration:
The curves of incidence of influenza in Munich, and of deaths in
London during the 1889 and subsequent epidemics. (_Greenwood._)
]
_Secondary type of epidemic._—There is a decided difference between the
curve of a primary wave as it appears in the onward rush of a new
pandemic and that of a secondary wave occurring at a greater or less
interval following the primary spread. A secondary epidemic affects,
according to Greenwood, a relatively small proportion of the population,
is slower in reaching its maximum, and thereafter declines slowly and
irregularly, more slowly than it increases. The distribution of the
curve is less symmetrical and there is less concentration around the
maximum. A secondary epidemic may be characterized by a much higher
fatality than a primary one.
We believe that the configuration of a secondary type of wave is due
chiefly although not entirely to a certain degree of residual immunity
in a large number of individuals remaining from the first spread. There
is a striking similarity between Chart I and Chart XXVIII, the latter
showing the measles incidence in epidemics among rural or chiefly
non-immune troops in the United States army. Chart XXIX shows a similar
epidemic among urban or chiefly immune individuals. Here the curves
correspond more to those of a secondary type of influenza epidemic. Thus
we see that, in the absence of immunity, other infectious diseases may
produce the primary type of curve, and that this curve is not a feature
of influenza alone.
A striking difference between the two types of waves of influenza is the
uniformity and relative constancy of the primary type as contrasted to
the great variation in the secondary type. The story of the first spread
of influenza in one community is usually similar to that of its spread
in any other community. Certain exceptions will be alluded to later. But
in the case of recurrent epidemics we may find them more severe or much
milder; we may find that they attack a large number of individuals or a
very few; we may even find an entire absence of recurrent epidemics in
certain communities. The primary curves are relatively uniform; the
secondary curves are variable.
Between 1889 and 1894 in England there were four epidemics. The first
was primary, symmetrical, and lasted between December and February,
1889–90. The second was asymmetrical and much more fatal in the
localities studied by Greenwood. It occurred in the spring and summer of
1891. There was a third epidemic in the autumn and winter of 1891–92 and
a fourth occurred from November, 1893 to January, 1894. The third
epidemic, according to Greenwood, showed some tendency to revert to the
primary type in respect to symmetry, while the fatality rate partook of
the character of a secondary epidemic.
Creighton writes: “That which chiefly distinguishes the influenza of the
end of the nineteenth century from all other invasions of the disease is
the revival of the epidemic in three successive seasons, the first
recurrence having been more fatal than the original outbreak, and the
second recurrence more fatal (in London at least) than the first. The
closest scrutiny of the old records, including the series of weekly
bills of mortality issued by the parish clerks of London for nearly two
hundred years, discovers no such recurrences of influenza on the great
scale in successive seasons.”
Greenwood, who has studied this subject in great detail in England,
discusses Creighton’s remarks as follows: “He would be a bold man who
challenged the accuracy of Creighton upon a point of historical
scholarship, and I have only to suggest that there are faint indications
of increased mortality in years following primary epidemics of influenza
prior to the nineteenth century. Thus 1675 was a year of primary
epidemic influenza, fully described in Sydenham’s Observationes Medicae.
“The nature of the succeeding constitutions is not clear, but the deaths
‘within the bills’ for 1676 were considerably more numerous than in
1675, although smallpox, fever and ‘griping of the guts’ were noticeably
less fatal.
“In the English Responsoria (1, 54) the epidemic constitution of 1679 is
described as a recurrence of that of 1675—that is, as having the
features of primary epidemic influenza. In the five following years
intermittents prevailed, and in one (1684) the mortality much exceeded
that of 1679, although the deaths from smallpox were fewer. Again, a
hundred years later, in 1782, there was a famous summer epidemic of
influenza in London which gave rise to much discussion. The London
mortalities in 1782 and 1783 were, however, almost equal, when the
smallpox deaths (which were nearly three times as numerous in 1783 as in
1782) are subtracted from the total mortality of each year.
“Whether these vague indications are sufficient to permit of our
thinking that the epidemic constitution of 1889–94 was not entirely
unprecedented is disputable. But the contrast of the latter period with
the preceding single epidemic of 1847–48 is striking; that was a primary
epidemic without important sequelae.
“We have now to consider whether our experience this year is concordant
with that of the early nineties, a reversion to the earlier type, or a
new phenomenon.”
After comparing the 1889 curves with those for the July, 1918, outbreak
in England, Greenwood concludes: “I believe that the evidence just
presented establishes a substantial identity between the summer outbreak
of 1918 and the primary wave of 1889–90. We do not need to appeal to any
new factor arising out of the war to account for it.
“I next consider the secondary epidemic which we are now experiencing
(October, 1918). Evidently our knowledge of the events in 1891 would
lead us to feel no surprise at the emergence of a secondary wave,
although we could not be sure that the precedent of 1847 would not be
followed.
“The summer epidemic of 1918 in the Royal Air Force included nearly 80
per cent. of the total incidence within the three weeks containing the
maximum, and the Munich epidemic included just over 80 per cent. within
the same limits. Now if the current epidemic has reached its maximum,
not more than 65 per cent. of the incidence will probably be so
concentrated, and the duration will therefore be longer than in the
summer; if, as suggested by the ratio of the last two ordinates, the
maximum is not yet attained, then the quota of the three first weeks is
likely to be still smaller and the complete duration still longer.
“The diagram of factory sickness leads to the same inference, which is
that, from the standpoint of prevalence, the present is a typical
secondary epidemic, congruent with that of 1891.
“It appears, then, that the origin of the summer epidemic must be
explained upon such epidemiological principles as will account for the
primary wave of 1889–90, that the current outbreak is in pari materia
with that of 1891, its excessive mortality being mainly due to the
accident of season, aided by the special circumstances of overcrowding
and fuel shortage which are due to the war. In a word, this is not
essentially a war epidemic.”
Wutzdorff found that in some towns, particularly in North Germany, the
1891–1892 wave was almost as extensive as that of 1889–90 had been in
other places, but that in general the morbidity in Germany was much
lower. He bases these conclusions on a study of the extent of crowding
in the hospitals in the two years, on statistics of government
physicians, etc.
In Europe the recurrent epidemics of 1891 increased as a rule very
gradually, developed slowly, reached their high point frequently after
many weeks, and as gradually decreased. The epidemic duration in the
winter of 1891–92 lasted four or five months. The morbidity in spite of
the longer duration was decidedly less. This is very different from the
explosive appearance of 1889 when the peak was reached in fourteen days
and the whole epidemic had been completed in six to eight weeks. There
were some exceptions to this rule, as in Yorkshire, England, where the
epidemic broke out suddenly between the 11th and 13th of April, 1891,
had reached its peak after ten days, and for another twenty days
declined. Especially interesting was Sheffield, where the first spread
began gradually and ran a slow course, while the second epidemic of 1891
began explosively, lasted a short time and declined rapidly, but showed
a significantly greater mortality than that of 1889.
The experiences in various communities in the United States have been
not unlike those described for European cities. Abbott in describing the
successive epidemics in Massachusetts remarked that the 1889–90 spread
manifested itself by a sudden rise in the mortality from influenza and
pneumonia, beginning about December 20th and culminating in the middle
week of January, thereafter falling off quite suddenly in February to
about the usual rate for these diseases. The second epidemic two years
later began with a more gradual rise in October and November and then
increased sharply in December, continued for nearly three weeks at its
maximum in January, and declined nearly as sharply as in the previous
epidemic two years before.
Winslow and Rogers who have studied the 1918 epidemic as it affected the
various towns of Connecticut observed that the outbreak in a given
community generally occupied a period of from six to eight weeks, and
was steep and abrupt in communities which were badly hit, flatter and
more gently sloping in those which escaped lightly. Also the outbreak
was more severe in communities receiving the infection early than in
those later affected.
_Mortality curves._—Pearl has studied the epidemic constitution of
influenza in forty-two of the large cities of the United States. He has
plotted the annual death rate per 1,000 population from all causes in
each week, from the week ended July 6, 1918, up to January 1, 1919, and
observed a very distinct difference in the type of curve for deaths from
all causes during the epidemic period in the various cities. These
differences have been chiefly in respect to the severity and suddenness
with which they were attacked. Thus Albany, Boston, Baltimore, Dayton
and Philadelphia show an initial explosive outbreak of great force,
while Atlanta, Indianapolis, Grand Rapids, Milwaukee and Minneapolis
exhibit a much slower and milder increase of the mortality rate. In
Albany and Baltimore the curve of the first epidemic outbreak rises to a
peak and declines at about the same rate. In Cleveland and St. Paul, on
the other hand, the rate of ascent to the peak is very rapid, while the
decline is slow and long drawn out.
Some of the cities, such as Albany, show but a single well defined peak
in the mortality curve. Others, such as Boston, New Orleans and San
Francisco show two peaks; while still others, like Louisville, show
three well marked peaks.
Usually the first was the highest and the second and third were
progressively lower. Milwaukee and St. Louis, on the other hand, showed
second peaks higher than the first. The usual phenomenon, however, was a
large first wave followed by smaller ones.
The highest, or maximum peak rate of mortality during the epidemic
varied greatly, from 31.6 per 1,000 in the case of Grand Rapids, to
158.3 per 1,000 in the case of Philadelphia.
The death rates which were of the most frequent occurrence were,
generally speaking, rates below 70 per 1,000 per week.
The date of the week in which the maximum peak rate occurred was
earliest in Boston and Cambridge, where it occurred October 5th, and
latest in Grand Rapids, Milwaukee and St. Louis (December 14th).
Thirty-one of the 40 cities studied had attained the peak rate of
mortality prior to November 2d. In the case of Milwaukee and St. Louis
the maximum peak was the second peak, whereas in Grand Rapids it was the
first peak that was so late. Sixty-five per cent. of the 40 cities
showed two distinct peaks in the mortality curve, while 15 per cent. had
one peak, and 8 or 20 per cent. had three peaks.
“It appears clearly that there was a definite tendency for the two-peak
cities to fall into two groups in respect of the time elapsing between
first and second peaks. About a third of them had the second mortality
peak around eight weeks after the first peak. The remaining two-thirds
had the second peak, on the average, about thirteen weeks after the
first. The three-peak curves had the second peak on an average 7.1 ± 0.3
weeks after the first, and the third peak on an average 13.1 ± 0.3 weeks
after the second. The cycle in the epidemic waves would therefore appear
to be nearly a multiple of seven weeks rather than the ten weeks
tentatively deduced from the dates of peaks. There the process of
averaging obscured the true relations.”
_Duration of explosive outbreak._—The range of the duration of the first
outbreak of epidemic mortality is great, varying from five weeks in
Richmond, Virginia, to twenty-three weeks in Atlanta, Georgia. Twenty of
the cities, one-half the total number, showed a duration of ten weeks or
less, while in the other half the duration was eleven weeks or more. The
mean duration of epidemic mortality in the first outbreak was 11.90 ±
0.55 weeks. The ascending limb of mortality rate was rapid in nearly all
cities. The descending limb was usually slower. In 34 of the 40 cities
it required four weeks or less time for the mortality rate to pass from
normal to its epidemic peak. But in only half as many (17) of the cities
did the rate come down from its peak to normal again in a period of four
weeks or less. The mean time from normal mortality rate to peak was 3.90
± 0.21 weeks. The mean time from peak mortality rate to normal was 8.00
± 0.50 weeks. Thus it took about twice as many weeks for the mortality
curve to come back from its peak to normal, as were required for the
increase from normal to peak at the beginning of the explosion. This is
on the average. The ascending limb occupied about a month and the
descending limb two months.
Pearl’s curves which have been copied in this report (Charts II to VII)
enable us to follow his conclusions. Pearl offers a partial explanation
for the variations in the different cities. There can be no doubt but
what many factors play a role in the causation of these variations, and
it is to be regretted that up to the present no statistics for smaller,
more homogeneous communities have as yet been reported which could be
compared with Pearl’s excellent work on the large cities of the country.
Were his work supplemented by records from smaller towns in which the
varying factors are less numerous, in which there is less occupational
variation, additional conclusions could probably be reached. The
unfortunate feature is that as a rule statistics from the smaller cities
and towns are less reliable.
From a detailed mathematical study of influenza in 39 of our largest
cities, done chiefly by the means of multiple correlation, with the hope
of being able to explain the differences in the epidemic curves of
weekly mortality in the various cities, Pearl concludes as follows:
“The general conclusion to which we come from an examination of the
correlation data assembled to this point is that these four general
demographic factors, density of population, geographical position, age
distribution of population, and rate of recent growth in population,
have practically nothing to do, either severally or collectively, with
bringing about those differences between the several cities in respect
to explosiveness of the outbreak of epidemic mortality in which we are
interested. Significantly causal or differentiating factors must be
sought elsewhere.”
CHART II.
[Illustration:
Death rates from all causes by weeks in certain large cities of the
United States during the winter of 1918–19. (_Pearl._)
]
CHART III.
[Illustration:
Death rates from all causes by weeks in certain large cities of the
United States during the winter of 1918–19. (_Pearl._)
]
CHART IV.
[Illustration:
Death rates from all causes by weeks in certain large cities of the
United States during the winter of 1918–19. (_Pearl._)
]
CHART V.
[Illustration:
Death rates from all causes by weeks in certain large cities of the
United States during the winter of 1918–19. (_Pearl._)
]
CHART VI.
[Illustration:
Death rates from all causes by weeks in certain large cities of the
United States during the winter of 1918–19. (_Pearl._)
]
CHART VII.
[Illustration:
Death rates from all causes by weeks in certain large cities of the
United States during the winter of 1918–19. (_Pearl._)
]
Concerning geographical position, he did find some slight relationship
with linear distance from the city of Boston, where the epidemic was
supposed first to have begun in this country:
“This result means that the greater the linear distance of a city from
Boston the less explosive did the outbreak of epidemic mortality in that
city tend to be. This is in accord with the general epidemiological rule
that the force of an epidemic tends to diminish as it spreads from its
primary or initial focus. It must be noted, however, that the
correlation coefficient in this case is not large. It is barely past the
value where it may safely be regarded as statistically significant. This
fact may probably be taken to mean that influenza does not follow the
epidemiological law referred to with anything like such precision as do
some other epidemic diseases, notably poliomyelitis.”
These factors having been found to be of little value in his attempt to
explain the varying curves in the 39 different cities, Pearl next
correlated the explosiveness of the epidemic mortality with deaths from
all causes, deaths from pulmonary tuberculosis, from organic heart
disease, from acute nephritis and Bright’s disease, from influenza, from
pneumonia (all forms), from typhoid fever, from cancer and from measles,
in the various cities.
“The outstanding fact which strikes one at once from this table is the
high order of the correlation which exists between the explosiveness of
the outbreak of epidemic mortality in these communities and the normal
death rate from certain causes of death in the same communities. In the
first four lines of the table the correlation coefficients range from
about 6 to more than 10 times the probable errors. There can be no
question as to the statistical significance of coefficients of such
magnitude.
“The highest correlation coefficient of all is that on the first line of
the table, for the correlation of epidemicity index with death rate from
all causes. The existence of this high correlation at once indicates
that an essential factor in determining the degree of explosiveness of
the outbreak of epidemic influenza in a particular city was the normal
mortality conditions prevailing in that city. In the group of
communities here dealt with, those cities which had a relatively high
normal death rate had also a relatively severe and explosive mortality
from the influenza epidemic. Similarly, cities which normally have a low
death rate had a relatively low, and not sharply explosive, increase in
mortality during the epidemic.
“It will also be noted that the correlation in the next three lines of
the table, namely those of pulmonary tuberculosis, so-called, organic
diseases of the heart, and chronic nephritis and Bright’s disease, are
of the same order of magnitude as that between the death rate from all
causes and the explosiveness of the epidemic outbreak of influenza.”
Pearl suggests that this correlation might arise because of differences
in the constitution of populations in the different cities, or, that it
was a factor of geographical position, such as the distance from the
Atlantic seaboard; but that even after correction of the results for age
distribution and geographical position, the net correlations were
actually higher than were the gross uncorrected correlations.
“We may conclude that the most significant factor yet discovered in
causing the observed wide variation amongst these 39 American cities in
respect of the explosiveness of the outbreak of epidemic influenza
mortality in the autumn of 1918 was the relative normal liability of the
inhabitants of the several cities to die of one or another of the three
great causes of death which primarily result from a functional breakdown
of one of the three fundamental organ systems of the animal body, the
lungs, the heart and the kidneys.”
Winslow and Rogers studied the relation of the pneumonia death rate from
1901 to 1916 to the influenza death rate of 1918 in 40 large cities of
the United States and found a distinct correlation. The cities which
have been characterized by a high pneumonia rate in the past are
precisely the cities which suffered most severally in the 1918 outbreak.
This is not due especially to virulent types of pneumonia organisms in
certain sections of the country because they found this same high
correlation between total death rates and influenza death rates, in the
same cities.
They believe that these high correlations may be the result of
weaknesses in the population due to high incidences of organic diseases
and tuberculosis in earlier years, or more probably that the correlation
is an indirect one, due to the relation between each of the factors
studied and one or more underlying conditions affecting both, such as
age distribution of the population, race distribution, or social and
economic conditions in the various cities studied. Or, finally, it may
be that the high rate from tuberculosis and organic disease in 1916 was
due to these latter factors, while the high incidence of influenza was
due chiefly to proximity to the original focus of infection. None of
these explanations are considered entirely satisfactory.
It is important to call attention to the fact that the American
observers quoted have been studying the death rate from influenza as it
is revealed in the increase of death rate from all causes, whereas
Leichtenstern and Wutzdorff, and Greenwood, in his studies in the Royal
Air Force have concerned themselves with _morbidity_. The comparison of
morbidity and mortality cannot be easily made as we will show when
discussing these two subjects, so we cannot conclude that the work of
Pearl and of Winslow and Rogers is at variance with the other work
quoted. The mortality curves form another characteristic of the local
spread of influenza in a community.
It is characteristic of influenza that the curve of deaths does not fall
as rapidly as does the curve for influenza cases. Thus in morbidity
curves we may expect to find a symmetrical curve for a primary epidemic,
but the mortality is rarely if ever symmetrical, the curve rising
rapidly and falling very much more slowly.
_Morbidity curves in 1920 recurrences._—The curves of influenza
incidence in the recurrence of 1920 have varied in different localities,
but in certain communities where the record has been carefully reported
the epidemic appears to be characterized by a symmetrical evolution and
usually a lower death rate as compared with 1918. The curve of incidence
in the State of Massachusetts in January, February and March, 1920, is
symmetrical, if anything falling away more rapidly than it ascends, and
the duration is at least ten weeks. The crest of the influenza wave in
Massachusetts was reached on February 4th, 5th and 6th. The peak is
recorded as being in the week of February 7th.
During the 1920 epidemic the author made a house-to-house canvass in six
representative districts in the city of Boston covering a population of
10,000 individuals. The curve of incidence of influenza corresponds
closely with the curves for the city and the state as a whole. The peak
was reached in the same week, the week ending February 7th, the curve
was symmetrical, and the duration of the entire epidemic was about the
same. The morbidity rate for 1920, according to our influenza census,
was but half of that for 1918 for the same population. The recurrent
epidemic as we will show later was decidedly milder (see Chart XVIII).
In Detroit the 1920 epidemic reached its peak for morbidity on the 9th
day, and that for mortality on the 16th. In 1918 the morbidity peak was
not attained until the 15th day and the death peak on the 22d. The
recurrent outbreak had nearly run its course within three weeks. The
following comparison between the influenza incidence in 1918 and 1920 in
Detroit is taken from a report by H. F. Vaughan, Commissioner of Health
for that city. In it is shown a comparison of the total figures on the
twenty-seventh day of each of the two epidemics:
_A Comparison of the 1918 and 1920 Epidemics of Influenza in Detroit.
Statistics Made to Include Through the Twenty-seventh Day of Each
Epidemic._
═══════════════════╤════════════╤════════════╤════════════╤════════════
│ │ │ Normal │ Excess
│ │Deaths from │ influenza │ influenza
│ Influenza │ influenza │ and │ and
│ cases │ and │ pneumonia │ pneumonia
│ │ pneumonia │ deaths for │deaths above
│ │ │this season │ normal
───────────────────┼────────────┼────────────┼────────────┼────────────
1920 (Jan.–Feb.) │ 11,202│ 1,642│ 197│ 1,445
1918 (Oct.–Nov.) │ 16,423│ 1,286│ 124│ 1,162
───────────────────┴────────────┴────────────┴────────────┴────────────
There had been fewer cases reported on the twenty-seventh day of the
1920 epidemic, but these had resulted in a greater number of deaths. On
this day the recurrent epidemic had run its course, while the 1918 one
was still in full swing. On the twenty-seventh day of 1918 there were
137 influenza cases reported and 49 deaths. On this day in 1920 there
were but 24 cases and 34 deaths. Thus the second outbreak was of shorter
duration, but was more deadly while it lasted.
Seven weeks of the 1920 epidemic in Detroit killed 0.20 per cent. of the
population, two out of every one thousand people. A similar period at
the beginning of the epidemic of 1918 witnessed the death of 0.17 per
cent. of the population. This was a smaller number, but the epidemic at
this time had not completed its course, and continued to be more or less
prevalent for twenty-one weeks, resulting finally in the death of 0.28
per cent. of the population. The recurrent epidemic was more highly
fatal, but, being of shorter duration, Detroit actually suffered less
from it.
SPREAD IN COUNTRIES AND CONTINENTS.
The spread of influenza is usually not limited to a single community.
Almost invariably it will travel on to another locality, carried thither
by human intercourse, and will there build again a local epidemiologic
picture more or less modified by changes in the environment and changes
in the virulence of the virus itself.
_Spread, in primary waves._—Reference to the table of epidemics in
history will show that in many of the epidemics and in most of the
widespread epidemics and pandemics there appears to have been a
definite, clearcut, direction of spread from one locality to others. In
the recent literature there has appeared considerable discussion
concerning the site of origin, the endemic focus of pandemic influenza.
Briefly the question raised is as to whether there are single or
multiple foci. We will for the time ignore this perplexing question. In
either case, after the influenza virus has once attained such
communicability as to produce a pandemic it does follow a direct course
over countries and continents. This may be followed in resumé in our
table.
The disease does not at any time spread more rapidly than the available
speed of human communication between the areas affected. If influenza
does appear simultaneously in two widely separated communities without
having been brought there from a common source it must be that it arose
spontaneously from simultaneous increase in virulence of the virus in
those localities.
Influenza was prevalent in Turkestan, Western Asia, in May of 1889. It
spread first to Tomsk in Siberia and did not appear in Petrograd until
the end of October. By the middle of November it had reached Berlin and
Paris, and one month later it was epidemic in New York and Boston. Four
months had been required for the disease to reach Petrograd from Bokhara
in Turkestan, while within two months thereafter it had traveled from
Russia to the United States. In both cases the rapidity of spread
corresponded to the rapidity of the means of communication of the
locality; the caravan in Turkestan and the transatlantic liner to
America. North America was widely infected in January of 1890. So, also,
Honolulu, Mexico, Hong Kong, Japan. Ceylon first experienced the
epidemic early in February, India at the end of the month, Borneo and
Australia on the first of March, Mandalay towards the first of May,
China and Iceland in July, Central Africa in August and Abyssinia in
November of 1890.
It should be noted that influenza was reported to have been prevalent in
Greenland at about the same time that it was in Bokhara. There appears
to have been no relationship between these two outbreaks.
The spread of the pandemic may be followed also by recording the period
of greatest mortality in the various cities. This period at Stockholm
followed that at Petrograd by three weeks, and that of Berlin by another
week. The period for Paris was a week later than for Berlin, that for
London another week later, and that for Dublin three weeks later than
that for London. The week of highest mortality in Dublin was later than
that for New York or Boston.
The earlier epidemics progressed more slowly. That of 1762 prevailed in
Germany in February, in London in April, in France in July, and in
America in October. In 1782 it attacked London in May, Exeter two weeks
later and Edinburgh early in June. In 1830–1832 the spread from Moscow
and Petrograd through Germany required no less than eight months to
cover the latter country.
In 1872 the time required for spread from Leipzig to Amsterdam was
eighteen days, the same time that was required for a merchant in the
latter town to reach Leipzig.
There are many instances on record in which influenza has passed by
small towns in its onward course to attack a larger city and only at
some later date has the small town, not on the main line of
communication, been affected. Not only is the speed of transportation
between two communities of importance, but also the volume of the
transportation undoubtedly plays a part in the rapidity of development
in a second locality. When the disease is carried by a vessel the first
places to be attacked are the seaports and the coast towns, be the land
a continent or an island. From there it spreads inland either rapidly or
slowly according to the transportation facilities. Formerly the question
was raised whether influenza spread in continuous lines or radiated in
circles. Naturally it follows the direct lines of communication, most of
which are radially distributed around large centers.
Leichtenstern calls attention to the fact that in the 1898 epidemic, as
in the previous one, the general direction of spread was from East to
West across Europe. This was also true of the epidemics of 1729, 1732,
1742, 1781, 1788, 1799, 1833, and 1889.
There have been in Europe two general routes followed by pandemics, a
Northern one through Russia and following the lines of travel into
Germany and through the countries of Europe; and a Southern path coming
from Asia, through Constantinople, and entering Europe from the South,
particularly Italy. With the latter, after reaching Europe, the spread
is northerly; with the former it is southerly, and usually Spain was the
country last infected.
In the United States as well, pandemic influenza usually has spread from
East to West, entering the country at or near New York or Boston, and
spreading West and South. This was true in the autumn epidemic of 1918.
_Spread in recurrences._—As a rule the manner of spread of a secondary
epidemic following the primary pandemic wave is quite different. At a
longer or shorter interval following the first spread the disease breaks
out anew in one locality or another, sometimes simultaneously in widely
separated districts. Sometimes we can distinguish a direction of spread
in the relatively small community affected, it frequently being observed
that the disease will start up in a large city which has experienced the
illness during the first pandemic, and from there will spread to small
nearby localities which may have remained free until that time. Again,
any clearcut direction of spread may be entirely lacking. It is rare
indeed that an epidemic following another by a short interval will
follow a definite line over an entire country or continent. Such an
example is, however, to be found in the epidemic of 1833, which traveled
over Europe from Russia, spreading to the west and the south and
following practically the identical path that it had taken in 1830. Even
so it was not as widespread, for while the epidemic of 1830 had covered
the entire earth, America appears to have escaped the second epidemic.
These disseminated and independent outbreaks are believed to arise from
endemic foci in which the virus has been deposited during the progress
of its first spread and in which the germ has survived until it has
acquired once again exalted virulence.
Usually these endemic outbreaks show in their local configuration, a
secondary type of wave. That this is not always the case we have already
indicated. The epidemic of 1732–1733 was a recurrence of that of
1729–1730. The epidemic of 1782 had as its source the epidemic of the
years 1780–1781. The epidemic of 1788 recurred until 1800, and was quite
possibly associated with those of 1802, 1803 and 1805–1806. That of 1830
recurred in 1831–1832. Next we have in 1833 the true pandemic
originating in Russia. Recurrences of the epidemic of 1836–1837 were
found in 1838 and in 1841. Those spreads which occurred in 1847 and 1848
found successors in the year 1851. In 1890 the influenza outbreaks were
as a rule single or isolated and occurred in only a few places of
Europe, particularly in Lisbon, Nürnberg, Paris, Copenhagen, Edinburgh,
Riga, London, etc. It is reported that there was an unusually severe
local outbreak in Japan in August, 1890. In 1891 no general direction of
spread was manifested, yet in heavily populated areas, or states rich in
lines of communication, especially those of Europe and North America,
one could frequently trace some definite direction followed by the
disease within these relatively small territories.
A. Netter made the following observation at that time: “La Grippe a fait
des explosions simultanées ou successives, et on n’a pu en aucune façon
subordonner ces différents foyers comme cela avait été possible en
1889–90. Il parait y avoir eu des reveils de l’épidémie sur divers
points.”
Leichtenstern describes the subsequent spread of the disease: “The
transfer of the disease by ships which played such an important role in
the first epidemic appeared to be insignificant in 1891, in spite of the
fact that influenza was present in many of the English colonies. The
third real epidemic spread of influenza was a true pandemic which began
in the autumn (October) of 1891 and lasted through the whole winter
until the spring of 1892. It involved all of Europe and North America
and spread to all other lands, but here again the geographic
distribution followed no rule. There was no spread of influenza from a
central point, no continuous spread following lines of communication,
and there was no longer an early predominance in the cities lying on the
lines of communication or in the larger cities and commercial centers,
as had been the case in the first epidemic. In England in 1891 the first
outbreaks occurred frequently in country districts. The epidemic raged
nearly four months in the northern part before it finally reached London
in May. The same was true of Australia.
“One peculiarity of the recurrent epidemic lay in the much more
contagious character of the disease and the remarkably greater
mortality. In Sheffield the mortality in the recurrent epidemic was
greater than in the pandemic, even though the epidemic picture was that
of a primary wave.”
By way of summary of our knowledge of the primary and secondary spread
in general up to the epidemic of 1918, we may enumerate the more
important characteristics:
1. Occurrence of true pandemics at wide intervals, primarily intervals
of several decades.
2. Indefinite knowledge and conflicting evidence regarding site and
manner of origin.
3. Apparent transmission chiefly or entirely through human intercourse.
4. Rapid spread over all countries, the rapidity roughly paralleling the
speed of human travel.
5. Rapid evolution of the disease in the communities where outbreaks
occur, with nearly equally rapid subsidence after several weeks’
duration.
6. Apparent lack of dependance on differences of wind or weather,
seasons or climate.
7. Generally low mortality in contrast to enormous morbidity. Variation
in the incidence of disastrous secondary infections.
8. Tendency to successive recurrences at short intervals.
SECTION II.
INFLUENZA EPIDEMICS SINCE 1893.
In this section of our report we will describe with as great accuracy as
our sources of information will permit, and in as great detail as space
will allow the events which have led up to the epidemics of 1918–20 and
the various phases of the epidemics themselves. Points of similarity
with previous epidemics will be made obvious; the differences, when of
significance, will be described and studied in detail.
OCCURRENCE SINCE 1893.
Attempts even today to determine when and where influenza has prevailed
in the world since the great pandemic of the last century are met with
great difficulties. There are several reasons for this, chief among
which is the absence of definite characteristics by which the disease
may be recognized. The isolated solitary case baffles positive
diagnosis. Nearly every year there are reports in the literature of
small outbreaks in institutions or communities in which the clinical
picture is that of epidemic influenza. As a rule the conclusion has been
in these cases that because the bacteriologic findings did not show a
predominance of Pfeiffer’s bacillus the epidemic was not true influenza.
This is particularly true in the outbreaks in which the streptococcus
predominated. Today our views concerning the bacteriology have changed
distinctly, and I believe it is safe to say that the predominance of a
streptococcus in a local epidemic in no way rules out influenza, and
that the only criteria by which we may judge are the clinical picture
and the evidence of high infectivity, together with the epidemiologic
characteristics of the local outbreak.
_Period 1893–1918._—A review of the medical literature between 1889 and
1918 gives one a certain impression which may be summarized as follows:
Between 1890 and 1900 the disease was in general more highly prevalent
in most localities than at any time during the preceding thirty years.
At no time during this decade did the annual death rate from influenza
in England and Wales fall to anywhere near the figures that had
prevailed consistently between 1860 and 1889. Between 1900 and 1915
there was a gradual diminution, but still not to the extent that had
prevailed previous to 1889. Since 1915 there appears to have been a
gradual increase. During the entire period there has been difficulty in
distinguishing between the disease in question and other respiratory
tract infections, particularly coryza, sore throat, tonsillitis, and
bronchitis. Many of the local epidemics which appear probably to have
been true influenza have had associated with them a high incidence of
sore throats. We describe this as sore throat, rather than tonsillitis,
because the clinician remarks that although the throat is sore there is
little if any demonstrable inflammation of the tonsils.
Chart VIII published by Sir Arthur Newsholme, showing the death rate per
million of population from influenza in England and Wales gives some
idea of the prevalence of the disease in the first part of the
interpandemic period in those countries. It should be remarked that the
record is for deaths from influenza only.
For records in this country it is convenient to refer to the death rate
in the State of Massachusetts; first, because the records in that State
have been carefully kept for a long period; and second, because
influenza has been carefully studied in this State during both epidemics
by two most competent epidemiologists. For the period preceding 1889 we
quote herewith from Abbott:
“For the past 45 years or more, or during the period of registration
which began with the year 1842, no epidemic of influenza has prevailed
within the State to such an extent as to have manifested itself in any
serious manner in the annual lists of deaths. An examination of the
registration reports for each year since 1842 shows that in no year were
recorded more than 100 deaths from this cause; the highest number from
influenza in a single year (92) occurred in 1857, and the least number
(8) in 1884. The average annual number of deaths from this cause
reported in the State for the period 1842 to 1888 was 38. The average
number during the first half of this period was greater than that of the
last half, especially when considered with reference to the increase of
population. From these statistics of nonepidemic influenza between the
years 1842 and 1888 it appears that its greatest prevalence, or rather
the years in which the mortality from this cause was greatest, were also
years of unusual mortality from pneumonia, and in some instances from
bronchitis.”
Frost has charted the death rate per 100,000 from influenza and from all
forms of pneumonia in Massachusetts by month, from 1887 to 1916. From it
he concludes that the epidemic of 1889–1892 developed in three distinct
phases, the first culminating in January, 1890, the second in April and
May, 1891, and the third in January, 1892. The mortality was higher in
1891 than in 1890, and still higher in 1892, while in 1893, although
there was no distinct epidemic, the pneumonia mortality for the year was
even higher than that of 1892. Frost remarks that this corresponds to
the experience in England, and that it apparently represents the general
experience in other countries (see charts IX and X).
CHART VIII.
[Illustration:
Death rates per million from influenza in England and Wales from 1845
to 1917. (_Newsholme._)
]
CHART IX.
[Illustration:
Monthly death rates per 100,000 from influenza and from pneumonia in
Massachusetts from 1887 to 1916. (_Frost._)
]
CHART X.
[Illustration:
Monthly death rates per 100,000 from influenza and pneumonia in three
cities of the United States from 1910 to 1918, inclusive. (_Frost._)
]
In the absence of comparable statistics for Massachusetts in 1917 and
1918, Frost has studied for those years certain other localities,
particularly Cleveland, San Francisco and New York City. The mortality
in all of these places, as well as in Massachusetts, was fairly regular
from 1910 to 1915, but in December of the latter year and January of
1916 there occurred in New York and Cleveland a sudden sharp rise in
mortality. This was not shown distinctly in the San Francisco curve, but
it was a rise which was almost universal and synchronous over the entire
registration area. It is of interest as indicating the operation of some
definite and widespread factor, and suggesting in this group of diseases
an epidemic tendency which is perhaps, as Frost remarks, not
sufficiently appreciated. In January of 1916 he found that influenza was
reported to be epidemic in twenty-two states, including all sections of
the country. The epidemic was very mild. In the early spring of 1918
there was another sharp rise, which we shall discuss in greater detail
later.
_Increase in 1900–1901._—Reference to Frost’s chart for Massachusetts
shows that there was also a rise in the curve around 1900. At this time
influenza was quite widely disseminated. Early in 1901 the Marine
Hospital Service made a canvass of all the states and several foreign
countries to determine the epidemic prevalence of influenza. The results
of the canvass were published in the Public Health Reports. The records
lack the detail, particularly in the description of clinical symptoms,
that is desirable in arriving at an identification, but the universal
agreement from all individuals reporting, in the comparatively high
morbidity and remarkably low mortality, together with the widespread
distribution, and the duration of the local epidemic leaves little doubt
as to the identity.
Influenza was reported present in October of 1900 in Los Angeles,
Milwaukee and New Orleans. In November it became prevalent in Toledo and
Cincinnati and in New York City. In December the disease was present in
Chicago, Albany, Philadelphia, San Francisco, Denver, Baltimore, Grand
Rapids, Columbus, O., Portland, Me., Detroit, Albuquerque and Omaha. In
January it was reported in New Haven, Boston, Washington, D. C.,
Indianapolis, Louisville, Ky., Wilmington, Del., Portland, Ore., and
Juneau, Alaska.
Although the disease was mild, in some localities a high proportion of
the population was attacked. Thus in New Haven it was estimated that 10
per cent. developed the disease, and in Los Angeles 20 per cent., while
in Wilmington, 40,000 were estimated to have become ill. In certain
small towns in Texas the incidence was especially high. In Pittsburgh,
Texas, ten per cent.; Laredo, 15 to 20 per cent.; Hearne, 50 per cent.;
and El Paso, 50 per cent. were attacked. The duration of the epidemic in
most localities was from four to six weeks.
Thus we see that in October, November and December of 1900 and January
of 1901 there was a widespread epidemic affecting all parts of the
United States. Many additional records in the Public Health Reports
coming from small towns have not been included in this summary.
At the same time an attempt was made to determine the prevalence in
foreign countries and letters were sent to the various United States
Consulates. It was discovered that the disease was mildly epidemic in
Denmark in October, in Berlin in November, in Cuba, British Columbia,
Ontario, Egypt, Paris, Mexico and the West Indies in December; in
Flanders, Porto Rico, Honolulu, in January of 1901; in Malta in
February, 1901; and in London and Ireland in March of that year. The
following countries reported that they had no influenza at the time:
Windward Islands, Jamaica, Bahamas, Brazil, India, Colombia, Costa Rica,
Ecuador, Honduras, Persia, Philippine Islands, Spain, Switzerland. The
disease was reported as being not of epidemic prevalence in the
following localities: Marseilles, Paris, Bremen, Hamburg, Mainz,
Stuttgart, Bristol, London, Liverpool, England as a whole, Scotland,
Amsterdam, Naples, Constantinople.
Reports from Switzerland and from Brazil stated that there had been no
influenza since the pandemic period 1889–1893. The death rate per
100,000 in Glasgow from influenza for 1896 was recorded as six; for
1897, twelve; for 1898, fifteen; 1899, twenty-two and for 1900,
twenty-seven.
The disease was present in Lima, Peru in March, 1900, and at Malta in
the same month. In Prague it was stated that ten per cent. of the
population had been attacked in the winter of 1901. In Sivas, Turkey,
fifty per cent. of a population of 50,000 were estimated to have been
taken ill within the winter months. It was reported from Valencia,
Spain, that there had been four or five visitations of influenza since
the preceding pandemic, each recurring invasion presenting a milder and
less expansive form than its predecessor. Very few deaths had been
recorded as directly due to influenza, but an increased mortality
followed the epidemics. In normal times the average mortality was ninety
deaths per week. After a visitation of influenza the number had
increased to as much as 160 per week. The population numbered 204,000.
_Period from 1901 to 1915._—Between 1900, with its wide distribution of
a very mild influenza, and 1915, there is very little mention of
epidemic prevalence of the disease. References which appeared in the
Public Health Reports during the interval are characterized chiefly by
their brevity, and by the absence of descriptive detail. They should
nevertheless be included.
In October of 1901 there was some increase of the disease in the
Hawaiian Islands, 110 cases being reported on the island of Kauai.
At the same time, C. Williams Bailey reported a mild form of influenza
existing in Georgetown, S. C., which was first considered to be hay
fever in consideration of the presence of the rice harvest season, but
which was finally decided, after careful investigation, to be true
influenza.
On July 21, 1902, the U. S. Consul at Canton, China, telegraphed that
influenza “was almost epidemic, plague sporadic in Canton.”
In 1903 the disease was reported as apparently prevalent at New Laredo,
Texas.
Surgeon Gassaway, of the Marine Hospital Service, reported from
Missouri, December 14, 1903, as follows: “There is a very decided
increase in the number of cases of influenza in this vicinity. Two have
been admitted within the last few days to this hospital, and several
cases have appeared among the patients under treatment. In these cases
the onset is sudden and the disease appears principally, at least at
first, to be confined to the nose and throat.”
Measles and influenza were reported prevalent in Barbados, West Indies,
during the month of December, 1904.
Sturrock describes a quite typical local epidemic in a British
institution in 1905.
Influenza was epidemic in Guayaquil and various other places in Ecuador
during the months of June and July, 1906.
Selter speaks of a true local epidemic of a disease clinically
resembling influenza which occurred in 1908 and extended over the
territory from France to the Rhine.
Hudeshagen mentions having examined bacteriologically cases of influenza
in the year 1914.
Ustvedt relates his experience at the Ullevaal Hospital up to September,
1918. Since 1890 there had been cases reported every year from the high
marks of 10,461 cases in Christiania in 1890 and 5,728 in 1901 to the
lowest figure, 138 in 1906. “The cases listed as influenza in the last
few years may have been merely a catarrhal fever. This is the more
probable as the cases were restricted to the winter months, while
influenza usually occurs at other seasons.”
Jundell believes that influenza is endemic at Stockholm, Sweden,
hundreds of cases being reported there each year. During the years
1912–1919 Pfeiffer’s bacillus has been found in ten per cent. of those
cases in which the diagnosis seemed certain.
A current comment in the Journal of the American Medical Association in
1912 remarks that epidemics of coryza, sore throat, and bronchitis
usually have been called influenza or grip because of the characteristic
contagiousness and the infectivity, the persistence of the symptoms, and
the tendency to prostration and mental depression. But this diagnosis
has not been satisfactorily confirmed by bacteriologists. An epidemic
according to the Journal, which occurred in Boston and which was called
sore throat, was studied by Richardson and others. They traced the
contagion to a streptococcus which apparently was spread by means of
milk. Müller and Seligman had recently carried out a study of an
influenza epidemic among children in Berlin and concluded that the
causative organism was a streptococcus, differing so much from the
ordinary germ that they used the term “grip streptococcus.” Davis and
Rosenau, according to the comment, had made a bacteriologic study of a
recent epidemic of sore throat in Chicago, and had demonstrated as the
exciting agent a streptococcus of peculiar characteristics, which in
many respects resembled the organism described by Müller and Seligman.
The Journal noted that these three epidemics occurring during the years
1911 and 1912 in widely separated communities were all caused by the
streptococcus, and cautioned against the proneness to call all such
epidemics grip. Today the predominance of the streptococcus would not
necessarily rule out influenza in our minds.
In the winter of 1913, C. L. Sherman had occasion to study carefully
fourteen cases of so-called influenza in the vicinity of Luverne,
Minnesota. Bacteriologic smears and cultures were made from the throat
and sputum in all cases. Bacillus influenzae was found in two of the
fourteen; pneumococcus in four and streptococcus in all. Tubercle
bacilli were found in one case. The onset of the disease was invariably
abrupt. The fever in all cases ranged between 101° and 104°; symptoms
indicative of infection of the upper respiratory tract were always
present. There was more or less sore throat in all. There was either
cough at the onset or else it appeared within 48 hours. Headache was
complained of by twelve of the fourteen; pains in the back and in the
limbs by thirteen, and nervous symptoms by six. Prostration out of all
proportion to the fever and other symptoms prevailed. Two developed an
otitis media and the streptococcus was isolated from the purulent
discharge in both cases. One patient had a complicating empyema, and one
an acute arthritis. Sherman also concluded that we are prone to call too
diverse diseases influenza.
Walb stated in 1913 that at Bonn during the preceding years there had
been numbers of cases of a febrile affection which seemed to be typical
influenza, but for which the pneumococcus appeared to be responsible.
They were never able to isolate the influenza bacillus, and according to
their statement the Hygienic Institute at Bonn, as well as that at
Berlin, had not “encountered an influenza bacillus within the preceding
ten years.”
C. T. Mayer described in 1913 a case of influenza in Buenos Ayres which
is of particular interest in view of one of the symptoms, cyanosis,
which was so prominent a feature in 1918. This appears to have been an
isolated case. The diagnosis wavered between miliary tuberculosis and
pneumonic plague, because of the high fever and intense cyanosis, with
nothing to explain the cyanosis on the part of the heart. There were
signs of severe congestion of both lungs, and notable enlargement of the
spleen. Bacteriologic examination was negative except for the presence
of Bacillus influenzae and Micrococcus catarrhalis. The patient
subsequently improved rapidly, and the lungs were entirely normal after
thirty days, thus ruling out the other two diseases.
A London letter to the Journal of the American Medical Association dated
February 5, 1915, runs as follows:
“Since the outbreak of the war the public health has been remarkably
good, but the record is now being threatened in the case of London, at
any rate, by an epidemic of influenza.
“The gastric symptoms which distinguished last year’s epidemic are
absent. The disease is most infectious. Whenever it has seized the
individual it has usually run through the entire household.
“Whole offices have succumbed, and as the mildness of the attack lures
the sufferer to continue his normal occupation, the disease has a full
opportunity of extending. A large number have resulted in
pleuro-pneumonia; otherwise the chief symptoms are headache, fever,
tonsillitis.”
Telling and Hann describe another clinical diagnosis of influenza, the
diagnosis being concurred in by Sir James Goodhart and Sir Clifford
Allbutt. The onset was absolutely sudden at a supper party on November
10, 1912. The patient had a slight rigor, and was compelled to go to
bed. In the night he had a longer and more severe rigor, with a
temperature of 103°. On the following morning he dressed, but another
chill sent him back to bed with a temperature still 103°, pulse 110,
regular, and remarkably dicrotic. There was no cough and no sore throat.
Another chill occurred in the evening. On November 12th the patient had
two chills, the temperature remaining steadily at 103° to 104°. The
patient complained much of nausea but did not vomit. On November 13th
the temperature remained up, there was no chill on this day; the spleen
was large and easily felt for the first time. On the 14th note was made
that there was no headache. On the 15th, 16th and 17th the temperature
began to fluctuate. On the 18th there were two severe rigors, and by the
19th the temperature suddenly fell to normal, with drenching sweat.
Throughout there was nothing to suggest pneumonia, and typhoid fever
appears to have been successfully ruled out.
An epidemic of influenza which prevailed in the city of Pittsburgh,
Pennsylvania, from December to February of 1907 and 1908, has been
described by J. A. Lichty. He says that the epidemic was as widespread,
though probably not quite as severe, as the pandemic of 1889. Whole
families, including servants and all associated with the household, were
afflicted in rapid succession. The onset was sudden and severe, the
usual symptoms of pain, all over, being most pronounced. The temperature
did not go unusually high, nor did it seem to be in accord with the
severity of the symptoms when the patient took to his bed. In typical
cases the attack lasted from two to three or four days. Peculiar to this
epidemic seemed to be the general complaint of sore throat. Upon
examination the throat rarely showed any other evidence of an abnormal
condition than a rather dark cyanotic blush, which was most intense over
the tonsils and faded out over the roof of the mouth. This was rarely
associated with any swelling or fever. Sinusitis and otitis media seem
to have been the two most frequent complications. The disease appeared
to be particularly fatal for chronic invalids. It was highly contagious.
Many of those physicians who were frequently exposed to the disease fell
victims.
At the same time C. H. Jones described an epidemic of the same disease
in Baltimore. The symptoms were described as headache, backache,
limb-ache, with a slight elevation of temperature, seldom more than
102°. Catarrhal symptoms developed secondarily and were not so prominent
a feature as in former epidemics. There were some gastric symptoms,
usually consisting of vomiting and nausea. Jones quotes no statistics,
but feels sure that the infection was more extensive than at any period
since 1895.
Coakley and Dench describe throat and ear complications as they saw them
in New York. From this we may assume that the disease was present at the
same time in New York City.
The following chart, derived from the U. S. Vital Statistics Report
shows the increase in the death rates from influenza in 1900 and 1901;
that of 1907 and 1908, and finally an increase to 26.4 per 100,000 in
1916, which reflects the epidemic beginning in the latter part of 1915:
_Influenza and Pneumonia Mortality in the United States Registration
Area for Each Year Since 1900._
═════════════════╤═════════════════════════════════════════════════════
Year. │ Annual death rates per 100,000.
─────────────────┼─────────────────┬─────────────────┬─────────────────
„ │ Pneumonia. │ Influenza. │ Combined
│ │ │ diseases.
─────────────────┼─────────────────┼─────────────────┼─────────────────
1900│ 158.6│ 22.8│ 181.4
1901│ 133.5│ 32.2│ 167.7
1902│ 124.7│ 10.1│ 134.8
1903│ 122.6│ 18.5│ 141.1
1904│ 136.3│ 20.2│ 156.5
1905│ 115.7│ 18.8│ 134.5
1906│ 110.8│ 10.3│ 121.1
1907│ 120.8│ 23.3│ 144.1
1908│ 98.8│ 21.3│ 120.1
1909│ 96.3│ 13.0│ 109.3
1910│ 147.7│ 14.4│ 162.1
1911│ 133.7│ 15.7│ 149.4
1912│ 132.3│ 10.3│ 142.6
1913│ 132.4│ 12.2│ 144.6
1914│ 127.0│ 9.1│ 136.1
1915│ 132.7│ 16.0│ 148.7
1916│ 137.3│ 26.4│ 163.7
─────────────────┴─────────────────┴─────────────────┴─────────────────
At best our information for these years is unsatisfactory. It is greatly
to be desired that individuals who have access not only to the current
medical literature, but also to the vital statistics and other records
for all countries possessing reliable records, and who are versed in the
newer mathematical methods of demography, establish definitely the
influenza prevalence and distribution during these interpandemic years.
The difficulty in this work is that mortality statistics are unreliable
and morbidity statistics are lacking.
_Influenza in 1915–1916._—Until the end of 1915 there was no widespread
distribution in the United States similar to that of 1900 and 1901, but
at that time there developed a widespread epidemic in this country of
similar or possibly slightly greater severity than that of fifteen years
previously. Reference to the last table will show that during 1916 the
annual death rate from influenza as reported in the United States Vital
Statistics reached the rate of 26.4 per 100,000. According to V. C.
Vaughan the literature of that time shows that this epidemic originated
in the West, first attracting attention at Denver, and gradually spread
over the country.
Dr. Dublin of the Metropolitan Life Insurance Company gives the
following table in which the deaths from influenza and pneumonia during
the months of December, 1914, and January, 1915, are compared with
deaths from the same cause during the months of December, 1915, and
January, 1916:
═══════════════╤═══════════════════════════╤═══════════════════════════
Name of city │ Deaths reported as due to │ Deaths reported as due to
│ influenza. │ pneumonia.
───────────────┼─────────────┬─────────────┼─────────────┬─────────────
„ │ In 1915–16. │ In 1914–15. │ In 1915–16. │ In 1914–15.
───────────────┼─────────────┼─────────────┼─────────────┼─────────────
Baltimore │ 57│ 12│ 219│ 101
Cincinnati │ 81│ 2│ 105│ 84
New Orleans │ 97│ 44│ 35│ 29
New York │ 494│ 62│ 2,067│ 1,207
Philadelphia │ 324│ 62│ 564│ 272
Providence │ 38│ 3│ 31│ 31
───────────────┼─────────────┼─────────────┼─────────────┼─────────────
Total │ 1,091│ 185│ 3,021│ 1,724
───────────────┴─────────────┴─────────────┴─────────────┴─────────────
Dublin states that the Industrial Department of the Metropolitan Life
Insurance Company, covering the entire country and embracing ten
millions of people, had deaths in the periods above mentioned, as
follows:
In December, 1914, and January, 1915, the number of deaths
attributed to influenza was 165
While in the corresponding months of 1915–1916 the deaths
attributed to influenza were 957
The deaths attributed to pneumonia in December, 1914, and
January, 1915, were 1,468
While the number of deaths attributed to the same cause in
December, 1915, and January, 1916, were 2,563
Coffey and others have reported an epidemic of influenza at Worcester,
Mass. during the first three weeks of January, 1916. During the first
three weeks of January, 1915, there were reported in that city
twenty-two deaths from respiratory diseases, making a total of 14.9 per
cent. of the total deaths. In the same period of 1916 there were
reported ninety-three deaths from acute respiratory diseases in the same
population.
Two of the more complete descriptions of the epidemic of the year
1915–16 are those by Mathers, and by Capps and Moody. Mathers reports
that: “During the winter of 1915–1916 the United States was visited by a
severe epidemic of acute respiratory infections which resembled in every
detail the great epidemic of 1890. This outbreak was apparently first
noticed in the Middle Western States, and it spread rapidly over the
entire country, taking a heavy toll of human life. December and January
were the months in which these infections were most prevalent, and the
epidemic had almost completely lost its impetus by March, 1916. During
the height of this epidemic in Chicago, sixty-one cases of the disease
were studied bacteriologically, and the results form the basis of this
paper.”
Mathers found hemolytic streptococci in forty-six instances, in all of
which they predominated. Green producing streptococci were found thirty
times, with one pure culture, and pneumococci thirty times with four
pure cultures. Staphylococci were isolated in fifty cases; Micrococcus
catarrhalis in six, and Friedländer’s bacillus in one case. The
influenza bacillus was found in only one instance, and then in small
numbers. The majority of the patients were studied early in the course
of the disease, and in the earliest, hemolytic streptococci were almost
constantly found, especially in the throat. In the atypical pneumonia
which followed many of the attacks of grip, hemolytic streptococci
predominated. In none of these was the Bacillus influenza found.
Mathers reported that coincident with the epidemic among humans there
was an epizootic of so-called influenza among horses. The symptoms are
very similar to that of the disease among humans. He isolated a
streptococcus as the predominating organism in the horses. The
streptococci from human and equine sources, although similar in many
characteristics, differed widely in pathogenicity, and seemed to be
highly parasitic for the specific hosts.
Capps and Moody found that in man most cases began rather abruptly, with
coryza, pharyngitis, laryngitis, or bronchitis.
“The chief complications were inflammation of the accessory sinuses of
the head, and bronchopneumonia, the latter being responsible for most of
the fatalities. None of these symptoms taken alone would justify the
distinctive name of grip. But the widespread and almost simultaneous
onset of this fairly uniform symptom group and the rapid cessation of
the epidemic after a few weeks reminded physicians generally of the
great grip pandemic of 1889–1890. This resemblance was further
strengthened by the unusual prostration lasting days or weeks after even
mild attacks. The older practitioners can recall no similar epidemic
during the twenty-five years intervening between 1890 and this year. The
numerous epidemics of septic sore throat have all been entirely
different in their symptomatology, and all were restricted to certain
localities. The term “grip,” therefore, seems justified from a clinical
standpoint.
“The public health reports offer evidence of an unusual prevalence of
pneumonia in the larger cities. Nicolas calls attention to the fact that
the incidence of grip was greatest in those cities in which the
mortality from pneumonia was most strikingly increased.”
Capps and Moody found that as a rule the white blood counts in the
individuals sick with influenza were 10,000 or less. A number showed
true leucopenia. Less frequently there was a leucocytosis up to 15,000
or higher.
_Influenza between 1916 and 1918._—Zinsser cites Dr. George Draper, who
believes that he observed at Fort Riley in the winter of 1917 epidemic
cases of influenza. He believes that for Europe too there is evidence
that influenza was endemic during the years preceding the great
outbreak, and that a number of minor epidemic explosions had occurred in
the years just preceding 1918:
“MacNeal who has investigated military reports particularly, states that
small epidemics occurred in the British Army in 1916 and 1917. A chart
constructed by him from the American Expeditionary Force reports shows
that a considerable rise in reported influenza cases took place in
November and December, 1917, and in January, 1918, gradually declining
toward spring. MacNeal, compiling the data available in the office of
the Chief Surgeon, A. E. F., states that the influenza morbidity
reported per 100,000 for succeeding months in 1917, were as follows:
July 321
August 438
September 404
October 1,050
November 1,980
December 2,480
“Robertson, who studied many of the secondary pneumonias which came to
autopsy at this time found an unusual type of lobular pneumonia in which
Pfeiffer bacilli were frequently found. In many of these cases the
organisms could be obtained from the nasal sinuses and antra. Similar
findings were reported by British bacteriologists (Hammond, Rolland and
Shore, and Abrahams, Hallows, Eyre and French), who studied the cases
that occurred in the reports by Austrian physicians in reference to
outbreaks of typical influenza on the Austro-Russian front early in
1917.
“There seems little doubt, therefore, that for some years before the
pandemic of 1918 influenza was endemic in many parts both of Europe and
of America. As early as 1915–1916 Frost finds evidences of limited
epidemic outbreaks in the United States. During the winter immediately
preceding the true beginning of the pandemic small outbreaks occurred
among the allied troops in France, the British troops in England and
probably among American troops gathered in home concentration camps as
well. MacNeal in a summary of the conditions prevailing among American
troops in France concludes that epidemic influenza in that country
originated from the endemic foci there existing, and that the disease
was probably carried from Europe to the United States by shipping. The
former assumption; namely, that the epidemic occurrence of the disease
may have been due to the fact that an enormous and concentrated newly
introduced material of susceptibles may have been lighted into flame at
the numerous endemic smoulders, may well be correct. The latter,
however, concerning the transportation of the disease from Europe to
America may justly be questioned. For, in the first place, Frost’s
studies have shown that prepandemic outbreaks were quite as frequent in
the United States as in Europe during 1915 and 1916, and, though we have
no proof of this, there is reason to believe that influenza was
prevalent in concentration camps during 1917.”
Carnwath, after remarking that the epidemic began in the British Army in
France in April, 1918, says that according to the reports of the
Influenza Committee of the Advisory Board this was not the first time
that Pfeiffer’s bacillus had appeared in the armies. On the contrary, it
had frequently been found in cases of bronchopneumonia, especially
during the winter of 1916–1917. It is doubtful, however, whether much
importance, from the epidemiologic point of view, attaches to these
sporadic findings of the Pfeiffer bacillus.
Influenza was reported in the year 1917, but this year, as well as the
epidemic of 1916, becomes involved in a determination of the date of
onset of the great pandemic of 1918.
THE PANDEMIC OF 1918.
The date and site of onset of the great pandemic are subjects concerning
which there is no conclusive information. There have been small
outbreaks of clinical influenza with epidemic tendencies at one place or
another during nearly all of the intervening years since 1889. In all of
them the question is open as to whether they were true influenza, and
also assuming that some were true influenza, how many of them should be
so included. There are some who believe that the increase of morbidity
following the measles epidemic in the United States Army camps in the
winter of 1917–18 is genetically associated with the great pandemic. In
short, there is no one point in the last few years at which we may say
that influenza which had previously been non-existent started at a focus
and spread throughout the world.
It follows from the experience of 1889 that we should at least attempt
to find an endemic focus and to follow the progression of the disease.
It is safe to say that once having become pandemic the disease spread as
it did thirty years previously. Experience in this country, where the
autumn spread began in the New England States and continued West and
South; knowledge of the late spread to remote localities; the fact that
the disease first appeared in England, etc. in sea coast towns; the
introduction of the influenza into new countries at seaport towns, after
the arrival of infected ships, all coincide well with the past history.
But which of the several local epidemics of the preceding years was the
direct progenitor of the great pandemic? In order to follow more clearly
the development of the facts we will record here the various hypotheses
that will come up for consideration as to the site of origin of the
disease.
1. Influenza is endemic in some one locality, such as Turkestan in Asia,
from which place the disease spreads throughout the earth at intervals,
after having acquired in some way greatly increased virulence. The local
outbreaks of interepidemic times are not due to the virus which causes
the great pandemics and should be called pseudo-influenza in contrast to
influenza vera. Following the pandemic it is true, however, that for a
succession of years local outbreaks occur, due to the pandemic virus
which has been left deposited in small endemic foci. These disappear in
the course of a few years.
2. The second hypothesis is similar to the first, except that in it is
considered the possibility of there being more than one endemic focus,
at least two, one in the old world and one in the new. Although
Leichtenstern believed in the first hypothesis he did not deny the
possibility of the second.
“There have been in the past several well described influenza epidemics
limited to North America. Furthermore true pandemics have occurred at
the same time in North America and in Europe. We can suggest the
hypothesis that there is a permanent endemic focus, just as in central
Asia and Russia, existing in the southern part of North America. The
following facts concerning the last pandemic period favor this idea.
“As early as May, 1889, influenza began in Athabasca (British North
America) and in the summer of 1889, in Greenland. It is especially
interesting to hear of an extensive influenza epidemic which in the
middle or toward the end of December, 1889, broke out in the Northwest
Territory of British North America, in Manitoba, in the Island of
Vancouver, similar to that in the east of Canada and Quebec. A spread of
the epidemic, which attacked Boston and New York on December 17th, to
the above territories, far away and connected by very poor
transportation facilities, is certainly improbable, especially in
consideration of the time at which the two epidemics occurred.
“We are told that the invasion and the outbreak of influenza in these
vast territories occurred at practically the same time at such widely
separated places as Fort MacLeod, Saskatchewan, Prince Albert and other
military posts, and furthermore in isolated Indian camps and tribes
between which there was little or no communication.
“These facts also indicate that we are considering primary endemic
pandemics analogous to the one which broke out in July, 1889, in Central
Asia.”
3. The virus of influenza is more or less uniformly distributed
throughout the world. We may say that it is endemic in many localities,
as is the case with the meningococcus. Quite frequently in one locality
or another the virus acquires increased virulence and causes a small
local epidemic which may even spread to adjoining territories. It is
possible that the virus in two or more separated localities may become
more invasive simultaneously, thus causing widely separated and
unrelated outbreaks. As a rule the virulence does not become so great as
to cause a true pandemic, but at rare intervals, usually of decades, or
thereabouts, the epidemic virus becomes so greatly enhanced, perhaps
from passage to new territory and through non-immune individuals, that
it eventually commences on its wild career around the earth. Perhaps the
_pandemic_ variety usually comes from one particular locality among the
many endemic spots. Perhaps always from the same locality or perhaps at
times even simultaneously from many different ones. It is possible even
that an increased virulence develops simultaneously in all localities.
This third hypothesis develops into a discussion as to whether the small
interpandemic epidemics are true influenza or some other disease.
Again, Leichtenstern, although he does not favor it, recognizes the
possibility of this theory:
“Whether the small local epidemics reported by Kormann in Coburg in 1878
and by O. Seifert in Würzburg in 1883 are the same as the true epidemic
influenza is at present uncertain. Some of the complications, such as
swelling of the neck glands, and especially frequently parotitis,
purpura, scurvy, indicate that the epidemic in Russia, in 1856–1858,
reported by Kasin, was not the true influenza.
“When W. Zülzer writes in 1886 of an epidemic in Berlin in which many
thousands of individuals were attacked, the question might arise, is
this the same influenza which three years later passed through the
entire world and which in Berlin was believed by the same physicians to
be a new disease?
“The evidence is better in the case of the epidemic reported by von den
Velden in 1874–75. First, because of the complication with pneumonia and
especially because at the same time the disease sprang up in several
places in France, South Germany and the Rhine Provinces. It is very
doubtful whether epidemics described in 1855 and 1862 in Iceland, in
1870 in Philadelphia, in 1875 in Scotland, in 1876 in the Fiji Islands,
in 1887 in several places of England, in October, 1889 in Natal, in
November, 1889 in Jamaica and Prince Edward Island, was the true
influenza, even though the complications of pneumonia in the last named
epidemics favor this assumption. As regards the influenza epidemic which
attacked specially the school children of Pleshey and Great-Waltham and
from which fifty per cent. became ill in November and December, 1889,
whereas the pandemic was known to have begun there in January, 1890—the
high percentage of school children that were attacked renders the
conclusion that this was influenza very doubtful.
“It is an entirely different matter concerning the last epidemic in
which the epidemiologic compilations, based on retrospective diagnoses
suggest that in many places of Germany the ‘first case’ of even small
epidemic outbreaks was observed as early as the summer and autumn of
1889; in other words, several months before the outbreak of the true
pandemic in December.”
Leichtenstern believed that the so-called catarrhal fever and epidemics
of “cold” which some have been accustomed to call grip or influenza are
not the true disease, although he admits that there is no pathognomonic
sign by which the diseases may be differentiated. He expected that
search for the influenza bacillus which had recently been discovered
would enable investigators to determine by its presence or absence
whether or not these local epidemics are true influenza.
This, of course, would depend on the proof that the influenza bacillus
is the cause of the disease. If the many local influenza outbreaks which
Hirsch has collected in his exhaustive historical tables are the same
disease as true influenza, then the picture of influenza must be
considered as rather protean. Leichtenstern adds that this is a
possibility which from present information we cannot deny. He writes:
“If such is the case we must give the following epidemiological
definition of influenza: Influenza is a specific, infectious disease
usually occurring epidemically which, however, is endemic over the
entire earth, as indicated by outbreaks of cases, and which, after years
and decades have passed, breaks out in epidemic proportions. It is
recognized nearly every year in one or another place on the earth where
it becomes epidemic. From time to time from some point or center, or
from several points, as for instance simultaneously in the old and new
world, and for reasons unknown to us, an enormous increase in virulence
of the specific virus occurs and with it a great increase in the
contagiousness of the disease. Those are the times when influenza
spreads in mighty epidemics over wide stretches of land and portions of
the earth, or over the whole earth. Our common epidemic influenza or
grip, occurring practically isolated or in very small outbreaks, belongs
to the same type of disease as the pandemic variety, but is due to a
mitigated form of the causative organism, one of decreased virulence and
of shorter viability.
“_Provisionally, however, we will hold_ until the proof has been
obtained by bacteriological methods that influenza nostras and influenza
pandemica are two entirely different diseases, just as are cholera
nostras and asiatica. Accordingly, we will divide the diseases
designated as influenza in the following way:
“1. Influenza vera, caused by the Pfeiffer bacillus.
“2. The endemic-epidemic influenza vera which arises from the germ
remaining after the spread of the influenza pandemic and which is caused
by the same germ, the bacillus of Pfeiffer. The duration of this endemic
state of influenza vera may last years in single localities.
“3. The endemic influenza nostras, or pseudo-influenza or catarrhal
fever, commonly called grip, a disease sui generis. The germs causing
this disease are at present as little known as are those of cholera
nostras.”
Parkes, in 1876, recognized these possibilities: “The exact spot has not
been made out. Two opinions prevail. First, one focus; second, many
foci. Each nation, in turn, attributes the disease to its neighbor and
from the names so given one can follow the direction of the epidemic.”
Noah Webster believed that in 1698, 1757, 1761 and 1781 it originated
first in America. Hirsch believed that some of the epidemics had
probably originated in North America.
We find then that after the pandemic of the last century the same
epidemiologic questions had arisen that have come into such prominence
during the present period. As a rule those who have quoted the
epidemiologists of 1890 to 1900 have mentioned the first hypothesis and
have failed to allude to the fact that the other two were considered. So
we see that the subject was by no means settled even at that time, and
that if we should discover that the 1918 pandemic cannot be traced to a
single endemic focus our results will not be absolutely contradictory to
those of the last century.
Returning to a consideration of the period 1916–1918, we observe from
reference to Frost’s diagram that in the spring of 1918 there was a
sharp and general rise in mortality from influenza and pneumonia. Frost
reports that in the larger cities on the Atlantic seaboard this increase
occurred generally during January, February and March, when pneumonia
mortality normally reaches its maximum. The increase was not so evident
in all these cities as it was in New York City. In the rest of the
country, especially in the Central and Western States, the increase
occurred in April, a month during which pneumonia mortality is generally
on the decline, and was sufficient to constitute an unmistakable
departure from the normal. The increased mortality rate extended quite
generally into May and in some areas still longer. This is the first
increase after 1916 that is pictured in the mortality statistics for the
country at large.
There are some who believe that they saw influenza in mild form in the
United States army in the year 1917. V. C. Vaughan has investigated this
possibility and from a study of the sick and wounded charts decided that
there was no relation between influenza and the pneumonia which was
prevalent in 1917, and which usually was secondary to measles, being
caused by the streptococcus in the majority of localities. The lack of
association between influenza and pneumonia in 1917 and the direct
association in 1918 is well brought out by a comparison of the figures
in the two following charts, prepared by V. C. Vaughan:
_Pneumonia as a Sequel to Respiratory Diseases._
(All troops in United States in 1917.)
─────────────────┬─────────────────┬─────────────────┬─────────────────
│ │ No. of cases │ Per cent. of
Primary diseases.│ No. of cases. │ followed by │cases followed by
│ │ pneumonia. │ pneumonia.
─────────────────┼─────────────────┼─────────────────┼─────────────────
Measles │ 47,573│ 2,075│ 4.37
Scarlet Fever │ 1,966│ 54│ 2.75
German Measles │ 8,982│ 39│ 0.43
Bronchitis │ 41,233│ 20│ 0.049
Influenza │ 32,248│ 19│ 0.059
Meningitis │ 1,027│ 13│ 1.27
Tonsillitis │ 43,021│ 7│ 0.016
Pulmonary │ 6,799│ 6│ 0.088
tuberculosis │ │ │
Laryngitis │ 4,633│ 2│ 0.043
Diphtheria │ 1,163│ 1│ 0.086
Mumps │ 21,725│ 0│ 0.000
Pharyngitis │ 8,096│ 0│ 0.000
─────────────────┴─────────────────┴─────────────────┴─────────────────
_Influenza and Pneumonia in Last Four Months of 1918._
Number of cases of influenza 338,343
Number of cases of influenza followed by pneumonia 50,700
Number of deaths from influenza-pneumonia 17,700
Stallybrass, who has studied the influenza and pneumonia deaths in
Liverpool, England, since the 1889 pandemic, states that in every year
there had been reflected in the curves evidence of periodic increase in
deaths from influenza and pneumonia, and he states that from 1914 onward
there has been a progressive increase in the annual number of influenzal
deaths with the single exception of 1917.
It becomes evident that we cannot with the information at hand find any
one locality in which the disease was prevalent sufficiently ahead of
the pandemic and to the exclusion of other localities, so that we might
determine accurately the site of origin. The next step will be, then, to
discover as accurately as possible the date at which various communities
were first definitely attacked by the great pandemic, and to search out
the locality first affected.
DATE OF FIRST INCREASED PREVALENCE IN VARIOUS LOCALITIES.
From table II which gives the earliest recorded dates of increased
prevalence in different localities, we can gain a fairly accurate idea
as to the direction and manner of spread of the disease during the
pandemic. Influenza was first noticed in the United States early in
March, 1918. By the end of the month it had become more disseminated in
very mild form over many of the States east of the Mississippi and a few
West of that line. The following month the disease appeared in France.
In the American Expeditionary Forces in France it first appeared at the
base ports which were receiving troops from the United States. During
this month the disease had reached the allied Western front, the German
front had become infected and probably the disease had started on its
travel inward into enemy country. In May the disease was reported
present in Scotland, Spain, Greece and Egypt. In June England became
infected, as also Switzerland, Germany, Austria and Norway. In this
month the disease had reached as far as South America and India. In
China, on the 15th of June, there was reported an epidemic of a disease
resembling dengue which affected fifty per cent. of the population in
Chefoo and Shanghai. This disease may well have been influenza. During
July the disease had spread through Germany, appearing according to
German reports in the cities toward the West earlier than in Berlin and
other more Eastern cities, including Vienna. In July the disease was
present in other countries of Europe and was again reported in China and
India.
TABLE II.
_The spread of influenza in 1918._
═══════════╤════════════╤═════════════╤═══════════════╤════════════════
Month. │ Date. │ Country. │ City. │ Authority
│ │ │ │ quoted.
───────────┼────────────┼─────────────┼───────────────┼────────────────
March │ │_China_ │ │McNalty,
│ │ │ │ Carnwath.
│ │Japanese Navy│ │McNalty,
│ │ │ │ Carnwath.
│ │_Japan_ │ │Jour. Am. Med.
│ │ │ │ Assn.
│ │ │Civilian │
│ │_France_ │ Population at│MacNeal.
│ │ │ Chaumont │
│ 5│_United │ │
│ │ States_ │ │
│ │Kansas │Camp Funston │Opie.
│ │Missouri │Kansas City │V. C. Vaughan.
│ │Illinois │Chicago │Frost.
│ │Ohio │Columbus │V. C. Vaughan.
│ │Michigan │Detroit │V. C. Vaughan.
│ 18│Georgia │Camp Greenleaf │V. C. Vaughan.
│ │ │Atlanta │V. C. Vaughan.
│ 28│S. Carolina │Camp Sevier │W. T. Vaughan.
│ 30│Kansas │Haskell │Public Health
│ │ │ │ Reports.
───────────┼────────────┼─────────────┼───────────────┼────────────────
│ │_United │Various points │Public Health
April │ │ States_ │ from Norfolk │ Reports.
│ │ │ to Louisiana │
│ │Mississippi │Camp Shelby │V. C. Vaughan.
│ │Georgia │Camp Hancock │Forbes and
│ │ │ │ Snyder.
│ 30│California │San Quentin │Stanley.
│ │ │ Prison │
│ │_France_ │ │Netter.
│ │ │ │Chauffard.
│ │ │ │Messary.
│ │ │ │Longcope.
│ │ │Brest (American│
│ 1│ │ Expeditionary│V. C. Vaughan.
│ │ │ Forces) │
│ │ │British │
│ │ │ Expeditionary│Carnwath.
│ │ │ Forces │
│ │ │Allied Western │Public Health
│ │ │ Front │ Reports.
│ 1│ │German Western │Gins.
│ │ │ Front │
───────────┼────────────┼─────────────┼───────────────┼────────────────
May │ │_France_ │Chaumont │Zinsser.
│ │_Scotland_ │Glasgow Dunlop,│Carnwath.
│ │ │ │Office
│ │_Spain_ │Madrid │ International
│ │ │ │ d’Hygiène
│ │ │ │ Publique.
│ │_Greece_ │Athens │Filtzos.
│ │ │ │Teissoniere,
│ │_Macedonia_ │French Army │ Beguet and
│ │ │ │ Jolly.
│ │ │Egyptian │
│ │_Egypt_ │ Expeditionary│Benjafield.
│ │ │ Forces │
│ │_Italian │ │MacNeal.
│ │ Navy_ │ │
───────────┼────────────┼─────────────┼───────────────┼────────────────
June │ │_England_ │Portsmouth │Carnwath.
│ 15│ │Birmingham │Public Health
│ │ │ │ Reports.
│ 1│_Switzerland_│Zürich │Office
│ │ │ │ International
│ │ │ │d’Hygiène
│ │ │ │ Publique.
│ 1│_Germany_ │Frankfurt, A. │Deutsche. med.
│ │ │ M. │ Wehnschr.
│ 3│ │Strasbourg │Rose.
│ │ │ (Alsace) │
│ 25│ │Bonn │Koepchen.
│ At the end │ │{Berlin │Deutsche. med.
│of the month│ │ {North & │ Wehnschr.
│ │ │ South Germany│
│ Late│_Austria_ │Vienna │Bohm.
│ 15│_Norway_ │Christiania │Public Health
│ │ │ │ Reports.
│ 15│_China_(?) │Chefoo │Public Health
│ │ │ │ Reports.
│ 16│_Brazil_ │Santos │Public Health
│ │ │ │ Reports.
│ 22│_India_ │Bombay │Public Health
│ │ │ │ Reports.
│ │_Porto Rico_ │ │Atiles.
│ │Philippine │ │Hernando
│ │ Islands │ │
│ │ │ │
───────────┼────────────┼─────────────┼───────────────┼────────────────
July │ 1│_Germany_ │Dresden │Schmorl.
│ │ │ │Office
│ │_Italy_ │ │ International
│ │ │ │ d’Hygiène
│ │ │ │ Publique.
│ 13│_Sweden_ │Malmo │
│ │ │Gothenburg │Frost and
│ │ │ │ Sydenstricker.
│ Late 27│_Netherlands_│Flushing │Public Health
│ │ │ │ Reports.
│ │_China_ │Chungking │Public Health
│ │ │ │ Reports.
│ │_India_ │Calcutta │Malone.
───────────┼────────────┼─────────────┼───────────────┼────────────────
August │ │_India_ │Punjab │Jour. Am. Med.
│ │ │ │ Assn.
│ 3│_West Indies_│Guadeloupe │Public Health
│ │ │ │ Reports.
│ │_United │Boston │Second Spread.
│ │ States_ │ │
───────────┼────────────┼─────────────┼───────────────┼────────────────
September │ │_Denmark_ │ │Frost and
│ │ │ │ Sydenstricker.
│ 11│_Republic of │ │Public Health
│ │ Salvador_ │ │ Reports.
│ 16│_Honduras_ │ │Frost and
│ │ │ │ Sydenstricker.
│ 25│_Bermuda_ │ │Frost and
│ │ │ │ Sydenstricker.
│ 30│_Jamaica_ │ │Frost and
│ │ │ │ Sydenstricker.
│ │_Mexico_ │Santa Cruz │Frost and
│ │ │ │ Sydenstricker.
│ 21│_Canada_ │Victoriaville │Frost and
│ │ │ │ Sydenstricker.
│ │ │Quebec │
│ │ │Hamilton │
│ 30│_Portugal_ │Lisbon │Public Health
│ │ │ │ Reports.
│ 28│_Morocco_ │Tangier │Frost and
│ │ │ │ Sydenstricker.
│ 14│_South Africa│ │Frost and
│ │ Union_ │ │ Sydenstricker.
│ 16│_Senegal_ │Dakar │Public Health
│ │ │ │ Reports.
│ 16│_Sierra │Freetown │Public Health
│ │ Leone_ │ │ Reports.
│ │_Korea_ │ │Schofield.
│ │_United │West and South │
│ │ States_ │ from Boston │
───────────┼────────────┼─────────────┼───────────────┼────────────────
October │ Early│_Alaska_ │ │Governor’s
│ │ │ │ Annual Report.
│ 1│_Russia_ │Archangel │Frost and
│ │ │ │ Sydenstricker.
│ │_Peru_ │Lima │Soldan.
│ │_Uruguay_ │Montevideo │Frost and
│ │ │ │ Sydenstricker.
│ 25│_Venezuela_ │ │Frost and
│ │ │ │ Sydenstricker.
│ 11│_Guatemala_ │ │Frost and
│ │ │ │ Sydenstricker.
│ 12│_Costa Rica_ │Limon │Frost and
│ │ │ │ Sydenstricker.
│ 26│_Colombia_ │Begota, │Frost and
│ │ │ Barranguilla.│ Sydenstricker.
│ │ │Cartagena, │Frost and
│ │ │ Peru. │ Sydenstricker.
│ 9│_Cuba_ │Camagney, │Frost and
│ │ │ Nuevitas │ Sydenstricker.
│ 22│_Azores_ │ │Public Health
│ │ │ │ Reports.
│ 18│_Canary │ │
│ │ Islands_ │ │
│ 19│_Madagascar_ │ │Frost and
│ │ │ │ Sydenstricker.
│ 17│_Australia_ │ │Frost and
│ │ │ │ Sydenstricker.
│ 19│_New Zealand_│ │Frost and
│ │ │ │ Sydenstricker.
│ │_Hawaii_ │Honolulu │Frost and
│ │ │ │ Sydenstricker.
───────────┼────────────┼─────────────┼───────────────┼────────────────
November │ │_British │ │Rose.
│ │ Guiana_ │ │
│ │_Dutch │Paramaribo │Frost and
│ │ Guiana_ │ │ Sydenstricker.
│ 22│_Samoa_ │Apia │Frost and
│ │ │ │ Sydenstricker.
│ │_Arabia_ │Aden │Frost and
│ │ │ │ Sydenstricker.
│ │_Iceland_ │ │Erlendsson.
───────────┼────────────┼─────────────┼───────────────┼────────────────
December │ │_Paraguay_ │Paraguay, │Frost and
│ │ │ Asuncion │ Sydenstricker.
│ │_Dominican │La Plata, │Frost and
│ 19│ Republic_ │ Puerto Plata,│ Sydenstricker.
│ │ │ Santo Domingo│
│ │_Lapland_ │ │Macklin.
│ 8│_Society │ │Frost and
│ │ Islands_ │ │ Sydenstricker.
│ 3│_Tonga │ │Frost and
│ │ Islands_ │ │ Sydenstricker.
│ │_Fiji │ │Frost and
│ │ Islands_ │ │ Sydenstricker.
───────────┴────────────┴─────────────┴───────────────┴────────────────
During its course through Europe influenza had developed a greatly
heightened virulence and toward the end of August it again appeared in
the United States apparently traveling in a reverse direction from that
of its first spread and, entering the country at Boston, it spread to
the West and South until the entire country was covered. The West Indies
were invaded early in August and in the same month the disease had
spread through India as far as the Punjab. In September the epidemic
continued through the West Indies, attacked Mexico and Canada, and had
attained such remote localities as the South Africa Union, Senegal and
Korea. In October the spread was particularly distributed through South
America, and in this month again remote localities such as Alaska, New
Zealand, the Hawaiian Islands, Australia, and Madagascar were reached.
Islands, which although not very remote, were isolated except for the
arrival of occasional ships, such as Cuba, the Azores and the Canary
Islands, were first reported attacked in October. In November the spread
continued throughout the world, and among the more remote localities
should be mentioned Samoa, Arabia, Iceland. In December, Lapland, the
Society Islands and the Fiji Islands were invaded (see Chart XI).
CHART XI.
[Illustration:
Cinematogram showing the spread of influenza in 1918 from a
presumptive primary focus in the United States.
]
It is particularly of interest to follow the spread of the disease in
Europe. Perhaps the chief characteristic is the distribution equally to
the north and south of France, a country which appears to have been
invaded early. In May it spread to Scotland and to Spain, Greece and
Egypt. In June the spread was in three directions, to England and Norway
on the North, to Switzerland, Germany and Austria on the East, and again
into Spain and Italy on the South.
The correctness of the foregoing description of the spread of influenza
depends first, upon the accuracy of the authorities quoted, and
particularly upon our having discovered the earliest report for each
country. The author believes that the information as obtained for the
United States represents nearly the true state of affairs, and that the
error present is negligible. The information obtained for France is
based upon the statements of excellent investigators, Netter, Chauffard
and Massary, for the French population, and MacNeal, Zinsser and
Longcope, for the American Expeditionary Forces. Here the statements
agree both for the military and for the civil population that there was
no widespread influenza in France much before April 1st. Also, the
author feels that the information for England and Scotland is
authoritative and will not later be changed. It is based particularly
upon the excellent reports by Carnwath, who has investigated the subject
in great detail. The excerpts from the German literature, although not
abundant, are practically unanimous in agreeing as to the date of
invasion in Germany. The reports from the remaining countries of Europe
have been less abundant, and frequently the author has been forced to
rely upon a report by only one individual; but while the date may be in
error, yet the month of occurrence is probably correct.
For other continents, Asia, Africa and South America, the reports as far
as they go appear reliable, but it is impossible to prove that at an
earlier date there was not a very mild epidemic in some one of these
localities, similar to the earlier epidemic in the United States, which
escaped detection. It is particularly important, in view of the 1889
experience, that we obtain if possible fuller information on the
earliest time of the appearance of the disease in China and other parts
of Asia, and that we determine whether there was a spread from that
continent to America previous to March, 1918.
Several factors have added considerably to the difficulty in tracing the
site of origin of the 1918 epidemic and its direction of spread. The
principal of these have been the speed of modern travel, the character
of modern commerce, and the existence of a state of war. The channels of
the commerce of today radiate nearly from all points to all other points
of the civilized world. No longer are there a few preeminent lanes of
travel, such as there were in 1580 when the epidemic spread clearly from
Constantinople to Venice and on to Hungary and Germany, finally finding
its way to Norway, Sweden, Denmark and Russia. The war has made it
difficult to know accurately the date and direction of spread in enemy
countries. We have practically no information, except that in the public
press, from Russia and the Balkan States. By October of 1918 the severe
form of the disease had become prevalent in every continent, and by
December it had reached the farthest islands of the Southern Pacific
ocean.
The apparent difference in the direction of spread between 1889 and 1918
makes comparison of rapidity difficult. But if we take as our starting
point the time at which each epidemic became prevalent in commercial
centers of Europe and the time at which it finally reached localities
well off the usual paths of commerce we will see that there is some
difference, the disease spreading more rapidly in the recent epidemic,
but that the difference is no greater than could be accounted for by the
more modern means of communication. From April, 1918, when the disease
appeared in France, to October, when it was reported in Madagascar, is
six months. From October, 1889, with the disease prevailing in
Petrograd, to July, 1890, when it appeared in Madagascar, is nine
months. It required seven months after the disease became epidemic in
France this time for it to appear in Iceland, and nine months in
1889–90.
The earliest recorded epidemic of influenza in the United States in the
spring of 1918 (but which was not recognized to be such until later)
appears to have been that at Camp Funston, described by Opie and his
associates as having appeared in that Camp March 5th. The epidemic swept
quickly throughout the Camp and spent itself as rapidly. A second wave
appeared in April and in May a third, both of which were almost entirely
limited to newly drafted men brought into camp subsequent to the
preceding outbreaks. Correlated with each of these three outbreaks was a
period of increased incidence of pneumonia and bronchitis, frequently
occurring in influenza cases. These complicating diseases were prevalent
in the organizations attacked by the influenza and maintained the same
relation to the length of service of the men affected.
The next report of influenza in the United States was from the
Oglethorpe camps, beginning about March, 18, 1918. Within two weeks
every organization in Camp Forrest and the Reserve Officers Training
Camp was affected. After about three weeks the epidemic subsided
rapidly. Fourteen hundred and sixty-eight cases were sent to the
hospital out of a total strength of 28,586. It is estimated that 2,900
cases had occurred. The clinical symptomatology and the epidemic
characteristics were described in detail.
On March 28th the author had occasion to observe a similar epidemic at
Camp Sevier, South Carolina, which appears to have attacked a smaller
proportion of the troops in camp, but which showed the same
epidemiologic picture. A note in the Public Health Reports states that
on March 30, 1918, the occurrence of eighteen cases of influenza, of
severe type, from which three deaths resulted, was reported at Haskell,
Kansas. This is the earliest report we have been able to find concerning
the disease in civil communities. That for Chicago was practically
contemporary. The Commissioner of Health of Chicago states in his
special report on the autumn epidemic, that in March, 1918, distinct
epidemics resembling influenza were observed in certain portions of that
city.
According to Public Health Reports, fevers of an undetermined nature
were reported during April and May at various points from Norfolk to
Louisiana. “An examination of the records and reports of the physicians
who had treated these cases leads to the belief that these fevers were
mainly influenza of mild type.” It is possible, however, that all cases
reported were not of the same disease, and in one locality in Louisiana
dengue may have occurred.
Fleisher states that during the latter part of March and early part of
April, 1918, there occurred at Camp Wadsworth an epidemic of measles and
practically concomitant with it an epidemic form of bronchopneumonia
associated with empyema. During this time there were some 200 cases of
measles and twenty-one cases of bronchopneumonia or empyema in which a
hemolytic streptococcus was the causative agent. He makes no mention of
any epidemic of influenza either in mild or severe form, occurring at
this period.
Forbes and Snyder reported that during the month of April, 1918, a
highly contagious, but comparatively mild infection of the respiratory
tract was epidemic in Camp Hancock. Several thousand men in the command
were infected, but relatively few were ill enough to be sent to the
hospital. The only fatal case occurred early in the epidemic, and it was
the observations made in this case which prompted the study made by
Forbes and Snyder.
The fatal case had the subjective symptoms familiar to influenza. The
physical findings were similar to those occurring in influenza in the
later epidemics. The leucocyte count was 4,300. A blood culture showed
in twenty-four hours a heavy growth of small non-motile, gram-negative
bacilli which the authors concluded to be Bacillus influenzae. The
leucocyte counts made at five hour intervals on a later date were
respectively, 3,400, 2,200 and 2,300. A second blood culture taken on
April 10th, a day later, also showed a pure culture of the same
organism. The leucocyte count had risen to 5,600. At necropsy a
confluent bronchopneumonia was found. There was no pleural effusion and
the other viscera showed nothing remarkable. Bacillus influenzae was
recovered from cultures taken from the lung and spleen.
Throughout this epidemic the clinical picture of the disease was
characteristic. Nearly every patient gave as the initial symptoms
backache, headache, slight cough or sore throat. Conjunctivitis and a
marked injection of the soft palate were noted in ninety per cent. of
the cases. In addition, a slight or moderate general adenopathy was
often observed. The face was flushed and in a few cases the skin of the
thorax presented a mild erythema. In three cases a provisional diagnosis
of scarlet fever was made until the blood count showed a leucopenia.
Leucopenia was characteristic of all cases.
During the early April epidemic at this camp, nasopharyngeal cultures
showed an organism resembling Bacillus influenzae in seventeen out of
thirty-three cases, but the identity of the organism was not established
by subcultures. In ten cases in which sputum examinations were made,
Bacillus influenzae was found in only four; streptococci were present in
six. Blood cultures on twenty consecutive non-fatal cases, only one of
which was complicated by bronchopneumonia, were all negative.
V. C. Vaughan reports that at Camp Shelby, Hattiesburg, Miss., there was
in April a division of troops numbering about 26,000. An epidemic of
mild influenza struck this camp in April, 1918, and within ten days
there were about 2,000 cases. This included not only those who were sent
to the hospitals, but also those who were cared for in barracks. This
was the only division that remained in this country without change of
station from April until the fall of 1918. During the summer this camp
received 20,000 recruits. In October, 1918, the virulent form of
influenza reached this camp. It confined itself almost exclusively to
the recruits of the summer, and scarcely touched the men who had lived
through the epidemic of April. Not only the 2,000 who had the disease in
April, but the 24,000 who apparently were not affected, escaped the fall
epidemic.
Vaughan also remarks that in March and April of 1918 there was an
unusually high death rate from pneumonia in Atlanta, Ga., Kansas City,
Mo., Detroit, Mich., and Columbus, Ohio, while in the autumn epidemic
these cities suffered rather less than the average. In view of the
experience at Camp Shelby he reasons that there was probably mild
influenza in these cities in March and April of 1918. It may be stated
that in the mortality statistics for 1918, the abnormally high death
rates for respiratory diseases during March and April were present
throughout the registration area of the United States.
The first reports that we have been able to discover concerning
influenza on the Pacific Coast are for the month of April. Stanley
reports three successive waves of epidemic influenza at San Quentin
Prison, Cal. The first began on April 30, 1918, with the entrance into
the institution of a prisoner who was sick on admission.
Following the disease in its possible spread to the next continent we
are inclined to conclude that it was carried to France with the great
body of men traveling to that country from the United States. MacNeal
and Longcope both report that in the first outbreak in the American
Expeditionary Forces the earliest recorded epidemic appeared about April
1, 1918, in a rest camp near Bordeaux. It reached its height April 22d
and ceased May 5th. According to V. C. Vaughan a mild epidemic of
influenza and pneumonia prevailed at Brest and in that vicinity from
April 1st to July 31st, 1918. During this time fifty cases of influenza,
twenty-six of which developed pneumonia, with two deaths were admitted
to the United States Naval Base Hospital at Brest. The disease was
prevalent at the same time among the French civil, military and naval
groups in the same locality. We see then that in the American
Expeditionary Forces at any rate the disease first occurred in two base
ports receiving troops from the United States. In May, 1918, a second
outbreak was reported from Tours, which lasted from May 1st to May 24th
and affected 117 persons. Zinsser reports an epidemic at Chaumont during
May and from this time until July more or less extensive epidemics
occurred throughout the entire American Expeditionary Forces.
Longcope remarks that the disease was likewise prevalent at this time
among the French population and in parts of the British Army. The
Influenza Committee of the British Advisory Board determined that in the
first British Army the disease became prevalent around May 18th.
Carnwath states that in the British Army in France the epidemic began by
a few local outbreaks in the first and second Armies in April and May,
1918. Later it spread to the first, third and fourth Armies and affected
a very large proportion of the troops.
Small describes two epidemics of influenza in one of the largest General
Hospitals of the British Expeditionary Force in France. He says that the
first wave began in April, 1918.
The fact that MacNeal, as we have previously recorded, believed that
there was influenza in France in 1917, must not be overlooked. Those
earlier cases were scattered and did not so far as we know occur in the
form of small epidemics. Even if these were true influenza it is
reasonable to assume that they were sporadic cases and were not
genetically associated with the epidemic spreading from America and
daily increasing in virulence, which we are now following. MacNeal
concludes that epidemic influenza in France originated from the endemic
foci existing there, and that the disease was probably carried from
Europe to the United States by shipping. The author’s opinion regarding
the first direction of spread is that the reverse condition was the
actual process. Zinsser likewise holds the latter view.
A most important observation made by MacNeal is that French physicians
practicing among the civilian population were perfectly familiar with
the disease when it appeared at Chaumont in April, 1918, that they
designated it as La Grippe, and stated that it had been extensively
prevalent in the civilian population of Chaumont from March 15th to May
15th, 1918. These observations of influenza occurring in France at
almost the same date as the first outbreaks in the United States is a
matter of great interest. It has also been stated by McNalty and by
Carnwath, who quotes Kabeshima and Lee, that the disease was prevalent
in epidemic form in China and Japan in March, 1918. We have here three
foci from which the disease may have primarily originated. There are two
possibilities; first, that it originated in all three foci (and perhaps
others), and spread to all parts of the world from each; second, that
the virus, distributed throughout the world, acquired high virulence in
all three localities, causing small epidemic outbreaks, but that the
virus from only one of these places finally became so exalted as to
cause the pandemic. Did the _pandemic_ disease originate simultaneously
in France, in China and in the United States? One fact seems certain,
that the influenza which attacked our troops in Europe was influenza
imported from the United States. We have seen that it first appeared in
the American Expeditionary forces at the base ports. Alberto Lutraria,
Health Commissioner of Italy, has reported that the disease was brought
to that country from America. A point of significance is the fact that
during March and April there was an unusually large troop movement from
the United States to the American Expeditionary Forces.
MacNeal says: “The suggestion that the epidemic was introduced from
America is supported by the fact that it appeared at a time when large
numbers of Americans were arriving in Europe, which is indeed an
outstanding feature correlated in time with the onset of the epidemic.”
According to the report of the Influenza Committee, the disease was
first seen in epidemic form in April and May in the British Armies in
France, but that was not the first time that Pfeiffer’s bacillus had
appeared within the armies. It had frequently been found in cases of
bronchopneumonia, especially during the winter of 1916–17. Carnwath
remarks that it is doubtful whether much importance from an
epidemiologic point of view attaches to these sporadic findings of the
influenza bacillus. In an outbreak of measles and rubella—complicated by
purulent bronchitis—which attacked men belonging to the draft of troops
from New Zealand between January 1st and March 8th, 1918, the bacillus
influenzae was present in twenty-four of the forty sputa examined, and
was grown in culture in twenty-one cases. Sellards made somewhat similar
observations on measles patients at Camp Devens.
Concerning the French population, Chauffard, Messary and Netter, all
remark that the first cases in France developed in April with possibly
some cases before that time, and that there were undoubtedly cases in
the German Army in April.
We see then that by April the disease has been transferred to France and
is prevalent in the various armies. It is natural to assume that the
battle front would present no great obstacle to the spread of the
disease into the German Army. Gins remarks that the disease was present
on the German West front among the troops as early as April, 1918, and
that it spread from there more rapidly to the South than to the North.
During the month of May we observe the spread of the disease to Great
Britain, where Carnwath, who has made an exhaustive study of the spread
in Great Britain, believes that it was imported by the troops from
France. Its first recorded appearance in Glasgow was in May. Dunlop, in
reporting the successive epidemics in Scotland, observed that in
addition to the three well marked epidemics there was a mild one
recognizable in Glasgow in May, and that in that city the death rate
rose from 14.1 to 20.1, and the weekly number of deaths from pneumonia
and bronchitis from 36 to 107.
In England the disease first attracted attention in June, appearing
first in the coast towns, chiefly at the beginning among the military
and naval forces. The civilian population was severely affected only
later. The ports which were earlier attacked were Portsmouth,
Southampton and Liverpool. Inland towns suffered more severely later.
In the same month that the disease broke out in Scotland it appeared in
Spain. The Inspector General of Health in that country reported that an
epidemic of the disease began at Madrid in the last half of May, 1918,
at a period when there was an unusually large gathering of people in the
city. Within a short time it had spread rapidly through all the
provinces. The increase in death rate became marked on the 27th of May
and reached its peak on the 31st, at which time the rate was twice that
of the average annual death rate for that period of the year. During the
following week there was some oscillation around the peak and then the
curve fell away. The epidemic was particularly severe at Madrid,
Badajoz, and Seville. It was mild at Barcelona.
MacNeal remarks: “In Spain the disease appeared in epidemic form about
the middle of May and this outbreak received great publicity, sufficient
to lead to the popular appellation of Spanish influenza. The very rapid
and extensive spread of the disease in Spain would indicate that it had
been introduced from without rather than transformed from the endemic
state in that country. This also appears to accord with the view of
those who have studied the epidemic in Spain.”
Filtzos reports that influenza first appeared in Greece toward the end
of May, 1918. The symptoms were slight and the people who were attacked
suffered for three or four days with fever, accompanied by nervous
symptoms. It was called at the time “Spanish Fever”. Beginning with
September the epidemic became worse and caused a considerable rise in
mortality. Complications with bronchopneumonia appeared. The decrease in
incidence began toward the middle of December, 1918.
According to Benjafield, the pandemic first commenced in the Egyptian
Expeditionary Force in May, 1918, but the maximum incidence was not
reached until September and October. The cases during the earlier period
of the epidemic were on the whole mild in type and of short duration,
only a very small proportion being complicated by bronchopneumonia. The
epidemic continued from November, through February, 1919, but the number
of cases showed a marked decrease during the last two months.
The month of June saw the spread into England which we have already
described, and the continuation from the German West front back into the
enemy territory.
Rose reports that on the 3d of June, 1918, in Strasbourg the first cases
of influenza were reported in his hospital and that by the 15th of the
month the disease was practically epidemic. Wachter in reporting cases
from Frankfurt a. M. says that the cases of influenza in that city
appeared from the beginning of June, 1918. Schmorl remarks that
influenza became epidemic in Dresden in the beginning of July, 1918.
According to Koepchen, the disease was epidemic in Bonn the 25th of
June.
An editorial comment in the Deutsche medizinische Wochenschrift, July 4,
1918, remarks that the influenza pandemic “which probably has spread
from Spain in the last few days” has appeared in several places in
Germany in the South and the North, and in Berlin. According to the
information received up to that time the disease was of short duration
and without severe complications. The issue of July 11th reports that
the influenza epidemic appears to have already passed its peak in Berlin
and that in Süddeutschland the spread of the epidemic has become very
wide.
The Office International d’Hygiène Publique records that the pandemic
spread throughout Switzerland towards the end of June, 1918, after
having invaded a certain number of European states, coming from various
army fronts. It was at first of mild severity.
Böhm states that the deaths from pneumonia and influenza in Vienna began
to show an increase in the week ending July 30th. In August they
returned to the normal rate. The second wave occurred in Vienna in the
middle of September.
From the information at our disposal we are unable to determine from
what direction the pandemic entered either Switzerland or Austria. The
point of entry into Switzerland is of relatively little importance in
tracing the spread on the continent of Europe. Presumably it entered
from the north or northwest. The disease appeared in Berne in June,
reaching its height in that canton in the middle of July and dying out
in August (Sobernheim and Novkaovie).
Information of the place of entrance into Spain is also rather
indefinite. We are told that Barcelona was one of the cities attacked
early. Barcelona is situated on the Mediterranean near the French border
and is quite directly connected by commerce with Marseilles and other
French ports on the Mediterranean.
In June the disease had also spread to Norway and outside of Europe to
the West Indies, South America, India and China. A short notice in the
Public Health Reports tells us that epidemic influenza with an estimated
number of 1,500 cases began in Christiania, Norway, about June 15th.
Atiles relates that influenza appeared in Porto Rico in June, soon after
the arrival of a ship from Spain. It spread rapidly, and it is estimated
that at one time fully eight per cent. of the entire population had the
disease simultaneously, and that forty per cent. of the population were
affected during the epidemic.
The Health Officer at Bombay made report in July, 1918, on an
influenza-like disease then spreading throughout India. It was stated
that the disease was introduced into Bombay from overseas by a transport
which arrived May 31, 1918; that by June 22d the disease had become
epidemic at Bombay, and that it was present in July, 1918, at Calcutta
and Madras.
The rapid spread from Europe to distant India may be accounted for with
the same mechanism as that by which the disease was spread from America
to France and from France to England, viz. by army transports. The
occurrence of the disease in Porto Rico appears to have been definitely
connected with the arrival of a ship from Spain. A very short notice in
the Public Health Reports tells us that influenza was reported present
at Santos, Brazil, June 16, 1918. We are not informed as to how it
reached that place.
We have discovered no mention of influenza in China in June. It was
reported present in Chungking, China, July 27th. and at that time
one-half of the population was stated to be affected. Dengue was
reported prevalent at Chefoo, China, during the two weeks ended June 15,
1918, and a report from Shanghai of the same date describes the
prevalence of a disease resembling dengue and affecting about 50 per
cent. of the population. The disease in these two latter places may have
been influenza.
The epidemic made its appearance in Korea in September, 1918. Schofield
and Cynn, who report the epidemic, believe that the infection came from
Europe via Siberia. The disease spread from North to South along the
line of the Southern Manchurian Railway.
In August the disease was re-introduced into the United States and by
the end of that month it had acquired a foothold in Boston and vicinity
and rapidly spread to other parts of the country. The pandemic had
crossed the Atlantic in both directions in six months’ time.
In 1918 as in 1889 there are excellent descriptions of the conveyance of
the disease by vessels. The transfer from Spain to Porto Rico has been
mentioned. Escomel says that the outbreak in Rio de Janeiro was ascribed
to infection from a steamship from Spain, the same boat which later
visited Buenos Ayres and started the epidemic in the latter city.
According to a report to the Journal of the American Medical Association
from Mexico the epidemic invaded that country from the North at Laredo
and followed the course from North to South. From a similar source the
same Journal reports that the influenza spread from Buenos Ayres as a
primary focus to Paraguay and there acquired greater virulence.
Hernando reports from the Philippine Islands that influenza was
estimated to have attacked forty per cent. of the total population of
7,000,000 the mortality being about 2.5 per cent. of those attacked. The
epidemic really began in June, although it did not assume great severity
until October. The group of ages that suffered most were those between
ten and twenty-nine years. The disease did not seem to be imported,
since cases were returned before any ships arrived from infected
countries, although after the importation of cases it assumed a more
severe form. The June epidemic seemed to confer a certain degree of
immunity during the second outbreak of the disease in October.
Erlendsson reports that the influenza when it appeared in Iceland in
November, 1918, corresponded in character with that in other portions of
the world. Macklin gives an interesting description of the epidemic as
it occurred in Lapland. The onset in that territory was probably in
November. He found that many individuals recovered in two or three days
and were about their work again feeling perfectly well. If, however,
they contracted pneumonia, about fifty per cent. died.
“The Laplanders had a very thorough if unsympathetic way of dealing with
their cases. The settlements were composed of wooden huts, small but
generally well made and warm. A common type consisted of but one room,
used by the family for all purposes. Better class Laps had better huts,
with two or three rooms. In each settlement one of the single-room huts
had been set apart, and into this each case of sickness as it arose was
unceremoniously pushed; and none were permitted to return to their own
huts until completely recovered. Whilst there they received practically
no attention, and no healthy person ever entered to attend to their
wants. Occasionally a bowl of water or reindeer milk was hastily passed
in at the door, or a huge chunk of reindeer meat thrown in, uncooked and
uncarved.
“We visited every settlement within our reach and entered these huts.
The stench on opening the door met one like a poison blast and the rooms
were nearly always ill lighted and dark. The patients lay littered about
the floor in a crowded mass, fully dressed in clothes and boots (most of
them had no socks), and with no other cover but an occasional greasy
rug. Although the outside air was cold and the ground snow-covered, the
temperature inside, maintained by the combined mass of bodies, was
generally sufficiently high. The patients in these huts included both
sexes and all ages; some, when we entered, sat up and with flushed faces
and dull, uncomprehending eyes watched us listlessly. Others lay
restlessly twisting about, quite incapable of taking any interest or of
answering any questions.”
The epidemic struck Alaska in October, invading first the towns of the
sea coast, being very evidently brought thither by steamer. Travel to
the interior was stopped and so the latter escaped, to a great extent,
the outbreak. At Kodiak and on Cook Inlet, the mortality was extremely
high. Whole villages of esquimaux lost their entire adult population.
Many infants were frozen in their dead mothers’ arms.
_Influenza in China._—We have been able to follow the pandemic quite
consecutively as it has spread around the world, from a first outbreak
in the United States in March, 1918. We repeat that the disease was
presumably present in Europe and elsewhere previous to that time, as it
was in America, but the particular virus which ultimately acquired
sufficient virulence to produce the pandemic may well be that which came
from North America. Did this virus arise from an endemic focus in this
continent, or was it transported to us at a somewhat earlier date from
Asia?
McNalty states that influenza was present in China and in the Japanese
Navy in March of 1918. He gives no reference. Carnwath makes the same
statement and gives as reference the report of Kabeshima and Lee. The
author has not been able to obtain this report.
The Health Officer of Shanghai made the following report for May, 1918:
“Towards the end of the month, reports were received of outbreaks of
‘fever’ which rapidly affected a large proportion of the employees of
various offices, shops, police stations, etc. As a result of clinical
and laboratory observations of cases admitted to the Chinese Isolation
Hospital the disease was recognized as epidemic influenza. The same
disease was reported to have appeared in Peking before reaching
Shanghai, but subsequent reports showed that most of the river ports
were almost simultaneously infected; that is to say the rate of spread
conformed to the rate of conveyance by railways and boats of infected
persons;”
In November of 1918 an editorial note in the China Medical Journal reads
as follows:
“From nearly all parts of China reports are being sent to the newspapers
of the occurrence of a severe epidemic of disease which seems to
manifest itself in various forms. In Wusuch, where the disease is called
‘the five days’ plague’ the symptoms are said to be not unlike those of
cholera, death in some cases ensuing in less than a day. In other cases
it is complicated by severe and often fatal pneumonia. At Anking many
cases have all the symptoms of typhoid fever, but the mortality is great
and sudden. In one house four people died within a few hours of each
other, and in another house eight persons out of eleven died. At Wuhu
and other of the lower Yangtze ports it is said to resemble dengue fever
and the mortality is so great that undertakers are finding it difficult
to meet the demand for coffins. In Shansi, where the victims literally
number thousands, the disease is regarded as influenza. In Peking fully
fifty per cent. of the Chinese have been affected and the mortality has
been heavy. Accurate reports from medical men in these cities would be
very instructive.”
The author has the following personal communication from Doctor Arthur
Stanley of the Health Department of the Shanghai Municipal Council.
“Influenza fever appeared during the recent epidemic in Shanghai towards
the end of May 1918. It swept over the whole country like a tidal wave.
You may take it that it spread like most rapid extant means of transit.
A primary source of origin was not made known.”
It is to be hoped that more definite and concurrent information will be
forthcoming in the case of China. A thorough search of the literature as
reviewed for China and Japan in the China Medical Journal reveals no
description of the disease previous to April or May of 1918.
Nevertheless we must assume that, until contradictory reports are made,
the disease was present in those countries in March as stated by
Carnwath.
AUTUMN SPREAD IN THE UNITED STATES.
By the first of July, 1918, convalescent cases of influenza began to
appear among members of the crews of transports and other vessels
arriving in Boston from European ports. The number of such cases on each
ship was usually not more than four or five, but Woodward records that
in one or two instances between twenty and twenty-five individuals were
sick on incoming vessels. None of these were seriously ill, none were
sent to the hospital, and none died. The disease in this class of
persons did not become severe until late August. Woodward has found on
inquiry among practising physicians that typical cases of influenza were
seen with notable frequency in private practice in the vicinity of
Boston during the month of August, and that they had developed no
serious complications, the only after effect being the marked
prostration.
These mild preliminary cases failed to attract attention; first, because
of their relative scarcity, and second because of their benign
character. Public attention was first directed to the influenza in
Boston by the apparently sudden appearance during the week ending August
28th of about fifty cases at the Naval Station at Commonwealth Pier.
Within the next two weeks over 2,000 cases had occurred in the Naval
forces of the First Naval District. One week later there was a similar
sudden outbreak in the Aviation School and among the Naval Radio men at
the Massachusetts Institute of Technology. The first death in Boston was
reported on September 8th.
The peak of daily incidence in Boston occurred around the first of
October. In the week ending October 5th a total of 1,214 deaths from
influenza and pneumonia was reported, while by the third week of October
this total had fallen to less than 600, and for the week ending November
9th was down to 47. Around November 15th the number of cases rather
suddenly increased and this recurrent wave lasted for about ten days. By
the 25th the rate was back to what it had been around the first of the
same month. On or about December 1st the incidence again rose and
continued increasing daily, to reach its peak in a severe recrudescence
around December 31st.
There are conflicting reports concerning the date of first appearance of
the epidemic at Camp Devens, Massachusetts. Woodward says that a sudden
and very significant increase was reported during the third week in
August in the number of cases of pneumonia occurring in the army
cantonment at Camp Devens, seeming to justify the statement that an
influenza epidemic may have started among the soldiers there even before
it appeared in the naval forces. Soper, on the other hand, as well as
Howard and Love in their official report, place the date of the first
case at Devens as September 7th. Soper remarks: “The Devens epidemic is
supposed to have commenced on September 7, 1918, in D Company, 42d
Infantry. On that date a case of supposed meningitis was sent to the
hospital from this company; on the following day twelve cases were sent
for observation. These proved to be influenza. By the 16th thirty-seven
cases had gone from the same company.” Howard and Love state, “The first
authentic cases of virulent influenza of the great autumn pandemic among
troops in the United States appeared on September 7, 1918, at Camp
Devens, Mass.” These statements by Howard and Love do not eliminate the
possibility of earlier and less virulent unrecognized cases. Wooley, who
was camp epidemiologist, reports that influenza began at Camp Devens on
the 8th of September, 1918. It reached its acme on the 16th, 17th and
18th of the month and then rapidly declined, almost completely vanishing
about the middle of November. He makes no observation as to whether a
mild form of the disease was or was not present in the camp in March and
April preceding.
Influenza entered Massachusetts at Boston. Reeks reports that it entered
Connecticut at New London, the cases coming primarily from the
experimental station and from Fort Trumbull, where vessels from foreign
ports had discharged patients. He believes that the disease was first
introduced by ships arriving in New London from abroad and by men from
the Boston Navy Yard, but numerous foci developed in a short period of
time in various parts of the state. Many of these had appeared by the
middle of September, and the source, according to Winslow and Rogers,
was traced to military establishments, chiefly Camp Devens. In
Wallingford, Willimantic, Hartland, Rockville and Danbury, all of which
towns were attacked early in the epidemic, investigation showed that the
disease developed in each case two or three days after visits of
soldiers from Camp Devens. In Connecticut the epidemic spread, beginning
at New London, chiefly from east to west, reaching its peak in the
Eastern section around October 4th, in the central section October 15th,
and in the Western part of the state around October 24th. Towns which
had been infected early by visitors from military establishments reached
the climax sooner than other towns nearby. In spreading from New London
north and west the large cities of Connecticut were successively
invaded, New Haven and Hartford reaching their crest about ten days
later than New London, while Fairfield County did not reach its acme
until later than New Haven.
In the cities along the New England coast we see then that the disease
reached epidemic proportions early in September. By September 21st it
had become epidemic in a wide area along the Atlantic coast extending
from the Southern part of Maine to Virginia, as well as in a number of
localities scattered over the entire country. By September 28th, areas
adjacent to the centers in which the epidemic had already appeared were
affected, suggesting radial movement from these centers. By that time
the greater part of the New England States, the North Atlantic and
Central States, and some of the Gulf and Pacific Coast States had become
involved. By October 5th the pandemic had apparently reached all parts
of the country with the exception of the more isolated rural districts
and some areas in the Central States and Mountain States. Within an
additional ten days even these areas, with the exception of the very
remote rural districts, had been reached by the epidemic. Within four
weeks the disease had become distributed to all sections of the country,
and within six weeks from its first epidemic prevalence in Boston
practically the entire country had been invaded.
Sydenstricker in a preliminary report remarks on the fact that the
disease reached an epidemic stage in a number of localities in the
central, northern, southern and western sections at about the same time
as it did in the area along the northeastern coast. “The possibility is
suggested, therefore, that sources of infection existed in at least some
of the larger population centers, well distributed through the country,
some time before the disease appeared as a nation-wide epidemic. The
apparent radial spread of the epidemic from certain centers would seem
to strengthen this hypothesis. It may also be noted that there is
evidence, the collection of which has not yet been completed, pointing
to the existence of cases of the disease in various centers, probably
widely distributed, weeks before they were definitely recognized as
influenza. The possibility that these foci themselves had a common focus
is by no means excluded, of course, but there is as yet no conclusive
evidence that would warrant the statement that the starting point of the
epidemic was Boston or any specific locality.”
Dublin, from a study of the statistics of the Metropolitan Life
Insurance Company, finds that the virulence of the influenza, as
indicated by the mortality rate, was greatest along the Atlantic Coast
and became progressively less as it progressed westward. There was one
exception. The mortality was high in San Francisco, higher than in other
western communities. Dublin believes that quite possibly there was a
double infection in San Francisco in the fall of 1918, one coming from
the East and of small caliber, while the other came either by way of the
Panama Canal or perhaps from Asia. The evidence in favor of two ways is
that Dublin finds that the peak of incidence in San Francisco and in
some other places on the Pacific Coast occurred sometime in advance of
the similar peak at points inland from the coast. This is not brought
out in Pearl’s chart, and the latter finds when considering the peak of
deaths that the peak for San Francisco was late. The peak in that city,
in Oakland, California, and in Los Angeles, was reached on the week
ending November 2d. Few cities had as late death peaks. Cleveland and
Pittsburgh reached their peak in the same week, St. Paul, Minnesota in
the week ending November 16th, and St. Louis, Milwaukee and Grand Rapids
not until the week ending December 14th. In the case of Milwaukee and
St. Louis these were the high peak dates but they were second peaks. In
the former the first peak occurred October 26th and in the latter
November 2d. In Grand Rapids the increase in mortality was clearcut by
the middle of October, although the peak was not reached until the week
ending December 14th. These statistics would indicate that San Francisco
was attacked, as evidenced by increase in death reports, relatively
late, and at about the time that would be necessary for the disease to
be carried across the continent.
In an article by Ely, Lloyd, Hitchcock and Nickson it is said that
influenza first appeared in the Puget Sound Navy Yard, near Seattle, on
September 17, 1918, and that it was introduced by a draft of 987 sailors
received from Philadelphia, a number of whom arrived ill, or came down
within a few hours after reaching their destination. As a result,
Seattle and the State of Washington were infected somewhat ahead of the
other West Coast States. According to the record, influenza did not
assume epidemic proportions in the State of Oregon for nearly a month
after this Navy Yard epidemic.
With army camps and cantonments situated in nearly every section of the
country it is difficult to follow the general direction of spread from
camp to camp. During the period of the epidemic, troop movements were in
general from West to East toward points of embarkation rather than in
the reverse direction. This was in the opposite direction to that taken
by the pandemic. Away from the coast there were, however, many movements
of troops from camp to camp, in the redistribution of forces. That these
troop movements were not discontinued during the epidemic is indicated
by the report of Howard and Love: “The virulent type of influenza had
spread rapidly from camp to camp, from the Atlantic seaboard to the
South and West, due to the continual interchange of personnel from
infected to non-infected camps. Such movements of troops at this time
were recognized as dangerous and inadvisable, and prompt recommendations
were made by the Medical Department that such movements be discontinued
or greatly restricted, if compatible with military interests, which, of
course, were at the time paramount. The War Department was unable to
approve any marked restriction of movement of men from camp to camp at
this time. One result of the free inter-communication of military
personnel was that practically all military stations in the United
States were in the throes of the epidemic at the same time.”
In addition to this means of inter-communication we had the possibility
of spread to the various camps by the ordinary course of civilian and
commercial travel as in spread to different communities, and also the
possibility of importing large amounts of virus at one time on the
incoming trains with new draft troops.
Soper gives the following order for camps attacked:
═════════════════╤═════════════════╤═════════════════╤═════════════════
Order. │ Camp. │ Location. │ Date.
─────────────────┼─────────────────┼─────────────────┼─────────────────
1│Devens │Massachusetts │Sept. 12
2│Upton │New York │Sept. 13
3│Lee │Virginia │Sept. 17
4│Dix │New Jersey │Sept. 18
4│Jackson │South Carolina │Sept. 18
│ │ │
5│Hoboken │New Jersey │Sept. 19
5│Syracuse │New York │Sept. 19
5│Gordon │Georgia │Sept. 19
5│Humphreys │Virginia │Sept. 19
6│Logan │Texas │Sept. 20
│ │ │
6│Funston │Kansas │Sept. 20
6│Meade │Maryland │Sept. 20
7│Grant │Illinois │Sept. 22
7│Taylor │Kentucky │Sept. 22
8│Sevier │South Carolina │Sept. 23
│ │ │
8│Lewis │Washington │Sept. 23
8│Newport News │Virginia │Sept. 23
9│Pike │Arkansas │Sept. 24
10│Beauregard │Louisiana │Sept. 25
10│Eustis │Virginia │Sept. 25
│ │ │
11│Greene │North Carolina │Sept. 26
11│McClellan │Alabama │Sept. 26
12│Kearney │California │Sept. 27
12│Bowie │Texas │Sept. 27
13│Johnston │Florida │Sept. 28
│ │ │
13│Sheridan │Alabama │Sept. 28
14│Sherman │Ohio │Sept. 29
14│Dodge │Iowa │Sept. 29
14│Shelby │Mississippi │Sept. 29
15│Custer │Michigan │Sept. 30
│ │ │
16│Travis │Texas │Oct. 1
17│Cody │New Mexico │Oct. 3
18│Forrest │Georgia │Oct. 6
19│MacArthur │Texas │Oct. 7
20│Wadsworth │South Carolina │Oct. 11
│ │ │
20│Wheeler │Georgia │Oct. 11
20│Greenleaf │Georgia │Oct. 11
─────────────────┴─────────────────┴─────────────────┴─────────────────
Howard and Love have established definitely that the extension of the
virulent influenza from Camp Devens to other camps south and west in
September, 1918, can be traced in many instances directly to the
interchange of military personnel from infected to non-infected camps.
The height of the September outbreak in the United States Army extended
over a period of about nine weeks, from Sept. 13th to November 15th, and
during this period over 20,000 deaths occurred among troops in the
United States alone in excess of the number that would have occurred, if
the disease death rate for the corresponding period of the preceding
year had prevailed.
It is interesting to note with respect to Camp Humphreys, Virginia, that
there were possibly some sporadic cases previous to the autumn outbreak.
Brewer in reporting on the epidemic in September and October records the
first case as having occurred shortly after July 1st. He makes no
mention of there having been any outbreak whatever prior to that date.
Between July 1st and September 12th there were only sporadic cases
diagnosed as influenza. The autumn outbreak began at Camp Humphreys
September 13th and ended October 18th.
RECRUDESCENCES.
We have already seen from the work of Pearl that recrudescences
following the original spread in any one locality were the rule rather
than the exception in this country. He found that in sixty-five per
cent. of the forty cities studied there were two distinct peaks in the
mortality curve and in twenty per cent. there were three, while only
fifteen per cent. had but one peak. The first peak was as a rule the
highest. Although there was no absolute regularity in the time of
occurrence of the recrudescences, Pearl established that the high peak
cities had the second peaks on an average 7.1 weeks after the first, and
the third peak on an average 13.1 weeks after the second. The two-peak
cities are divided into two classes, the first comprising about a third
of the total number, had the second mortality peak around eight weeks
after the first, while the remaining two-thirds had the second peak
about thirteen weeks after the first. The cycle in the epidemic wave
appears to be nearly a multiple of seven weeks. He suggests that the
smaller group of two-peak cities with early second peak may have been
cities which at the time were presumably destined to show a third
distinct wave and peak of mortality, but in which for some reason not
now apparent the third wave did not eventuate. In contradistinction the
larger group of two-peak cities with the second peak occurring around
thirteen weeks after the first are presumably cities in which the
complex of factors determining the form of the mortality curve was such
as to lead definitely to a two and only two-peak curve. In three-peak
cities the first interval was around seven weeks, the second around
thirteen weeks. The two-peak cities with an interval around thirteen
were probably not destined, according to Pearl, to have another
repetition, but those with an interval of seven were presumably destined
to have a second interval, the thirteen-week interval, which for some
reason did not occur.
This raises the question of periodicity, a subject which we will discuss
at a more appropriate place.
This experience of recrudescences was similar in the American
Expeditionary Forces. The first outbreak lasted through April and May
and into June. The second came in September and October. The spring
epidemic had been characterized by mildness and was known as three-day
fever, but in the autumn, complications of the respiratory tract
predominated in the symptom complex. By August 18th a severe epidemic
had occurred in an artillery camp at La Valdahon in the Jura Mountains,
near Bezançon. Early in September a larger epidemic occurred in an
artillery camp near Bordeaux. The epidemic in our troops in France, as
well as in the French civil and military population, reached its height
during October. The Service of Supply was more heavily affected than
were the troops situated on the battle front. The morbidity rate
appeared to have been almost the same as that in the United States. That
it was not quite as high has been shown by Howard and Love. Longcope
states that it prevailed particularly among the troops at the base ports
where during a part of the epidemic transports laden with infected
troops were being landed; in those organizations which contained the
largest number of replacement troops; and in organizations being moved
on troop trains, where the men were necessarily closely crowded.
The second outbreak subsided during the early part of November. A third
occurred in January and February, very much as it had done in the United
States. In the interval between the second and third recurrences there
was no time at which the entire Expeditionary Forces were free from the
disease. The author had occasion to study an outbreak occurring early in
December in the 26th Division stationed in rest area at Montigny-le-Roi.
In this outbreak the respiratory complications predominated, as in
October, and the mortality was comparatively high. We had had occasion
to study the same disease at Camp Sevier, South Carolina in September
and early October, 1918, and in two different localities in France in
December, 1918, and February, 1919, and found that the clinical
characteristics were identical on both continents.
The more severe recurrence in England, in October, has been carefully
studied. In fact this recurrence was almost universal in all countries.
The autumn epidemic has been reported as being at its height in October,
1918, in such widely separated localities as the United States, England,
France, Greece, Brazil, India, Japan and Korea.
In Europe at any rate the third wave occurring in the winter of 1919 was
quite generally distributed. At about the same time the disease broke
out in England, making a third wave in less than a year. Once again the
third attack began less suddenly and less violently and resulted in a
lower number of fatalities. During February there was reported to have
been a great increase in the number of cases in Paris. It had terminated
by March 27, 1919. In March the disease broke out anew, this time
assuming grave proportions, not only in that city but in several of the
Departments.
The second recrudescence has also been reported as being present in
Spain.
On May 5, 1919, report was received from Buenos Ayres that in one of the
concentration zones for naval troops located in the harbor there had
been an epidemic of short duration, but with high morbidity, with two
hundred cases being frequently reported each day.
Just as Pearl has observed a certain periodic recrudescence in the
United States, there has been described a similar periodicity in
England. The interval, however, is described as twelve weeks. The first
wave began in July and died down about the end of August, running a two
months course. Twelve weeks after the commencement of the first wave, at
the beginning of October, the second appeared. It had disappeared around
the middle of December. Again, twelve weeks from the beginning of the
second wave, that is, in January, the third appeared.
RECURRENCES IN WINTER OF 1919–1920.
We distinguish between the flareups following the autumn spread of 1918,
and which lasted until the spring of 1919, and yet another widely
distributed recurrence in the winter of 1920. We have called the former
recrudescences to distinguish them in point of time from the latter, but
do not imply thereby any difference in the character or origin of the
secondary waves. Between them all there occurred almost continuously
isolated or solitary cases of influenza which served to keep the fires
smouldering. In our own work in the city of Boston we found record of
scattered infrequent cases of clinical influenza of apparently low
infectivity in every month from March, 1919, until the recurrence in
January, 1920.
Moreover, in some localities there were during this interval small
epidemic outbreaks. Thus a report from Lisbon, Portugal, on June 1,
1919, states that the deaths from influenza in that city during the
preceding two weeks had been more than the total deaths from all causes
during the preceding four months. A report from London, October 30,
1919, states that during the preceding few weeks there had been in the
ninety-six great towns of England and Wales a slight but gradual
increase in the number of deaths attributed to the disease, and a
coincident rise in the number of notifications of acute primary and
acute influenzal pneumonia. The feeling at that time was that the
increase was associated with prevailing meteorological conditions, and
did not apparently signify more than the usual variation in respiratory
diseases which was to be expected at that season of the year. On
November 3, 1919, the disease was reported prevailing at Chile and it
was spreading throughout Bolivia. At the same time influenza had spread
over the entire country surrounding Buenos Ayres and had even reached
the neighboring city of Montevideo. In the latter part of November more
than 2,000 cases had been reported at Lemaies, about fifteen miles
northeast of Granada, Spain.
_The winter of 1920._—In the United States the death rates from
influenza and pneumonia in the large cities over the entire country were
below the usual average from May, 1919, until January 1, 1920. In the
week ending January 17th there was a sharp increase in the
influenza-pneumonia rate, which occurred simultaneously in Kansas City
and Chicago. In the latter city an excess over the average was not
reached until some days later, but the maximum mortality occurred in the
week ending January 31st, while in Kansas City the mortality did not
reach its height until one week later. New York, Washington, San
Francisco, Milwaukee and St. Paul soon followed with an increase in the
week ending January 24th, and in the subsequent two weeks many other
cities were added to the list. By February 14th thirty-two out of the
thirty-six large cities reporting had an increase in the death rate from
influenza and pneumonia as compared with the same period in 1917. The
maximum was reached at this time, and according to the Bureau of the
Census reports there were 7,059 deaths from influenza and pneumonia
during the week ending February 14th. In the next week the number of
deaths from these causes in the cities reporting had dropped to 5,088.
The February weekly average for 1917 was 1,489. In the week ending
February 14th, 267,643 cases of influenza were reported from forty-one
states; the excess annual death rate as compared with the average for
the period from 1910 to 1916 was 1,319.
In general the 1920 recurrence was decidedly milder than the autumn
outbreak of 1918. Certain cities, however, suffered severely,
particularly Detroit, Milwaukee, Kansas City, Minneapolis and St. Louis.
In these the death rate, while the epidemic lasted, was higher than that
of 1918. The duration of the epidemic was generally, however, shorter in
these cities. Columbus, Ohio, and Indianapolis suffered severely, but to
a less extent than the cities just mentioned. In Chicago the death rate
was not as high as in the fall of 1918, but it did rise far above the
point reached during the 1889–90 outbreak, and the influenza in the last
two weeks of January brought the total mortality for that month up to
5,149, the highest mortality in the history of the city with the
exception of October, 1918.
We have already discussed the recurrent epidemic as it was studied in
Detroit. The salient characteristics were a rapid and fairly symmetrical
evolution, a shorter duration than in 1918, a lower morbidity with a
higher mortality rate, and finally, a smaller total number of deaths
than in 1918.
The 1920 recurrence was widespread. It was not confined entirely to the
large cities. Semi-official reports from small towns and villages show
very much the same conditions as were observed in the larger cities. On
the whole, however, most communities, both large and small, suffered
less severely than in the first spread. The few exceptions to this were
distributed over the continent without uniformity.
The first among the large cities to show an increase in death rate from
the epidemic was Kansas City, in which the mortality first climbed in
the week ending January 17th. The following week there was an increased
rate in Chicago, New York and Milwaukee, and one week later, Boston,
Detroit, San Francisco and Philadelphia were affected. New Orleans was
one of the last large cities affected, not showing a definite increase
until the week ending February 14th. In contrast to the 1918 pandemic,
the influenza of 1920 showed no clearcut direction of spread, and was as
in the years following 1889 due, without doubt, to firing up of the
pandemic virus as it had been left scattered in many endemic foci
throughout the earth. There probably were instances of spread from the
larger centers to outlying districts, but there was no continuous spread
over large areas. The accompanying table shows clearly that the disease
this year commenced in the center of the continent, a fact which would
seem to disconnect it entirely from the late epidemics of 1919,
occurring in Europe:
_Annual death rates from all causes by week in certain large cities of
the United States from week ending January 3d to week ending February
21st._
═══════════════╤═══════════════════════════════════════════════════════
City. │ Week Ending
───────────────┼───────────────────────────┬───────────────────────────
„ │ January. │ February.
───────────────┼──────┬──────┬──────┬──────┼──────┬──────┬──────┬──────
„ │ 3│ 10│ 17│ 24│ 31│ 7│ 14│ 21
───────────────┼──────┼──────┼──────┼──────┼──────┼──────┼──────┼──────
Kansas City │ 16.3│ 15.8│ 19.3│ 32.7│ 39.5│ 61.5│ 44.0│ 29.1
Chicago │ 14.4│ 13.8│ 15.1│ 23.5│ 41.3│ 39.1│ 24.6│ 17.7
New York │ 14.0│ 15.3│ 14.6│ 19.5│ 28.0│ 35.0│ 35.1│ 24.8
Milwaukee │ 11.6│ 12.5│ 9.0│ 15.6│ 29.4│ 34.5│ 27.1│ 16.9
Detroit │ 13.7│ 13.0│ 14.2│ 15.5│ 33.9│ 60.9│ 42.9│ 21.6
Boston │ 16.8│ 16.9│ 14.1│ 16.8│ 20.3│ 27.1│ 33.7│ 32.1
San Francisco │ 16.5│ 15.4│ 19.6│ 19.2│ 22.9│ 25.2│ 31.8│ 28.8
Philadelphia │ 15.6│ 16.7│ 16.2│ 16.8│ 18.3│ 22.1│ 34.3│ 37.2
New Orleans │ 18.8│ 19.6│ 22.6│ 18.8│ 20.9│ 20.1│ 25.0│ 32.3
───────────────┴──────┴──────┴──────┴──────┴──────┴──────┴──────┴──────
The relative severity of the two epidemics in certain of the large
cities has been compared by H. F. Vaughan, and he has found as is seen
by the table that Kansas City and Detroit, two of the early cities
affected, had the highest mortality in 1920. Philadelphia in 1918 lost
nearly three times as many people as Detroit did in 1920. Detroit was
higher than Chicago in 1920, but lower in 1918.
_Per cent. of population killed by influenza._
═════════════════╤═════════════════╤═══════════════════════════════════
│ 1920. │ 1918–1919.
─────────────────┼─────────────────┼─────────────────┬─────────────────
│ First seven │ First seven │Twenty-one weeks.
│ weeks. │ weeks. │
─────────────────┼─────────────────┼─────────────────┼─────────────────
Detroit │ 0.20│ 0.17│ 0.28
Chicago │ 0.12│ 0.34│ 0.41
Kansas City │ 0.24│ 0.30│ 0.63
Philadelphia │ 0.10│ 0.76│ 0.82
New Orleans │ 0.05│ 0.55│ 0.77
─────────────────┴─────────────────┴─────────────────┴─────────────────
The following table taken from the “Final Influenza Bulletin,” by E. R.
Kelley, Commissioner of Health in Massachusetts, shows distinctly the
difference that must be always borne in mind between curves of influenza
incidence and death curves. In his table the mortality climbed first on
the week ending January 13th, as in the table above, but the increase in
influenza cases began at least one week earlier. It is characteristic of
influenza epidemics that the rise of mortality curves follows that of
morbidity by about a week:
_Influenza and pneumonia cases in Massachusetts in the first three
months of 1920._
═══════════════════════════╤═════════════════════╤═════════════════════
│ Influenza. │ Lobar pneumonia.
───────────────────────────┼──────────┬──────────┼──────────┬──────────
│ Cases. │ Deaths. │ Cases. │ Deaths.
───────────────────────────┼──────────┼──────────┼──────────┼──────────
Week ending January 3d │ 41│ 0│ 109│ 9
Week ending January 10th │ 46│ 2│ 142│ 50
Week ending January 17th │ 58│ 0│ 145│ 52
Week ending January 24th │ 489│ 4│ 201│ 56
Week ending January 31st │ 4,495│ 48│ 313│ 96
Week ending February 7th │ 9,627│ 272│ 382│ 212
Week ending February 14th │ 10,747│ 133│ 583│ 140
Week ending February 21st │ 5,601│ 181│ 510│ 147
Week ending February 28th │ 2,375│ 147│ 313│ 114
Week ending March 6th │ 1,144│ 54│ 206│ 34
Week ending March 13th │ 490│ 31│ 130│ 54
Week ending March 20th │ 254│ 20│ 105│ 44
Week ending March 27th │ 147│ 14│ 102│ 94
Week ending April 3d │ 218│ 6│ 97│ 12
───────────────────────────┴──────────┴──────────┴──────────┴──────────
In Massachusetts in the first three months of 1920 there were reported
35,633 cases of influenza and 3,158 of lobar pneumonia, with 906 deaths
from the former disease and 1102 from the latter. The case rate per
100,000 from influenza was 883.4; from lobar pneumonia, 78.3; the death
rate from influenza, 22.4; from lobar pneumonia, 27.4; and the fatality
per cent. from the former disease was 2.5, and from the latter, 34.9.
The epidemics in Detroit and Boston both showed a symmetrical evolution
and a single wave. This appears to have been the more frequent type of
recurrence in this country. There are examples of the secondary curve.
At the Great Lakes Naval Training Station the epidemic began during the
week ending January 17th. On January 12th there were fifty-one cases.
The peak was reached on the third day with the admission of 182 new
cases during twenty-four hours. Although the peak came early the decline
was less rapid and there were four secondary peaks, but the outbreak
terminated on the twenty-fourth day. On the whole the epidemic was less
severe than in 1918. Pneumonia was a complication in about ten per cent.
of the reported cases of influenza at the training station.
On the European continent there were similar recurrences in the first
three months of 1920. In the large towns of England the recorded deaths
from influenza made an increase in a steady curve from sixty-six in the
last week of January until the week ending March 27th. After that date
there was a gradual falling off. That the situation was in no way as
serious as it was at the same time in the American cities and in certain
other parts of Europe is indicated by an annotation in the Lancet of
March 6th. According to this annotation, the weekly totals of deaths
attributed to influenza in London and the 96 great towns had on the
whole tended to increase in the early part of 1920, but the absolute
increment was so small and the necessary uncertainty of classification
so great that no unfavorable inferences could be drawn from these
fluctuations alone. On the other hand, the notifications of cases of
pneumonia increased appreciably, too much to be set down as a mere
chance fluctuation. But notification for this disease had not been in
force long enough to enable accurate comparison. There were no
indications of epidemic influenza in any of the large factories situated
throughout the country. But on the other hand there was proof of the
existence of epidemic influenza of an infectious, but relatively
non-fatal type in certain large schools situated in the South and
Southwest of England.
The annotation concludes that influenza was epidemic in a few localized
English and Welsh communities, and that the type was similar to, but
less severe than that of 1918–19.
In the city of Paris between the 11th and 31st of January there was a
very definite increase in the death rate from inflammation of the
respiratory tract above the average for other years.
Renon and Mignot studied 141 cases of influenza (71 men and 70 women)
during January and February, 1920, at L’Hopital Necker. Fifteen of the
141 died. According to these observers the grip of 1920 attacked all
ages in contradistinction to the 1918 epidemic which affected especially
the young and vigorous. One-third of their group were over forty years
of age, while some were seventy and eighty years old. In spite of this
the disease remained relatively mild. Sixty-four were cases of simple
grip. Forty-three had associated bronchitis and pulmonary congestion and
edema. Twenty-seven had pneumonia. One had acute pulmonary edema. There
were cases of influenza in tuberculosis individuals. One developed an
acute serofibrinous pleurisy. One had purulent pleurisy, and one
meningitis.
In Copenhagen there occurred between the 18th and 24th of January, 1920,
1,204 cases of influenza with four deaths; in the following week, from
the 25th to the 31st of January, 7,445 cases with forty-two deaths; from
the 1st to the 7th of February, 11,038 cases with 207 deaths; from the
8th to the 14th of February, 8,308 cases and 327 deaths. This is to be
contrasted with the month of December, 1919, in which there were 1,845
cases of influenza in Denmark, of which only 272 were at Copenhagen. In
Christiania, Norway, during the week of January 25th to 31st, there
occurred eleven deaths from influenza, whereas during the preceding two
weeks there had not been a single death from this disease.
In December, 1919, there were reported in Switzerland only 511 cases of
influenza. During the month of January, 1920, this increased to 13,162,
and in February to 83,008, the estimated population being 4,000,000.
From February the disease decreased in prevalence. In Zurich, with a
population of 210,000, the epidemic resulted in 14,534 cases. The first
increase began around January 4th. The total number of cases for January
was 1,071. In February the records of the four weeks showed 2,721,
4,140, 3,341 and 1,899 cases, respectively; in March the decrease was
rapid, 886, 442 and 45 cases being reported in the first three weeks.
The total number of deaths, mostly due to pneumonia, was 229, a
mortality of 1.5 per cent.
During 1920 epidemics were also observed in Valencia, Santander and
other towns in Spain, and in Mexico City. In the latter city the number
of deaths was reported as 1,649, as contrasted with 3,000 in 1918.
INCUBATION PERIOD.
An accurate determination of the period of incubation in influenza
presents great difficulties. The large number of cases with the
consequent multiple opportunities for infection in the case of every
individual add to the difficulty. Under any circumstances the period is
very short. Parkes, many years before the 1889 epidemic, believed that
an incubative period sometimes exists; that it was sometimes very short
and sometimes of many days duration.
“In the Transactions of the College of Physicians it is stated that in
the epidemic of 1782, seventeen persons came to London to an hotel, and
on the following day three were attacked with influenza. Haygarth says
that a gentleman came to Chester from London, on the 24th of May, 1782,
ill of influenza; a lady, into whose family he came, was seized on the
26th, and was the first case in the town. Haygarth states, evidently
with the view to point out the possibility of a direct contagion, that
the gentleman was engaged to be, and was afterwards, married to this
lady. In this case the longest possible incubative period was two days.
In 1782 a family landed at Harwich, from Portugal, and came to London
directly; the day after their arrival the lady, two servants and two
children were all seized. Two men-of-war arrived at Gravesend from the
West Indies; three Custom-house officers went on board; a few hours
afterwards the crews of both vessels were attacked. Some other cases are
on record where the incubative period, if it existed, could not have
been more than a single day. On the other hand, some cases are on record
in which the incubative period must have been two or three weeks.”
Leichtenstern believed that the usual incubation period is from one to
three days although some cases have been reported in which it is without
doubt no longer than twelve hours. Parsons in reporting for England also
gives the incubation period as from one to three days as a rule.
It is reported in France in 1918 that in one institution thirty-one
cases out of thirty-three individuals occurred within three days, all of
them infected by one nurse.
MacDonald and Lyth report in the British Medical Journal for November,
1918, an interesting observation concerning the incubation period in
influenza. These two individuals were traveling from London to York in
the same compartment with an individual who was just convalescing from
influenza. Exactly forty-one hours after being on the train with this
individual, they both came down with the disease. One suffered lightly
while the other was severely ill. The wife and two children of the
latter contracted the disease in turn, and with them also the first
symptoms appeared suddenly after a delay of about forty-eight hours.
Stanley, in studying the epidemics of influenza in San Quentin Prison,
found that as a rule there was an increase in incidence following the
Sunday picture shows. This usually occurred on Tuesdays and Wednesdays,
giving an apparent incubation period of from thirty-six to sixty hours.
He tabulated the records of twenty-nine individuals who had presumably
become exposed at the show and found that the incubation period averaged
about forty-eight hours.
The majority of observers give the incubation period as from twenty-four
hours to four or five days, most often two or three days.
PREDISPOSING CAUSES.
Not every individual acquires influenza. There are those who assume that
the disease is so wide spread that every individual in each community
attacked has been actually exposed to the disease. In that case there
must be a certain amount of natural immunity which protects around sixty
to eighty per cent. of most populations from the disease. The other
extreme would be that every exposed individual falls victim to the
disease and that only twenty to thirty or forty per cent. are actually
exposed. The true state probably lies between these two extremes.
Nevertheless it is a fact that some individuals naturally insusceptible
to the disease fall victim as a result of the action of some extraneous
force, something which lowers their resistance. Raw recruits in the army
camps in the fall of 1918 contracted the disease in much greater
proportion than did the hardened soldiers. Fatigue, intercurrent
illness, environmental changes and exposure to inclement weather may all
predispose to infection in the individual. Greenwood found that the
compulsory rationing of food in England during the war was probably not
a predisposing cause of infection. The incidence of the disease in the
South Africa Union where food was abundant was even higher than that for
the British Isles. Hamer calls attention to the fact that the ages of
highest incidence during the pandemic were those ages in which the diet
was perhaps more restricted than in other ages. This, however, is but
one factor and cannot be accepted as conclusive.
It had been suggested that in the army camps in the United States
typhoid vaccination during the epidemic predisposed to the disease. The
similarity of the symptoms in vaccine reaction and in influenza may have
suggested this. V. C. Vaughan has investigated this possibility and
finds that those organizations in which anti-typhoid vaccine was
discontinued for a time after the appearance of the influenza suffered
quite as severely as those which submitted to vaccination.
Other predisposing causes, such as the incidence of crowding in a
household and the sanitary surroundings of the individual will be
discussed later.
PERIODICITY.
The phenomenon of occurrence of epidemic influenza in many countries,
even on different continents almost simultaneously and often without any
clearcut progressive spread from one of these countries to another
raises the question of periodicity in influenza. Is this simultaneous
occurrence due to some mechanism in the life cycle of the influenza
virus whereby it regularly acquires increased invasiveness, no matter
what its geographical distribution, or is it merely a feature of the
meteorologic conditions that makes the epidemic appear to be
simultaneous in widely scattered communities?
Influenza characteristically returns. An influenza period usually
comprises from three to five years, with one or two very mild epidemics
at the beginning which may frequently be overlooked, then of wide
pandemic spread, to be followed by endemic recurrences for as long as
two or three years. During these influenza periods the intervals between
waves are frequently so nearly equal or multiples of each other as to
force the question of a periodic law. Not only thus, but even on a
larger scale does the disease appear with a certain uniform regularity.
The great epidemics are separated frequently by intervals approximating
decades. Stallybrass calls attention to the epidemic years in England,
which are 1789–90, 1802–03, 1830–32, 1840–41, 1848–49 and 1851, 1854,
1869–70, 1879, 1890–91, 1898, and 1918–19. With the exception of 1854
all of these dates are around the end of a decennium.
Yet, again, in the successive waves of an individual epidemic, as has
been pointed out by Pearl, there is very roughly some periodicity.
Are these admittedly obvious phenomena fundamental features of the life
cycle of the influenza virus, or are they incidental, due to extrinsic
causes, changes in the pabulum, in the host as an individual, or in the
host as a community, or changes in climatic conditions? Is it a basic
feature upon which we must build our conception of the epidemiology of
epidemic influenza, or is it more a feature of chance? The evidence to
date is conflicting and incomplete. The answer lies in the future.
Periodicity in the acute infections is not a new subject. It has been
discussed in various other diseases, particularly in measles. For many
years epidemiologists in many parts of the world have reported the
observation of a periodicity in epidemics of measles. It is generally
regarded as an established fact that each locality suffers from epidemic
waves of this disease and that the period is somewhere about two years.
In certain relatively small localities in England where registration
statistics have been kept for many years the Health Officers count on an
epidemic every two years. In some places the epidemic is expected to
fall during the even years, while in others it occurs in the odd years.
Brownlee has been one of the foremost investigators in the periodicity
of influenza, but since his communication on that subject was very
brief, we take occasion to quote first from his article on the
periodicity of measles, thereby gaining a more comprehensive knowledge
of his theory, and at the same time becoming able to compare the
periodicity in the two diseases.
“The common explanation of the periodicity of epidemics of children’s
diseases is that the susceptible children take the disease in sufficient
numbers to limit the further spread. The epidemic thus dies out to recur
when a further sufficient number of susceptible children have
accumulated. This is quite a feasible theory and certainly explains the
periodicity of epidemics. The forms of epidemic curve which arise on
this hypothesis are not unlike those actually found, the differences
being no more than might be expected between a mathematical form based
on a hypothesis and the natural conditions to which the hypothesis is
only an approximation. This explanation, however, must fail if epidemics
of different periods can be shown to exist in the same town at the same
time, and I think this has been shown. In London, which on account of
its size might be assumed deserving of special treatment, the existence
of periods of different length have been demonstrated. In Edinburgh,
Glasgow, and Birmingham also it has been shown that epidemics with
periods in the neighborhood of ninety-eight weeks and one hundred and
ten weeks intermix. The same epidemicity even applies to districts in
London. In the West end of London we have almost a replica of what
occurs in Glasgow, Birmingham and Edinburgh. The main period there is 97
weeks, the secondary period 109.5 weeks. In the South of London one
period is that of 97 weeks, but almost equally prominent is that of 87
weeks. The whole evidence, therefore, seems to point to some condition
in the organism which produces the disease as the potent cause of the
difference rather than to the number of susceptible children. Compare
the _Paramoecium_ which under natural conditions divides asexually for
several hundred times and then dies out unless conjugation takes place.
The resting stage following conjugation persists for some time.
“There is, however, one point of great importance which must be
considered. If an epidemic begin in a definite locality and spread from
that locality, and if there is no loss of infectivity on the part of the
organism, it is demonstrable that a similar proportion of the population
should be attacked in each zone as the epidemic spreads outward. On the
other hand, if the organism lose the power of infecting with the lapse
of time, in each additional zone invaded the proportion of susceptible
persons infected should become smaller and smaller. Of course this might
not be true for any one epidemic, as in many parts of the area invaded
the population might be more or less susceptible because of recent
attack of the disease, but when an average of twenty outbreaks has been
taken this effect should be eliminated, the number of times the invading
organism comes into contact with an insusceptible population being
balanced by the number of times which it meets one more susceptible than
the average. The method of spread of epidemics on the average should
thus give some indication regarding the laws which determine the course
of the phenomenon. Now with regard to London, the clearest facts refer
to the 87-weeks, the 97-weeks and the 109.5-weeks period. The 97-weeks
period starts at the same time all over the city and there is no
evidence of any special center. The infection seems generalized. With
regard to the 87-weeks epidemic, however, the case is different. This
seems to start in St. Saviour’s Parish and to spread thence to
Camberwell, Lambeth, etc. In this epidemic the rate of spread can be
definitely measured. The maximum occurs later and later as the distance
from the center is increased and the percentage of children infected is
also easily observed to fall as the time increases. With regard to the
109.5 weeks’ period epidemic the facts are similar though not quite so
definite. This seems to show that for at least two strains of organisms
the epidemic ceases because the organism has lost its power of
infecting. It may be inferred that an epidemic ceases because the
organism varies in its potency to cause infection. A cycle of epidemics
now coinciding and now differing in their maxima can thus be explained.
Some kind of life cycle exists in the infecting organism. In this life
cycle high powers of infecting are attained probably after a resting
state: a period of activity follows and gives place to a period of rest;
the average length of the cycle is determined by the strain of the
organism.”
There are certain drawbacks to Brownlee’s work and conclusions. We quote
from V. C. Vaughan, who has discussed Brownlee’s work, not only because
of his good summary of the difficulties and disadvantages of the method,
but particularly because the same disadvantages and possibility of
inaccurate conclusions hold in the case of influenza.
“There is no reason for supposing that the virus of measles is
controlled in any way by our calendar. In order to get anywhere in
determining any law of periodicity in epidemics we must know the
morbidity and mortality of the disease by days, or at least by weeks. In
different parts of a large city there may be, and undoubtedly are,
epidemic waves of measles on the flow or on the ebb at the same time.
The best work that has been done along this line is that of Brownlee,
who has figured out epidemic waves of measles, based on the weekly
numbers of deaths in London between 1840 and 1912.
“The figures presented by Brownlee are of great value, and his theory is
fascinating and has much in its favor, not only in a study of epidemics
of measles, but of the other infectious diseases of infancy and
childhood, especially scarlet fever, whooping cough, and chicken-pox. In
order to solve the problem of periodicity in measles we must have more
exact information than we now possess. Brownlee’s figures pertain to
deaths only. There are, so far as we know, nowhere in the world
satisfactory statistics concerning morbidity in this disease. Deaths
from measles are so largely determined by the care bestowed upon the
sick and upon the extent to which secondary infection is prevented that
we are inclined to hesitate about the acceptance of a death rate or
number of deaths from this disease as an index to the virulence of the
organism causing the disease; in other words, we are not convinced that
the death rate in a given outbreak of this disease is a measure of the
virulence of the organism causing it. This involves the question whether
measles _per se_ is a disease of wide variation in malignancy or are the
widely different death rates observed in different epidemics due to
secondary infections. The streptococcus, a common invader of the body
during the progress of a measles infection, is known to possess a most
variable degree of malignancy. We are inclined to the opinion that if
all cases of measles could be recognized before secondary infection
occurs and could be cared for ideally the death rate from this disease
in different epidemics would be much more uniform than is now shown and
would be low. The greatest danger to life in an attack of measles lies
in the fact that the virus lowers the resistance of the body cells and
opens gateways to more deadly organisms, such as the streptococcus. We
believe that there are demonstrated facts which support these ideas.
Quite uniformly in measles there is a well marked leukopenia. As we now
interpret it, this means a decrease in the number of the forces that
naturally protect the body against the invasion of foreign cells. Again
as we interpret it, the failure of the body cells to respond to the
tuberculin test during a course of measles or soon thereafter is
evidence that the resistance of the body is lowered. If our
interpretation on these points be correct we fail to see how deaths from
measles can be properly employed as a standard in the measurement of the
virulence of the organism of the disease.”
Recognizing then the obvious disadvantages of the method, we will turn
to the work done on periodicity in influenza. We should call attention
at this point to the fact that the establishment of periodicity would
carry with it the assumption that the third of our three hypotheses
concerning the origin of influenza is the correct one. For example, the
July and autumn epidemic in England, as well as all occurring subsequent
to them, would be due to a virus or several viruses which have been
endemic in England since 1889, in fact since man has been in England,
and the epidemics and their recurrences would be due to increase in the
virulence of this local virus. The virus is distributed over the earth
and may become virulent periodically in many countries at the same time,
or if the periodicity is different on two continents the epidemics would
occur at different times.
Periodicity is not a new hypothesis. Hirsch denied any periodicity
distinct enough to be revealed by the comparatively crude statistical
methods of his time. Periodicity if present can only be revealed by
detailed and complicated mathematical procedures. Brownlee has
investigated the weekly number of deaths from influenza in London
between 1889 and 1896, and also up to the present time. He has compared
these with the weekly number of deaths from bronchitis and pneumonia in
London, the records of which have been available since 1870. By the
method of the periodogram he showed that there was a regular periodicity
of 33 weeks in deaths from influenza between the years 1889 and 1896,
but that in later years there was some considerable aberration. He
concluded that for some reason influenza periods tend to recur at
33-week intervals after the primary epidemic, and that the favorable
season for its recurrence is from January to the end of May. Should the
33d week fall in other than these winter months the epidemic may be mild
or even missed, appearing after another 33-week interval. Epidemic
influenza does not assume a form which causes any large number of deaths
until a bronchitic or pneumonic constitution has been established. The
fatal form is usually a disease of the winter or spring. He also found
that in the absence of influenza, bronchitis and pneumonia did not show
a 33-week periodicity, but when associated with influenza these
conditions also became periodic (33 weeks), and he assumes that this
change is definitely associated with the appearance of influenza.
Between 1876 and 1890 there was no tendency to the 33-week periodicity
with regard to bronchitis and pneumonia, but it was very marked between
1889 and 1896. During this epidemic period the deaths from pneumonia
precede those from influenza by one week and those of bronchitis precede
those of influenza by two weeks. The number of deaths from bronchitis
and pneumonia ascertained by this method of grouping is fully twice the
number obtained from influenza alone.
He believes that in these years, influenza appeared, on its epidemic
onset, first with bronchitic symptoms, later with pneumonic symptoms,
and lastly with those symptoms more definitely associated with influenza
proper. When the several sets of deaths are added together in 33-week
periods a very typical epidemic makes its appearance.
Brownlee finds that in the monthly statistics of Glasgow, Aberdeen,
Massachusetts, etc., there has been nothing differing essentially from
this phenomenon found in London.
Between 1876 and 1889 the annual curve for bronchitis and pneumonia
shows two maxima, one at the end of January and the second in the middle
of March. From March the decline in deaths from bronchitis is very
rapid. The disease re-appears around the beginning of October. During
the period 1889–96 the maximum number of deaths from bronchitis occurred
in the second week of January and the last week of February. Both of
these maxima are a fortnight before the maxima of the epidemics of
influenza. This suggests that the advent of influenza has brought a
change in the seasonal prevalence of bronchitis and supports the view
that the earlier portion of the influenza epidemic is associated with
bronchitic symptoms. The same phenomenon holds for pneumonia.
Brownlee was able to predict correctly the date of the recent 1920
epidemic. He did not attempt, however, to explain the short interval
between the summer and autumn, 1918, epidemics in England. He speaks of
the second as “aberrant.” In other words, it does not fall within his
classification. October is not a high respiratory disease month. The
epidemic should have been mild.
Stallybrass has confirmed Brownlee’s 33-week periodicity and suggests an
explanation for the “aberrant” October epidemic. Using periodograms with
a 33-week basis, and plotting deaths from influenza and respiratory
diseases from January, 1890, through January, 1920, he finds that the
most definite 33-week periodicity is shown during the years 1890–99.
During this period there is one maximum, when all 33-week periods are
superimposed, which occurs at the seventh week of the cycle. Beginning
about 1899 a new maximum appears in the nineteenth week of the cycle,
which continues to recur until the culminating point is reached in the
week ending October 26, 1918. An additional 66 weeks carries the date
forward to the first week in February, 1920. The maximum at the seventh
week of the periodogram during the years 1899–1913 is greatly diminished
from that in 1890–98. The periodogram for 1914–1919 shows clearly both
maxima, that in the seventh and that in the nineteenth weeks.
We quote Stallybrass in some detail (see Chart XII):
“Dr. John Brownlee pointed out that from July 13th to March 1st (the
maxima of the summer wave of 1918 and of the spring wave of 1919) is 33
weeks, but that the wave having its crest in this country on November 2,
1918, does not fall into the sequence, leaving one to infer that there
were two strains of the influenzal virus in operation.
“I supplement his investigation by the weekly deaths occurring in
Liverpool during the period 1890–1919 that were ascribed to influenza
and to all respiratory diseases. Prior to 1890 there were no deaths
attributed to influenza for a number of years.
“Closely corresponding with Brownlee’s observations on London by far the
most definite periodicity is shown during the years 1890–1899, during
which period there is one well marked maximumly at the seventh week of
the cycle. During the period 1899–1913 a new maximum in the nineteenth
week of the cycle comes into play and continues to recur until the
culminating point is reached in the week ending October 26, 1918, a week
earlier than in most English towns (Wave III); a further 66 weeks
carries one forward to the first week in February of this year, as
Brownlee pointed out, and the outbreaks that are being reported in
Japan, Paris, Chicago, New York, etc., would show that this strain has
punctually reappeared.
“There is also evidence in the table of a small maximum at the
twenty-seventh week of the cycle in the earlier sub-period, and at the
twenty-ninth week in the later sub-period; slight movements of the
maxima forwards or backwards in the cycle over a number of years may,
perhaps, indicate a periodicity slightly greater or less than 33 weeks.
The twenty-ninth week of the cycle fell on the weeks ending May 18,
1918, and January 10, 1919. An examination of the figures in Dr. Hope’s
annual report for Liverpool for 1918 shows that there was a definite
wave of influenza reaching its crest on May 18th (Wave I), and there is
also a definite rise in the deaths from influenza, respiratory diseases,
and from all causes, making a small peak in the week ending January 3,
1919, but it is hidden by the enormous waves of October and March, so
that it only appears as an irregularity in the curve; but it was noted
at the time that influenza had not declined in Liverpool in January in
the way that it had in practically all other English towns. These two
waves do not appear to have played a large part in this country, but the
outbreaks in the Grand Fleet in May, 1918, and also in Spain, Glasgow,
etc., may, perhaps, be attributed to it. In the United States in
January, 1919, it would appear to have played a much larger part. In a
large number of American cities two waves are experienced, the first
being the October wave; the crest of the second wave sometimes fell in
March, as did one of the crests in this country, but in a number of
instances, _e.g._, Cambridge, Washington, San Francisco, New Orleans,
etc., it fell in January, or to be exact, in the thirty-first and
thirty-second weeks of the cycle. The close relationship of Liverpool
and Glasgow with the United States through the incoming stream of
American troops may perhaps account for the presence of this May wave in
these two towns, and not the rest of England.
CHART XII.
[Illustration:
Periodogram based on the weekly influenza deaths in Liverpool between
1890 and 1919. The curves are based on a thirty-three week
periodicity. (_Stallybrass._)
]
“The third maximum in the fourth week of the cycle is represented during
the late outbreak by the waves culminating in Liverpool, and also the
greater number of English towns on the weeks ending July 13 (Wave II)
and March 1 (Wave IV). This is a 33-week interval. This wave recurred at
an interval of 32–34 weeks in a large number of English towns.
“Of 65 towns which experienced all three waves 47 (72 per cent.) had
their maxima in the summer and spring epidemics within an interval of
32–34 weeks; but comparing the week in which any given town had its
epidemic peak in the summer and autumn, and autumn and spring epidemics
only 27 (41 per cent.) and 31 (47 per cent.) respectively fell within
the limit of a week on either side. The time relationships of the maxima
in summer and spring were much closer to each other than they were to
the autumn maxima.
“If it should prove correct that there were three strains of the
influenzal virus, each with a periodicity of about 33 weeks, and that
simultaneously all three strains became enhanced in both virulence and
infectivity, then we are faced with a phenomenon without an exact
parallel, although the behavior of the meningococcal viruses during the
war presents some points of similarity. So far the weight of evidence
leans to such an exaltation of a widespread endemic strain or strains
rather than to dissemination from any particular focus in the world. In
any case doubtless a good deal of spread of infection took place.”
Spear takes exception to the work of Brownlee and Stallybrass, and
points out that the periodogram is not applicable to the study of
recurrent epidemics unless the recurring waves are of approximately
uniform “amplitude.” In that case nothing could be less appropriate for
this study than the influenza waves which vary from very small to
extremely high, as in 1918.
Spear describes two simple tests which he applied to demonstrate the
existence or non-existence of periodicity.
First he divided each of the last thirty years into 13 four-weekly
periods, and tabulated the frequency with which the observed week of
maximum mortality falls into one or other of the 13 groups. He
discovered that the climax of an influenza prevalence falls more
frequently in the second and third four-weekly period than in
others—_i.e._, the months of February and March. Had there been a
33-week periodicity there would have been an equal number of these
climaxes in each of the 13 divisions of the year.
Brownlee, according to Spear, was correct in his prediction that
influenza would occur in February, 1920, for the reason that January or
February is the most likely time for an influenza prevalence in any
year.
Spear’s second test of periodicity consisted in plotting the
interepidemic periods according to the number of weeks intervening. Were
there a 33-week periodicity, he says, that nearly all interepidemic
periods should fall in this group. As a matter of fact, more than twice
as many periods fall in the 42–58 weeks interval than in any other
interval. Fifteen fall within this period, six in the period 59–75
weeks, five in the period 8–24 weeks, and only four in the period 25–41
weeks. There was one in the period 76–92 and one 110 plus. Finally in
the thirty years 1890–1919 there were thirty-two climaxes or peaks in
the “influenza” mortality.
Spear concludes that if there is any periodicity it is around fifty
weeks, or a year.
The fallacy in the work of Stallybrass and of Brownlee, according to
him, is that the mortality in the third week of 1892, the twentieth week
of 1891, and the tenth week of 1895, and in the big epidemic of 1918 so
overshadowed all the other peaks that the smaller ones became lost in
these larger waves.
Brownlee does not claim a 33-week periodicity during interepidemic
periods. This part of Spear’s criticism is not valid.
Vaughan’s objections to the conclusions on measles hold equally well
with regard to influenza. Finally, we must remember that in parts, at
least, of the work of Brownlee and Stallybrass, they are not studying
chiefly influenza deaths, but deaths reported as due to bronchitis and
pneumonia.
After a study of the pros and cons of the question of periodicity the
author submits by way of summary his conclusions:
1. Influenza does tend to recur at intervals. It has not been proven
that these intervals are always of equal length.
2. At the present the opinions concerning the periods are divergent. We
have the 33-week periodicity of Brownlee and Stallybrass, the one-year
period of Spear, the seven-week intervals suggested by Pearl, and the
apparent twelve-week recurrences in England in 1918 and 1919.
3. It is to be noted that particularly in the work of Stallybrass, in
order to prove his periodicity, he finds it necessary at times to quote
epidemics occurring, not in England, but in fairly remote parts of the
world, as in the United States and Japan. We have shown that in the
interval between 1918 and 1920 an epidemic could be discovered somewhere
on the earth in many months, perhaps even in every month during this
interval. It is to be regretted that following the criticism by Spear
there has been no further report, so far as we know, by either Brownlee
or Stallybrass.
4. It is quite possible, even probable, that influenza is endemic in
mild form throughout the interpandemic years in England, as well as in
many, or all other countries, but it is equally possible or probable
that the particular virus which gave rise to the pandemic was not one
which simultaneously increased in virulence in all countries, but was
one which had its origin in one comparatively well localized focus.
5. Our own theory does not explain the autumn recurrence in 1918 in
England, following that of May, June and July. We have traced the
original spread to England and have left it at that point. We have again
taken it up in the autumn when it became severe, and was returned to the
United States. The interval of quiescence in England and elsewhere may
need further explanation. Two alternative hypotheses suggest themselves:
First, that the autumn recrudescence is entirely comparable to later
ones, and is but a manifestation of the characteristic feature of
recurrence in influenza. Had the autumn epidemic been mild and had it
not so overshadowed all others, we would have classified it with those
of early 1919 as being merely recrudescences of the summer spread.
Evidence, particularly in favor of this, is the report of Greenwood
previously mentioned which shows that in England the autumn spread
partook of the nature of a secondary type of epidemic, as compared with
the primary type in the summer.
The second hypothesis is that the occurrence in the summer in England of
an epidemic due to a virus imported from America or France or China,
with its consequent increase in morbidity, so enhanced the virulence of
a local endemic British virus that the latter produced the autumn
epidemic. We see no necessity for complicating the question by the
assumption of this second hypothesis.
6. Whether or not there is a regular periodicity of a definite number of
weeks in the case of influenza, the fact remains beyond cavil that one
of the dominant characteristics of epidemic influenza is its recurrence
at intervals. The evidence is ample that the disease is distributed
throughout many countries in interepidemic times and that intermittent
outbreaks of large or small extent occur.
The most striking phenomenon is the fact that in March of 1918 influenza
is reported as having been present in China, in the United States and in
France. It is scarcely possible that the disease in its epidemic form
could have been carried from any one of these three points to the other
two in the remarkably short time between the onset of the three
outbreaks. We are faced with the phenomenon of a simultaneous exaltation
of the influenza virus in three remotely separated countries of the
world. This one fact more than any other indicates that the fluctuation
in virulence is dependent upon some factor intrinsic in the virus itself
and not upon environmental factors.
It is impossible at the present time to decide whether the world
epidemic spread simultaneously from these three foci or whether in only
one of these three the virus became so exalted as to produce pandemic
prevalence. All we can say is that we are able to trace consecutively
the spread of the influenza from the focus in the United States
throughout the world. The information upon which we base our findings is
not statistical, and as we have previously said this latter type of
demographic study should be brought into use to either corroborate or
disprove our findings.
VIRULENCE ENHANCEMENT.
Before attempting to study the mechanism of origin of the 1918 pandemic
it is highly essential that we devote some attention to a consideration
of the processes by which the germs of infection, particularly the virus
of influenza, may develop an increase in virulence. Followers of the
theory of periodicity would base virulence enhancement primarily on some
intrinsic property of the virus itself. We know from past experience and
particularly from animal experiments that this is not the only manner by
which virulence may be increased.
As far as we know there is no new infectious disease. Individuals who
delve into the history of the past inform us of more and more diseases
which were well known to the ancients. We are frequently amazed at the
variety of diseases now known to be infectious that were very correctly
described by the Hippocratic writers. The infectious diseases are with
us always and live nearly always in man, the host. There are few
exceptions. Very few of the contagious viruses can live for any long
period of time outside of the human body. A few, such as the plague
bacillus, may live on other hosts, but these are the exception. The
remarkable feature is that for long periods of time the virus exists in
the host in a quiescent state and only at intervals does it become
highly invasive and thereby produces epidemics of greater or less
extent. Under what conditions does the metamorphosis of the
microorganisms occur?
Topley, in the Goulstonian lectures, discusses this subject. He says:
“The first difficulty with which we were faced in forming any theory of
the spread of bacterial infection, which should conform to the known
facts of epidemiology, was to find some explanation of the perpetuation
of the virus during interepidemic periods. The bacteriologic data which
have accumulated, especially during the last twenty years, have shown
that the causative agents of specific diseases are to be found in
apparently normal persons who give no history of having been in contact
with the disease in question, as well as in contact with actual cases of
the disease. Moreover, the organisms in question have been shown, in
certain cases, to persist for long periods of time in or upon the
tissues of their hosts, and we must always remember that the difficulty
of bacteriologic technic is likely to lead to a serious under-estimate.
Clinical and epidemiologic investigations have yielded confirmatory
evidence, and we are thus left with a conception of the virus of a given
disease being distributed fairly widely throughout the world as an
apparently harmless parasite on the human host, but taking on during
epidemic periods a new and sinister role, only to relapse again into
comparative quiescence as the epidemic subsides.”
He explains the rise of the epidemic wave as follows: “There are at
least three possible explanations—an increase in the power of the
parasite to produce disease, a decrease in the resistance of the host,
and some attraction in the surrounding circumstances which favor the
transference of parasites from case to case without any alteration of
the pathogenicity of the one or in the resistance of the other. The
third of these hypotheses may, I think, be disregarded. That alterations
in environment may be the determining cause in initiating an outbreak of
bacterial disease is probable enough; but they will almost certainly act
through the variations which they bring about in the other two factors.
The whole of bacteriologic knowledge is clearly against the occurrence
of a considerable epidemic in which the pathogenicity of the parasite
and the resistance of the host remain constant. Again, while we may well
believe a lowered resistance of a certain number of the host-species to
be an important factor in the initiation of the process, yet we cannot
believe that it is the whole story. The widespread ravages of many
epidemics would seem altogether to preclude such an explanation. We seem
forced therefore to the conclusion that an increase in the pathogenicity
of the specific parasite is an essential factor in the rise of
epidemics, excluding from this category small sporadic outbreaks which
may be due to the introduction of a fully virulent parasite by a healthy
carrier in some other way.”
If a disease like measles is quiescent in a given community it must be
that in that locality the hosts and parasites are existing in a state of
biological equilibrium. They are living in a state somewhat akin to
symbiosis. Such a condition could be attained either by a diminution of
the invasive powers of the parasite, or by an increase in resistance of
the host. Probably both elements are active; as the relative immunity of
the host rises the infectivity or virulence of the parasite must rise to
an equal extent to maintain the equilibrium. If this were true we would
find that in those localities in which the disease is endemic and where
the population is relatively resistant there is a normally more virulent
virus in existence. A stranger coming into such a community would, in
view of his lower resistance to the virus, be more susceptible of
becoming actively infected. There would, however, be little danger of an
epidemic spread because the number of susceptibles would, roughly, be
limited to the number of strangers in the community. If, however, an
individual from the community carrying the more virulent virus were to
travel to another community where the greater proportion of the
population was relatively less immune the field would be fertile for the
beginning of an epidemic. Furthermore, there is the possibility of an
outbreak in the first community if there should occur gross changes in
its constitution; another infectious disease, a redistribution of the
population with greater crowding, anything to change the balance between
host and parasite.
Theobald Smith has described this possibility very clearly:
“During the elimination of the more virulent races of microorganisms,
there goes on as well a gradual weeding out of the most susceptible
hosts. In a state of nature in which medical science plays no part,
there must occur a slight rise in the resistance of individuals, due to
selection and perhaps acquired immunity, which meets the decline of
virulence on the part of microbes until a certain norm or equilibrium
between the two has been established. The equilibrium is different for
every different species of microorganism, and is disturbed by any
changes affecting the condition of the host or the means of transmission
of the parasite. One result of the operation of this law is the low
mortality of endemic as compared with epidemic diseases. Certain animal
diseases while confined to the enzootic territory, cause only
occasional, sporadic disease, but as soon as they are carried beyond
this territory epizootics of high mortality may result. Climate in some
cases enters as an important factor, but the most important, perhaps, is
the slight elevation in virulence brought about by a more highly
resistant host. The most susceptible animals are weeded out and the rest
strengthened by non-fatal attacks. The virulence of the microbe rises
slightly to maintain the equilibrium. In passing into a hitherto
unmolested territory, the disease rises to the level of an epizootic
until an equilibrium has been established.
“The same is true of human diseases, among which smallpox is a
conspicuous example. The great pandemics of influenza, which seem to
travel from east to west every one or two decades, soon give away to
sporadic cases, and the careful work of many bacteriologists would
indicate that the influenza bacilli found at present have fallen to the
level of secondary invaders, and are parasites of the respiratory tract
in many affections.”
Smith describes his hypothesis that the tendency of microbes in
perfecting the parasitic habit is to act solely on the defensive. The
aim of microorganisms, if we may speak of such, is to become able to
live unharmed on the host. If they kill the host they have lost their
home. The biologic tendency would be in this case for diseases which
were once acute to become more and more chronic and indolent.
The extremely virulent parasite, which kills its host, will die with the
host unless it has effected a means of exit before its death and escapes
into a new host. For this reason Pasteur failed to exterminate the
rabbits of Australia. He believed that with races of the bacillus of
rabbit septicemia, which were very virulent, and which destroyed life
very quickly, all that would be necessary was to start the disease among
the rabbits of Australia and that it would tend to spread and would kill
off all of the rabbits. But the parasite killed the animals before it
had perfected for itself a means of escape from the body and thereupon
died.
“From the biologic standpoint which I have endeavored to present, we may
conceive of all highly pathogenic bacteria as incompletely adapted
parasites, or parasites which have escaped from their customary
environment into another in which they are struggling to adapt
themselves, and to establish some equilibrium between themselves and
their host. The less complete the adaptation, the more virulent the
disease produced. The final outcome is a harmless parasitism or some
well-established disease of little or no fatality, unless other
parasites complicate the invasion. The logical inference to be drawn
from the theory of a slowly progressive parasitism would be that in the
long run mortality from infectious diseases would be greatly reduced
through the operation of natural causes. But morbidity would not be
diminished, possibly greatly increased by the wider and wider diffusion
of these parasites, or potential disease producers. The few still highly
mortal plagues would eventually settle down to sporadic infections or
else disappear wholly because of adverse conditions to which they cannot
adapt themselves.
“In this mutual adaptation of microorganism to host, there is, however,
nothing to hinder a rise in virulence in place of the gradual decline if
proper conditions exist. In fact, it is not very difficult to furnish
adequate explanations for the recrudescence and activities of many
diseases today, though the natural tendencies are toward a decline in
virulence. In the more or less rapid changes in our environment due to
industrial and social movements the natural equilibrium between host and
parasite established for a given climate, locality, and race or
nationality is often seriously disturbed and epidemics of hitherto
sporadic diseases result.
“These illustrations indicate that so-called natural law does not stand
in the way of our having highly virulent types of disease, if we are
ignorant enough to cultivate them. The microorganism is sufficiently
plastic to shape itself for an upward as well as a downward movement.
Among the most formidable of the obstacles toward a steady decline of
mortality is the continual movement of individuals and masses from one
part of the world to another, whereby the partly adapted parasites
become planted as it were into new soil and the original equilibrium
destroyed. These various races of disease germs become widely
disseminated by so-called germ carriers, and epidemics here and there
light up their unseen paths.”
An example of increasing virulence from changing environmental
conditions, is the experience in the United States Army camps in 1917
and 1918 with the streptococcus. This microorganism, which at first was
but a secondary invader, particularly to measles, became so exalted in
virulence that it soon became the cause of primary disease. This is
likewise true of the various secondary invaders of the influenza
epidemics. They become so highly virulent that they dominate the picture
in the later stages. The organisms included in this group are
particularly the streptococcus, the various pneumococci, and the
meningococcus. Probably the tubercle bacillus should be added to this
list.
It requires a certain amount of time for such organisms to attain
increased virulence. The earliest cases in any epidemic are
comparatively very mild. Thus Major Billings, epidemiologist at Camp
Custer, says that for the first five days of the autumn influenza
epidemic in that camp the cases admitted to the hospital were very mild
in character and were recorded as simple bronchitis and pharyngitis, of
no great severity, the majority soon recovering. Five days after the
first case was admitted, however, the entire symptom complex seemed to
change, and the cases admitted to the hospital from then on were a very
different and much more severe type. Major Billings, after going over
the records, feels that both types of cases were the same disease, the
second being a more severe form. Woolley reports essentially the same
condition from Camp Devens.
The same phenomena were found in 1889. During the 1889 epidemic Prudden
examined by current bacteriologic methods seven cases of influenza and
six cases of influenza-pneumonia. In them he found staphylococcus
pyogenes aureus, streptococcus pyogenes, diplococcus pneumoniae, and in
other cases he found a streptococcus. He concludes that the use of
culture methods and media commonly employed has brought to light no
living germ which there is reason to believe has anything to do with
causing the disease. He emphasizes the probable importance of
streptococcus pyogenes in particular in inducing the various
complications.
At this point we should include for the sake of completeness reference
to a recent theory propounded by Sahli explaining influenza epidemics, a
theory to which we do not subscribe. He believes that the pneumococcus,
the streptococcus, the influenza bacillus, and possibly other organisms,
form a complex group, an obligate complex, a symbiosis, a higher unit,
which infects the organism as a unit. It is all of these organisms
acting together which produce the influenza. After infection has
occurred one or the other member of the group may develop
preferentially. In favor of this he says that in one of his cases the
sputum was swarming with influenza bacilli on one day, and that the next
day the sputum was a thick pure culture of the pneumococcus. He says
that if an ultramicroscopic germ should yet be discovered this would not
invalidate the theory, but would merely add another member to the group
forming the obligate complex virus unit.
_Meteorologic conditions._—Formerly attempts were made to demonstrate
etiologic relationships between the occurrence of influenza and unusual
conditions of the atmosphere. In most cases no relationship has been
discovered. Nevertheless it is conceivable that the changes in the
atmosphere, particularly seasonal variations, might influence the
virulence of the organism. It has been found that nearly all of the many
epidemics apparently originating in Russia took their origin there
either in the late autumn or in the winter months. The spread of
influenza appears to be uninfluenced by atmospheric conditions, but the
severity of the disease is definitely increased in the winter months,
and Leichtenstern believes that the development of a primary spread from
its point of origin is also influenced by the season. Hirsch found that
out of 175 correlated pandemics or epidemics, 50 occurred in the winter
between December and February, 85 in the spring from March to May, 16 in
the summer from June to August and 24 in the autumn.
The soil plays no part in the spread of the disease. It prevails on
every soil or geologic formation; on the mountain top, in the low
malarial swamps, in the tropics and within the arctic circle. Volcanic
eruptions, fogs, electrical conditions, ozone, direction of the wind,
have all been considered in previous epidemics and successively
eliminated as etiologic factors.
It must be stated, however, that Teissier, who investigated the
influenza in Russia in 1890 and has compared his conclusions at that
time with the results of investigation of the recent visitation,
believes that some particular cosmic conditions suddenly enhanced the
virulence of an endemic etiologic microorganism—probably some ordinary
germ—and that this opened the portals to secondary infections.
_Secondary invaders._—We have considered a possible manner in which the
virulence of the organism causing influenza may become enhanced.
Whatever this organism may be, another and equally important virulence
enhancement occurs in the opportunist group of the germs, so-called
secondary invaders of influenza. As we have previously remarked, it is a
characteristic of influenza outbreaks in all communities that the
earliest cases are very mild. Secondary infection has not as yet
obtained a foothold. After about a week the character of the illness
changes, becoming distinctly more severe. Billings reported that at Camp
Custer in the autumn of 1918 cases admitted to the hospital during the
first five days were very mild in character and were reported as simply
bronchitis or pharyngitis of no great severity, the majority soon
recovering. After this time the entire symptom complex seemed to change
and the cases admitted to the hospital were of a very different and more
severe type.
Benjafield reports that in the Egyptian Expeditionary Force the epidemic
commenced in May, 1918, and that the cases occurring during the earlier
portion of the epidemic were mild in type and of short duration, only a
very small proportion being complicated by bronchopneumonia. Wooley
found at Camp Devens that the first cases were of a mild form and were
usually diagnosed “naso-pharyngitis, acute catarrhal.” After a few days
the disease became more severe and pneumonia cases developed.
Bezançon found that among the repatriated French soldiers from
Switzerland those cases occurring in May and June had a much lower
severity than in the later epidemic. Zinsser’s description of the mild,
earlier epidemic in Chaumont has already been quoted.
The secondary invaders of pathogenic importance are the various forms of
the streptococcus and pneumococcus, the meningococcus, the
staphylococcus, and probably the tubercle bacillus and the influenza
bacillus. In the last epidemic as in that of thirty years previously,
the chief complications were bronchitis and pneumonia. Capps and Moody
found these to be the chief complications in December, 1915. Also they
found a high incidence of sinusitis. This has been a feature of the last
epidemic. Wooley cites a good example of the damage done by these
opportunist organisms when they are present. Among the troops stationed
at Camp Devens in the fall of 1918 pneumonia following influenza was
particularly prevalent in a battalion of negroes from the South. This
battalion had, a short time previously, passed through an epidemic of
pneumonia and Wooley believes that many of the blacks were harboring the
pneumococci which were only awaiting a favorable opportunity to invade
their hosts. The influenza furnished the required opportunity.
That the meningococcus should be classed in this group is certain. The
author observed at Camp Sevier cases of epidemic meningitis occurring in
various influenza wards scattered throughout the hospital, with no
demonstrable relationship. Usually there was but one case in a ward and
almost invariably meningitis occurred when convalescence was beginning.
No epidemic occurred in any ward. Others have reported actual epidemics
of meningitis following influenza. Moss found that a large proportion of
his influenza cases had the meningococcus in the circulating blood, as
demonstrated by culture. Fletcher cultivated meningococci from the lungs
in all of eleven autopsies, and in all eleven cases the influenza
bacillus was also present.
In considering the effect of influenza on the death rate in general, and
in considering the relationship of influenza to other diseases in
general, it is important to distinguish those diseases which are
apparently unrelated and those diseases which occur as direct
complications or sequelae. Bronchopneumonia, bronchitis, empyema, otitis
media, frequently tonsillitis and sometimes erysipelas, occur as
sequelae. Meningitis should frequently be included in this group.
Not only is there an increase in certain other diseases following
influenza outbreaks, genetically related, as we have seen, but also some
observers, particularly Crookshank, believe that previous to epidemic
influenza prevalences there occurs an increase in the incidence of other
entirely unrelated infectious diseases, such as poliomyelitis. This
theory of simultaneous increase in invasiveness of many apparently
unrelated germs is comparatively new and will probably receive deep
consideration in the future. For the present the information on the
subject is so limited that attempted conclusions would have no value.
ORIGIN OF THE 1918 PANDEMIC.
In discussing the spread of the 1918 pandemic over the earth, the author
has traced it from an apparent origin in the United States. Localized
early epidemics are reported simultaneously in the United States,
France, and China. From the literature at his disposal he has been
unable to find convincing proof of an earlier origin in Asia, but he did
emphasize at the time the necessity of a much more thorough study of
influenza in all countries to be made by more competent statisticians.
Nevertheless it is highly interesting to formulate an hypothesis which
appears to meet all demands, on the assumption that the disease
originated in America. In order to hold a theory with this basis we must
assume that the third of our previously mentioned hypotheses of the
origin of the disease is the more nearly correct.
Let us assume that in the interpandemic periods the influenza virus is
widely distributed over the earth, existing in an avirulent form. The
basis for this assumption is the previously described occurrence of
localized epidemics in interpandemic periods. The occurrence of solitary
cases, although of interest, could scarcely be considered as evidence of
the widespread distribution of the virus, but in the case of the small
outbreaks as in 1900, 1907 and 1915, and as in the numerous small
outbreaks described by Hirsch, the character of the epidemic curve is
characteristic. Let us, then, assume that the disease has been endemic
in the United States, together with other localities. It requires no
keen observation to discover in the years 1917 and 1918, Theobald
Smith’s “movement of individuals and masses from one part of the world
to another, whereby the partly adapted parasites become planted, as it
were, into new soil, and the original equilibrium is disturbed.” Not
only was there a tremendous redistribution and concentration of
individuals in our camps in this country, but also there was a further
disturbance of the equilibrium in the outbreak of other infectious
diseases, particularly measles. The effect of the measles epidemic on
the virulence of the streptococcus and allied organisms has been
discussed; presumably the same occurred with respect to the influenza
virus. Howard and Love report that approximately 40,512 cases of
influenza were reported in the United States Army during 1917. They
write:
“In 1917, the death rate for the acute respiratory diseases (influenza,
pneumonias and the common types) increased to 1.71. During the fall of
1917, after the camps were filled with drafted men, acute epidemic
diseases swept through a number of them. Measles was one of the most
prevalent and one of the most fatal of the infectious diseases that
occurred. It was noted during the fall and early winter that there were
a number of cases of pneumonia which were unlike the pneumonia that
ordinarily occurred. This was apparent both to the physicians in civil
life and in the army camps. It was reported by all classes of
practitioners that numerous cases of pneumonia were occurring which
resembled the pneumonia following measles, but occurring among men who
had not had measles recently. In a number of the camps, both in the
north and in the south, rather extensive epidemics of pneumonia occurred
and a number of deaths resulted. The same variety of pneumonia occurred
in the late winter and spring of 1918. In many of the camps pneumonia
was practically epidemic during March and April. In many camps a number
of cases occurred later in the spring and summer. It was again reported
by a number of medical men that these cases of pneumonia that were
occurring were different from the types of pneumonia ordinarily
encountered and very similar to pneumonia following measles, but, again,
that the cases occurred among men who had not had measles recently.”
MacNeal has observed similar conditions in the American Expeditionary
Forces in France in 1917:
“The American troops in France in 1917 began to show, as early as
October, 1917, a very considerable rise in the influenza morbidity. The
data available in the office of the Chief Surgeon, A. E. F., show an
influenza morbidity per 100,000 of 321 in July, 438 in August, and 404
in September, rising to 1,050 in October, 1,980 in November, and 2,480
in December, 1917, in which month the total number of new cases of
influenza reported was 3,520. That a considerable proportion of these
cases were actual infections with the bacillus of Pfeiffer is proven by
the necropsy findings in fatal cases of bronchitis and bronchopneumonia,
especially those performed by Major H. E. Robertson at Army Laboratory
No. 1, Neufchateau, in November and December, 1917, and January, 1918.
In these cases the bacillus of Pfeiffer was found in the scattered
patches of lung involved in the bronchopneumonia and also with great
frequency in the cranial sinuses. These necropsy findings were, at the
time, recognized as essentially new for young adult Americans, and, in a
discussion at Army Laboratory No. 1, during December, 1917, they were
considered as being of possible important significance for the future
morbidity of American soldiers in France. In the British Army in France
there is definite evidence of epidemics showing the same pathologic
condition, during the winter of 1916–17, and at Aldershot in September,
1917. There can be little, if any doubt that this disease was
essentially the same which attacked the American soldiers late in 1917.”
Schittenhelm and Schlecht have reported that a disease was studied among
the German troops on the Eastern front which resembled greatly the
influenza. It occurred from the beginning of August to the middle of
October, 1917. It attacked simultaneously and in epidemic form units and
divisions very widely separated over a large territory. It was
characterized clinically by a very sudden onset, in the greater number
of cases with chill, headache, pain in the extremities, sometimes
thoracic pain and cough. The fever lasted seven to nine days. The spleen
was enlarged in 11 per cent. of the individuals. There was diarrhea in
12 per cent., frequently conjunctivitis, and quite often a
scarlatiniform rash. Bacteriologic examination of the blood was
negative. There was usually leucopenia. No treatment seemed especially
efficacious. Aspirin gave the best results. The authors call attention
to the close similarity to influenza and also suggest that it might have
been due to transmission by insects as in pappataci fever or in dengue.
Carnwath concluded that the finding of influenza bacilli in necropsies
in British soldiers in 1917 was without epidemiologic significance in
considering the origin of the 1918 pandemic. He had studied the disease
among the British in detail and appeared to be of the opinion that the
first influenza morbidity of significance among the British troops did
not appear previous to April, 1918.
MacNeal further says: “The influenza rates per 100,000 of 1,050 in
November and 2,480 in December, 1917, really indicate a greater relative
prevalence of influenza at that time in the A. E. F. than occurred in
the fall of 1918, when the respective morbidity rates were 826 in
September, 2,176 in October, and 1,356 in November. The total number of
American troops in France was relatively small during that
winter—141,995 effective mean strength in December—so that the
prevalence of influenza did not lead to the recognition of an actual
epidemic. Furthermore, the overcrowding in quarters, which seems to have
had a definite relation to many of the later explosive outbreaks, had
not become such a distinct feature at that time. In addition, the cold,
wet weather, exposure and unusual living conditions furnished
explanations for the morbidity which were no longer adequate during the
hot weather of May and June, 1918. Until May, 1918, therefore, the
prevalence was that of an endemic disease, with perhaps an occasional
outbreak suggesting epidemic character.”
We admit that MacNeal’s report furnishes excellent evidence of an
independent origin in France. Two points should be borne in mind. First,
that MacNeal’s figures are not for the French, but for the Americans who
were transported to that country, and that we may consequently consider
influenza among the American Expeditionary Forces as being possibly from
the same source as influenza among the troops in our own country,—that
the American Expeditionary Forces may be considered a subdivision of the
American Army in the United States, equally well as a subdivision of the
French population; second, that we have been unable to find detailed
evidence of similar conditions occurring among the French troops or
French population, where the conditions have been ripe in a way since
1914. MacNeal records that in March and April, 1918, there was a great
increase in the number of troops brought over from the United States to
France. Previous to that time there had been 287,000 in that country and
during the two months 150,000 were added, with a consequent increase of
more than fifty per cent.
We should insert a word of caution regarding the diagnosis of influenza
among troops in the absence of any sign of an epidemic. Internists who
served in base hospitals during the war will agree that a diagnosis of
influenza is very frequently made on the admission card when the disease
turns out to be some other malady. This was not equally true in all
camps, but regimental surgeons could often be found who would transfer a
patient to the hospital with the diagnosis of influenza used almost
interchangeably with the diagnosis “Fever of unknown origin.” It would
be interesting to see statistics from one or two of those base hospitals
which were manned with especially competent internists, as to the
frequency with which the admission diagnosis of influenza remained
unchallenged in the hospital, during the year 1917.
There would be such cases in greater or smaller numbers. The magnitude
of this number would not influence our hypothesis.
Aside from this discussion of the disease among our troops in France it
is most important that we establish, if possible, the identity of the
disease reported among British troops in Northern France during the
winter of 1916–1917 and designated by the name “Purulent Bronchitis.”
The disease first appeared in December, 1916. It reached its height
during February and early March of 1917, and appears to have disappeared
early in the spring. Hammond, Rolland and Shore report that during
February and early March 45 per cent. of the necropsies under
observation showed the presence of purulent bronchitis, and they
remarked that the disease assumed such proportions as to constitute
almost a small epidemic. They described the clinical aspects as follows:
“The cases which came under our notice can be divided broadly into two
types: The first and more acute presents a clinical picture which
closely simulates ordinary lobar pneumonia with a sustained temperature
of about 103°, and expectoration at first blood-streaked—rather than
rusty—which, however, rapidly becomes quite purulent. The pulse-rate in
these cases is out of all proportion to the temperature in its rapidity.
Dyspnoea and cyanosis are prominent features. The patient usually dies
from ‘lung block,’ resulting in embarrassment of the right side of the
heart on the fifth or sixth day. For the last day or two there is often
incontinence of the feces, due, no doubt, to the condition of partial
asphyxia. The mental state is one of torpor; delirium is the exception.
“The second and less acute type is marked by a more swinging temperature
with a range of two or three degrees. The expectoration at first may be
frothy and mucopurulent, but it very soon assumes the typically purulent
character. This form may run a long course of from three to six weeks,
during which time the patient wastes a great deal and has frequent and
profuse sweats; indeed, at a certain stage the illness is most
suggestive of acute tubercular infection, and it is only by repeated
examination of the expectoration that the clinician can satisfy himself
he is not really over-looking a case of acute pulmonary tuberculosis.
The majority of our cases conforming to this type have ultimately
recovered, but the convalescence is slow and tedious.
“Onset.—Whilst a history of a previous catarrhal condition lasting for a
few days is often obtained, the disease quickly assumes an acute
character; we have been able to observe this in patients admitted into
this hospital with purulent bronchitis; we find the temperature is
between 102° and 103°, the pulse 120 or over, and the respiration about
35. The patient frequently complains of shivering and looks pathetically
miserable, but we have not seen an actual rigor. Despite his obvious
shortness of breath, the sisters have noticed that, at any rate at
first, he prefers a lateral position low down in the bed, and resents
any attempt to prop him up.
“Cough.—This for the first day or two may be irritable and distressing,
with a little frothy expectoration, but as the latter becomes more
purulent the cough is less troublesome, and soon the patient is
expectorating easily and frequently, until the later stages are reached;
when owing to increasing asphyxia the patient becomes more and more
torpid, the cough subsides, and hardly any secretion is brought up. This
failure becomes an added factor in bringing about a rapidly fatal
termination.
“Expectoration.—The sputum, with its yellowish-green purulent masses, is
very characteristic, and may be one of the first indications of the
serious nature of the illness the patient is suffering from.
“Temperature.—The fever of this complaint does not follow any very
constant type. In nearly all our cases the pyrexia was of sudden onset,
and for the first few days was more or less sustained at about 103°.
Later it conformed more to the swinging type with a range of several
degrees. In a few cases a curious gradual ante mortem drop has been
observed.
“Pulse.—Tachycardia is a very constant feature throughout the illness.
The rate is frequently well over 120, though the volume may remain
surprisingly good until immediately before death.
“Some degree of dyspnoea is always present, and is usually progressive,
though towards the end in the fatal cases when the mental acuteness is
dulled by the increasing asphyxia the patient is not distressed by its
presence. In some cases there have been paroxysmal exacerbations of the
breathlessness, accompanied by a state of panic, in which the patient
struggles wildly and tries to get out of bed in order to gain relief.
Cyanosis is another prominent feature throughout the illness. At first
it may not be more than duskiness, but in the later stages it becomes
very evident. It is only slightly relieved by oxygen; this, no doubt, is
partly explained by the difficulty in giving the oxygen efficiently,
owing to the patient’s objection to any mouthpiece that fits at all
tightly, and partly by the blocked condition of the bronchioles
interfering with the absorption of the oxygen.
“The condition usually begins with the presence of a moderate number of
sharp crepitant râles, often first heard in the region of the root of
the lung; these quickly become generalized. In the majority of the cases
signs of bronchopneumonia patches can be made out; these are generally
situated near the root of the lungs. In a certain number of cases these
patches spread and become confluent, giving practically all of the
physical signs of a lobar pneumonia. As the disease progresses the air
entry is diminished; on listening one is often struck by the small
volume of sound heard. The resonance of the lungs may also be lessened.
A slight pleuritic rub was heard in a few of our cases, but this was
soon masked by the bronchitis signs.”
Detailed sputum examination in twenty cases showed the presence of the
influenza bacillus in eighteen, and in ten out of these eighteen the
organism was isolated by culture. The next most frequent organism found
was the pneumococcus, which was present in thirteen cases. The
streptococcus was found in five.
Abrahams, Hallows, Eyre and French report the same epidemic:
“A typical case is as follows. The onset is usually acute; the early
symptoms are those of a ‘cold in the head.’ The temperature may be 101
or 102°, but there are no features to distinguish the condition from
acute ‘coryza’ or febricula, so that in the majority of cases the
patient does not report sick for two or three days, by which time he is
sent to the hospital. At this state two features attract particular
attention. First, the character of the expectoration: this consists of
thick pale yellow, almost pure pus, not the frothy expectoration
familiar in ordinary bronchitis; it has no particular odor and it
becomes increasingly abundant until in a day or two it may amount to
several ounces in the twenty-four hours. Secondly, the rapidity of the
patient’s breathing: this may be so evident that pneumonia suggests
itself, yet on examining the chest the only physical signs consist of
few or many rhonchi scattered widely, but most marked at the bases of
the lungs behind, associated with a wheezy vesicular murmur; resonance
everywhere is unimpaired and bronchial breathing is absent. A little
later a third point attracts notice; a peculiar dusky heliotrope type of
cyanosis of the face, lips, and ears, so characteristic as to hall-mark
the nature of the patient’s malady even on superficial inspection. By
this time dyspnoea is very pronounced; respiration consists of short,
shallow movements, which in bad cases amount almost to gasps,
reminiscent of the effects of gas poisoning. Recovery at this stage may
occur, but by the time the cyanosis has become at all pronounced the
prognosis is extremely bad, though the number of days the patient may
still live, in spite of the severity of his distress, is often
surprising. The character of the sputum remains the same throughout,
though sometimes it is blood-tinged or actual blood may be expectorated
instead of, or in addition to, the more typical pale yellow pus. In the
later stages of the illness areas of impaired note or of actual dullness
may be found, particularly over the posterior aspects of the lungs,
associated with bronchial breathing and crepitant râles. These may be
due to the progression of the purulent bronchitis into hypostatic
pneumonia, or into actual bronchopneumonia at the bases; or, on the
other hand, they may be due to massive collapse of the lungs secondary
to the bronchitis and obstruction of the bronchioles by pus. In a few
cases, not necessarily the most serious, a frank lobar pneumonia has
developed later, and has been followed by an empyema from which 15–30
ounces of thin pneumococcal pus has been aspirated—in one case alone was
resection of a rib unavoidable. The condition, however, is not primarily
a lobar or a bronchopneumonia, but a bronchitis, and although a small
amount of basal bronchopneumonia has been present in one or two of our
post-mortem examinations, in other fatal cases there has been no
bronchopneumonia at all, not even the smallest portions of either lung
being found to sink in water.
“We have no doubt that the condition is primarily an affection of the
bronchi and bronchioles, and not of the alveoli, though the alveoli may
be affected later if the patient survives long enough. In a typical
post-mortem examination it would be difficult, or almost impossible, to
define the actual cause of death unless one knew the clinical history.”
Abrahams and his collaborators describe in detail eight consecutive
cases. A study of the type of onset may be of help in determining the
character of the disease. The first patient had been subject to
bronchitis for years. He had been ill with cough and some pyrexia for
five days previous to his admission. There is no further description of
his admission symptoms. Case two was admitted on March 17th, having
taken ill the previous day with shivering, cold and pain in the chest.
The temperature was 104°, the pulse-rate 118, and the respirations were
44. The patient was very restless and had much dyspnoea but was not
cyanosed. The third patient had taken ill three days previous to
admission with symptoms of cold in the head and a sore throat. He
complained of headache and dry cough without expectoration, shortness of
breath, and a pain behind the sternum.
Case four was admitted with a history of having been out of sorts with a
cold and bronchial cough for ten days previously. On admission his
temperature was 103°, pulse-rate 112 and respiration-rate 36. He had
abundant blood-stained purulent sputum.
Case five is the first case that shows a type of onset distinctly
resembling that of influenza. The patient had been ill three days with
headache, cough and generalized pain previous to his admission. The
temperature on admission to the hospital was 103°, pulse-rate 112,
respiration-rate 20. There were no abnormal physical signs in the chest
on admission. They did appear two days later. Case six related that he
had been sleeping under canvas for three nights before coming to the
hospital, and that during the first of these nights he was taken ill
with a cold which became associated with a cough and increasing
shortness of breath. On admission there was slight cyanosis, and
dyspnoea was very pronounced. Shortly afterwards he became orthopnoeic,
with heliotrope cyanosis. On the slightest exertion, such as turning
over in bed, the cyanosis increased markedly, and although the
respiration-rate remained under forty when he was at rest, on the least
exertion it increased to nearly sixty. The sputum was purulent and
abundant, pale yellow, not frothy and not blood-stained, and the day
after admission contained Bacillus influenzae, pneumococcus and
Micrococcus catarrhalis.
Case seven had been ill seven days before admission with cough and
fever. On admission his temperature was 105°, pulse 116, respiration 24.
Case eight gave a history of having had a cough for eight days previous
to admission. This cough had not incapacitated him much at first, but he
became progressively worse during the four days before admission, with
increasing shortness of breath and abundant yellow sputum which he found
it difficult to raise. On admission dyspnoea with cyanosis was very
evident.
Even from these detailed clinical descriptions it is impossible to say
definitely whether the disease was or was not influenza. There is no
doubt, however, but that clinically the disease resembled more the
so-called streptococcus pneumonias that were observed in the United
States camps in the winter of 1917–18. The descriptions of the mode of
onset are particularly at variance with the onset as we know it in
influenza.
Those who believe that the influenza bacillus is the cause of influenza
maintain that the finding of this organism in a large per cent. of cases
by both groups of observers is valuable evidence. For reasons previously
stated we cannot agree.
Description of the epidemic features is not detailed enough to be of
assistance. The first group of authors remark that the disease
constituted “almost a small epidemic.” The second group say that six out
of eight cases in their series of candidly reported patients came from
one command. The former report on twenty cases, the latter on eight. The
latter remark that although they have dealt with only eight cases in
detail, they had a much larger number altogether. Presumably there were
a decidedly larger number of patients in both hospitals, but the actual
number is not stated. In short, we do not know whether the disease
appeared to be more or less epidemic than the apparently similar disease
among our troops in the winter of 1917–18.
Both groups of observers have described in some detail the pathology of
the cases which were necropsied. The author in attempting to obtain
further comparative information has submitted the pathologic
descriptions given by the British authors to Dr. E. W. Goodpasture, who
has very kindly pointed out the points of similarity and difference
between the gross and microscopic findings in these cases of purulent
bronchitis, and the same findings in typical influenza. He says that the
lung picture, as described, is not the same as that which was typical of
the acute influenza observed in the autumn of 1918 and again in the
winter of 1920. The characteristic picture in the latter is primarily an
extensive involvement of the alveolar structure, while as Abrahams and
his associates remarked, the condition in their case is primarily “an
affection of the bronchi and bronchioles, and not of the alveoli, though
the alveoli may be affected later, if the patient survives long enough.”
Goodpasture states that the pathology as described by the British
authors is very similar to the lung picture in interstitial
bronchopneumonia described by MacCallum for the post-measles and primary
bronchopneumonia among our troops in the winter of 1917–18. The
streptococcus and the influenza bacillus were dominant organisms in
MacCallum’s series. It also resembles the pathologic picture described
by Pfeiffer in his original article on one of the late recurrences of
the 1889–93 epidemics of influenza.
In summing up, we must admit that it is impossible to reach a definite
conclusion, but that both clinically and pathologically the disease
described among the British troops in 1916 and 1917 was not typical of
influenza as we have known it more recently. The similar conclusion
reached by Carnwath, presumably chiefly from epidemiologic
considerations, has already been described. We do not deny that this
“purulent bronchitis” _may_ have been influenza. On the contrary, it is
a part of our hypothesis that influenza under the proper conditions may
become epidemic in practically any land. But we do believe that the
evidence has not shown that the disease among the British troops in 1916
and 1917 was an etiologic precursor of the great pandemic.
To return to a discussion of influenza in China, we quote from an
article by Cadbury in the China Medical Journal: “Unfortunately no
health reports are available for the greater part of the Chinese
Republic. We have consulted, however, the Health Reports of the Shanghai
Municipal Council from 1898 to 1917, and among the total foreign deaths
we find that only the following were attributed to influenza: 1899, one
death; 1900, one death; 1907, four deaths; 1910, one death. After this
no deaths are recorded from this cause up to and including the year
1917.
“In the Hongkong Medical and Sanitary Reports, which give the total
deaths registered in the Colony, we have examined the records from 1909
to 1917. During these nine years only two deaths were attributed to
influenza, and both occurred in 1909.
“From a personal letter from Dr. Arthur Stanley, Health Officer in
Shanghai, dated February 11, 1919, I quote the following:
“‘As to influenza we had an attack beginning at the end of May and
lasting through June and again in the latter part of October and lasting
through November. The latter was somewhat more severe. The noteworthy
features were general absence of catarrhal symptoms, congestive pharynx
frequent, as also was a slight erythematous blush on the neck and chest,
which made one think at first of scarlet fever. Fatal pneumonia common
among the Chinese and Japanese, but among Europeans very little
pneumonia.’
“In his report for May, 1918, Dr. Stanley says that the disease was
reported to have reached Peking before it came to Shanghai, but
subsequent reports showed that most of the river ports were almost
simultaneously infected, the rate of spread conforming to the rate of
conveyance by railways and boats of infected persons. The mortality was
very low.
“Newspaper reports indicate that a third appearance of the disease in
Shanghai occurred from the middle of February, 1919, which was still
prevalent in April. The symptoms were much more severe.
“For Hongkong I quote from a personal letter from Dr. Hickling, the
Principal Medical Officer of Health, dated January 29, 1919:
“‘The epidemic of influenza in the spring was a very mild one, so far as
we can judge. The disease did not last more than a few days in most
cases. The recent epidemic (October, November, December and January) has
been much more severe, often lasting two or three weeks.’
“Only one death, which occurred on May 14th, was reported from Hongkong
in the spring. In the later epidemic the deaths reported were as
follows: October, 70; November, 95; December, 67. The first of these
deaths occurred on October 5th. The figures for January had not been
compiled, but the disease was diminishing.
“Dr. C. W. McKenny of Hongkong has kindly furnished me with the
following facts: ‘During the first five months of 1918 there were
twenty-two admissions for influenza to the Civil and Tung Wa hospitals
(3 in May). In June there were 269 cases with three deaths. In July,
August and September, 43 cases; and during October-November, 130 cases
with four deaths....
“‘The June epidemic in Canton appeared first at the Pui Ying School,
then among the employees of the Post Office, the staff of the Canton
Hospital, the Canton Christian College, and the Kung Yee Hospital. The
other schools entirely escaped. Eleven days were taken by the disease to
spread from one part of the city to the various other parts.’”
Plague appeared in the north of China in 1917, originating apparently in
inner Mongolia. The spread extended over quite an area, and it is
reported that this epidemic of pneumonic plague has been more extensive
than any since that of 1910–11. The disease was first reported prevalent
in Patsebolong December 6, 1917. The diagnosis was confirmed
bacteriologically, and there can be little doubt but that the cases of
plague reported in various parts of China even up to March 18th were
true plague, and not unrecognized influenza.
SECTION III.
In the following section of our report we shall have frequent occasion
to refer to a series of investigations conducted by the author in the
City of Boston during the 1920 influenza epidemic. We will explain in
some detail at this point the nature of the work done and the methods
used, in order that the subsequent references will be readily
intelligible.
AN INVESTIGATION OF INFLUENZA IN BOSTON DURING THE WINTER OF 1920.
Following every widespread epidemic interest centers in the question as
to how much havoc the disease has wrought, what proportion of the
population fell victim, and how many of these died. With regard to
influenza the vital statistics of all countries are decidedly
insufficient in furnishing this information.
In nearly all countries influenza is not a reportable disease. Usually,
as was the case in the United States in 1918, the disease was made
reportable during the epidemic, but this took effect usually at least
two weeks after the epidemic had started in a community. Further, there
is probably not a single community in which the reported cases of
influenza reach to anywhere near the total of actual cases. The question
of diagnosis, which is not always easy even in the presence of a
pandemic, causes some physicians to hesitate to report cases. Other
physicians “play safe” and report nearly everything as influenza.
Finally, in the period of an epidemic, the physicians are so pressed
with caring for the sick that they very naturally neglect to report
cases as they occur.
It becomes necessary, therefore, in collecting evidence in civil
populations, of the morbidity and fatality from influenza, to obtain
additional information to that available to the Health Officer.
The method which may be relied upon to give the most accurate data
consists in house-to-house surveys made soon after an epidemic, in which
competent inspectors obtain detailed information concerning the illness
or freedom from illness of every individual in the areas canvassed. The
majority of individuals interviewed will not have had the disease, and
it is therefore essential that in such a census a large enough
population be covered that the resulting figures will be truly
representative of the population at large.
Toward the end of January, 1920, when the recurrent epidemic was at its
height in Boston, the author undertook with the aid of thirteen trained
social service workers, and one physician, who was a graduate of the
Harvard School of Public Health, to make a sickness census of 10,000
individuals. Six districts were chosen in different sections of the
city, representing six different economic and social groups. Great care
was exercised in selecting the districts, so that the population in each
might be as homogeneous as possible regarding economic and sanitary
status, as well as race, and living conditions in general.
We have sought to clarify and to abbreviate our description of the
characteristics of the various districts by incorporating a map,
together with photographs of typical streets in each district. One who
compares these streets as they are seen in the photographs would
scarcely find it necessary to enter the buildings in order to discover
the living conditions of the occupants (Chart XIII).
CHART XIII.
[Illustration:
Map of greater Boston showing the distribution of the districts
covered by the author’s house census.
]
District I includes an Italian population of 2,000 individuals, one-half
of which live in the most congested portion of the city (see photograph)
known as the North End, while the other half, living in East Boston, are
slightly less crowded.
District II, in South Boston, consists of 2,000 individuals almost
entirely of Irish race stock.
[Illustration:
FIG. 1.—District 1. Italian tenements. Very congested and very poor.
]
District III, like District I, consists of three groups living in very
similar environment to the two groups of the first district, but
composed chiefly of Jewish race stock of various nationalities. The
photograph for this district represents the area in the “West Side” near
the Charles River Basin. The area in the “South End” is of similar type,
while the area in East Boston is housed similarly to the Italian
district in East Boston. The dwellings in both of these latter districts
correspond to those shown in the second photograph of District II.
While the first three districts comprise tenement areas, some poor and
the remainder very poor, Districts IV and V represent the middle class,
and consist nearly entirely of “Duplex” and “Three-Decker” buildings.
The first of these comprises 1,000 individuals of mixed race and
nationality, the type broadly spoken of as American. The second consists
of a Jewish population of 1,600.
[Illustration:
FIG. 2.—District 2. Irish tenements. Congested and poor.
]
[Illustration:
FIG. 3.—Another street in the Irish tenement district.
]
[Illustration:
FIG. 4.—District 3. Jewish tenements. Very congested. Very poor.
]
[Illustration:
FIG. 5.—District 4. Middle class. Mixed American population.
]
[Illustration:
FIG. 6.—District 5. Middle class. Jewish population. Moderately
well-to-do.
]
[Illustration:
FIG. 7.—District 6. Well-to-do population. Mixed American.
]
In District VI are included 1,400 individuals belonging to the
well-to-do and moderately wealthy families of Brookline.
The six districts may be considered as representative of the various
strata of society, so that we are enabled to study the influenza and its
mode of action under varying environment. We have selected areas in the
city consisting of households or homes rather than boarding houses and
rooming populations. After a few attempts in the latter group we became
convinced that the information obtained in rooming houses was utterly
valueless. In the Jewish districts we were able, through the kind
co-operation of the Federated Jewish Charities, to use trained Jewish
Social Service Workers, each of whom had previously worked in the
district assigned to her, thereby possessing the confidence of the
inhabitants. They were also able to speak the language. One-half of the
Italian district was surveyed by an Italian physician and the other half
by an American Social Service Worker who knew the Italian language.
The information obtained was recorded on printed forms, which were
filled out in accordance with detailed written instructions. Form “A”
contained the necessary information concerning the family as a whole,
including statistical data of each individual, description of the
dwelling, of the sanitary condition, of the economic status, etc. Form
“B” was filled out for each individual and gave detailed information as
to the occupation and illnesses during the 1918–19 or the 1920 influenza
epidemics, or during the interval. Form “B” was so arranged that the
inspector was not called upon to make the diagnosis of influenza, but to
record the various symptoms as described by the patient. The decision as
to the diagnosis was made later, by the author. All blank spaces were
filled in with either a positive or negative answer, so that the
reviewer knew that all questions had been asked and answered. (See
Appendix.)
The inspection was begun on February 9th, at the height of the epidemic.
All records were turned in and reviewed by the author, who blue-penciled
obvious inaccuracies and incorporated directions and questions in those
instances where he desired further information. The records were then
returned to the inspectors who, at the termination of the epidemic early
in March, surveyed the entire 10,000 a second time, checking up their
first record, correcting any inaccuracies, and adding records of
additional cases of influenza which had occurred in the interval.
The most careful statistical surveys and compilations are not without
error. We have gone into considerable detail in the preceding
description in order to demonstrate the several checks that have been
made upon the work, without which information others would be unable to
judge of the accuracy or value of our work.
_Diagnostic standards for the 1918 epidemic._—All cases of illness
recorded on the reports, which have occurred during either the 1918 or
the 1920 epidemics, or in the interval between them, have been put into
four groups as regards diagnosis of influenza. Cases are designated as
“Yes,” “Probable,” “Doubtful,” and “No.”
Cases of illness occurring during the months of 1918 and 1919 in which
influenza was epidemic and in which the patient remembers that he had
the more definite symptoms, (fever, headache, backache, pain in the
extremities, pneumonia) and in which he was sick at least three days and
in bed at least one day, have been designated as “Yes.” The symptoms
chosen are those most likely to be remembered. The individual frequently
does not remember all. Statements of the absence of fever are often
unreliable. Usually the headache, backache or pain in the extremities,
or even all of these are well recollected.
Cases occurring particularly during the epidemic period in which the
more definite symptoms are unknown, but who were sick three days or
longer and who were in bed at least one day, were probably influenza.
This is particularly true if there were no other symptoms suggestive of
some other definite disease. Such cases were designated “Probable.”
Cases have been designated as doubtful when the evidence of illness
falls short of the above desiderata. Cases of true influenza may fall
into this group, either because of the extreme mildness of the symptoms
and course or because of the inaccurate memory of the individual
concerning the events of his illness sixteen months previously. Our
results show that the group of doubtful cases is relatively very small
and the number of true cases lost in this group will be negligible.
One important reason for adhering to the above classification is that it
corresponds closely with that used by Frost and Sydenstricker, so that
our results may easily be compared with theirs.
_Standards for 1920._—For 1920 the illnesses were so recent in the minds
of the patients that we have required rather full information for making
the diagnosis of “Yes.” For this designation certain symptoms are
arbitrarily required. Certain additional symptoms, if present, serve to
strengthen the diagnosis of influenza. The required symptoms are fever,
confinement to bed for one day or more and at least two out of the
following three, headache, backache and pain in the extremities. The
additional symptoms which influence the classification are sudden onset,
prostration, lachrymation, epistaxis, and cough.
Cases designated as probable are those in which the symptoms as
enumerated above are incomplete in one or more details, but yet in which
the diagnosis of influenza would be justified. “Probable,” therefore,
means that the case is to be accepted among the list of true influenza
cases. This is particularly so when the case occurs during the epidemic
period.
“Doubtful” applies to those cases in which the evidence although
suggestive of influenza, is not complete enough to warrant such a
diagnosis. The doubtful feature may be in the lack of too great a number
of the symptoms enumerated, or the presence of symptoms which might be
due to some other disease. Certain cases occurring at the same time with
other cases of typical influenza in the same household, and which would
otherwise have been recorded as doubtful, have been marked either
“Probable” or “Yes.”
_Standards of severity._—A purely arbitrary classification of severity
has been adopted. Probably no two observers would agree exactly on a
classification of this nature, but for the purposes of this study the
following will suit all requirements provided the standard used is
carried in mind throughout the comparison.
If a patient with influenza is under medical care, and the case is one
of ordinary severity, the usual period in which the individual is
advised to remain in bed is one week. This is the basis of the criteria
of severity.
_Mild._—A case is recorded as mild if the individual has remained in bed
three days or less; _Average_, if in bed four to seven days; _Severe_,
if in bed over seven days. _Pneumonia._ This designation is added to
that of “severe” only in case the physician made such a diagnosis, or if
the evidence under “symptomatology” leaves no doubt as to the condition.
Examples of individual exceptions to the preceding general
classification are as follows: An individual in bed two days, but sick
for three weeks might be recorded as average. A mother, with a family of
sick children and who spent no time in bed may have been a severe case
of influenza. In fact, we have allowed ourselves a certain latitude in
individual cases in classifying both the diagnosis and the severity of
the disease.
In the final tabulation we have included both the “Yes” and the
“Probable” as being cases of influenza. This has been done after a
careful comparison of both groups.
As a check upon the reliability of the work we have compared our results
for the 1918 epidemic with those reported by Frost and Sydenstricker and
have discovered that with regard to the general subject discussed in
both studies there is close agreement. This is important in view of the
long period that has elapsed between the first pandemic and the time of
our survey, and because we are unable to compare our tables of incidence
for 1918 with those for the city or the state at large. Our own records
do not place the date of occurrence of the disease in 1918 any more
closely than by month.
We have compared our 1920 incidence curves with those of Massachusetts
and find a close correspondence, particularly in the date of onset,
peak, and disappearance of the epidemic. We have done likewise for the
occurrence of the disease in the city of Boston at large (Chart XIV).
In the past but few house-to-house canvasses have been made with
relation to influenza. Auerbach, following the 1889 epidemic, collected
statistics on 200 families distributed throughout the city of Cologne.
Abbott, while not conducting a canvass, did obtain a certain amount of
valuable information by letters addressed to physicians, institutions
and corporations throughout the State of Massachusetts.
There is fairly abundant literature on the disease as it occurred in
institutions. Moody and Capps, in a study of the epidemic in Chicago in
December, 1915 and January, 1916, made a survey of the personnel and
inmates of four institutions in that city. Among other rather numerous
statistical compilations from institutions we may mention that of
Hamilton and Leonard which was devoted particularly to a study of
immunity, and that of Stanley at San Quentin Prison, California.
Garvie has reported his personal experience with influenza in an
industrial area and discusses the disease as it has occurred in families
in his private practice.
Carnwath reports a “block census” undertaken by Dr. Niven in Manchester,
England. This is of the same nature as our own work. Reeks has made a
detailed house survey of 2,757 persons in New Britain, Connecticut. D.
W. Baker has conducted somewhat similar surveys for the New York
Department of Health, and Winslow and Rogers quote the excellent record
of the Visiting Nurse Association of New Haven, in which they have
information for all of the families cared for by the nurses. This,
however, is a collected group and does not correspond with the so-called
block census.
CHART XIV.
[Illustration:
Chart showing the actual incidence of influenza in Boston by weeks and
the actual incidence among the 10,000 individuals surveyed by weeks
during the first three months of 1920.
Full Line—incidence in the entire city based upon reports to the
Health Commissioner.
Dotted Line—incidence in the six districts surveyed.
]
The most comprehensive and detailed work that has been done in this line
is that reported by Frost and Sydenstricker and by Frost, the first
being the result of a canvass of 46,535 persons in Maryland, and the
second a similar report based on a canvass of 130,033 persons in several
different cities of the United States. We shall have occasion to refer
to these later.
MORBIDITY.
There has been great actual variation in the morbidity from influenza in
the various epidemics and even in different localities during single
epidemics. Previous to 1889 there were no reliable statistics for the
disease incidence, and subsequent to that date the records, for the
reasons previously mentioned, have still been not entirely adequate.
In the history of influenza morbidity, as in that of its mortality, we
must content ourselves for information prior to the nineteenth century
with the very general estimates made by contemporary historians. During
the last century the statistics have been more numerous and more nearly
correct. As far back as the first recognized pandemic, 1510, the
extremely high morbidity has been a recognized characteristic. Thomas
Short in speaking of this pandemic says, “The disease ... attacked at
once and raged all over Europe, not missing a family and scarce a
person.”
Pasquier in 1557 spoke of the disease as common to all individuals, and
Valleriola describes the widespread distribution of the epidemic
throughout the whole of France during that year. It spared neither sex,
age, nor rank, neither children nor aged, rich nor poor. The mortality,
however, was low, “children only, dying.” Again, Thomas Short remarks,
“This disease seized most countries very suddenly when it entered,
catching thousands the same moment.”
Of the second pandemic, 1580, Short says, “Though all had it, few died
in these countries except such as were let blood of, or had unsound
viscera.”
Thomas Sydenham remarks that in the epidemic of 1675 no one escaped,
whatever might be his age or temperament, and the disease ran throughout
whole families at once.
Molineux recorded concerning 1693, “All conditions of persons were
attacked, those residing in the country as well as those in the city;
those who lived in the fresh air and those who kept to their rooms;
those who were very strong and hardy were taken in the same manner as
the weak and spoiled; men, women and children, persons of all ranks and
stations in life, the youngest as well as the oldest.”
Schrock tells us that in Augsburg in 1712 not a house was spared by the
disease. According to Waldschmidt in Kiel, ten and more persons were
frequently taken ill in one house, and Slevogt says that the disease was
fearful because so many persons contracted it at the same time. The
disease was, however, not dangerous, for Slevogt continues: “Fear soon
vanished when it was seen that although it had spread all over the city,
it left the sick with equal rapidity.”
It is estimated that in the epidemic of 1729–1730, 60,000 people
developed the disease in Rome, 50,000 in Mayence, and 14,000 in Turin.
In London “barely one per cent. escaped.” In Lausanne one-half of the
population, then estimated at 4,000, was stricken. In Vienna over 60,000
persons were affected. In the monasteries of Paris so many of the
inmates were suffering from the disease that no services could be held.
Huxham is quoted in Thomson’s “Annals” as declaring concerning the
epidemic of 1732–33: “Not a house was free from it, the beggar’s hut and
the nobleman’s palace were alike subject to its attack, scarce a person
escaping either in town or country; old and young, strong and infirm,
shared the same fate.”
Finkler writes as follows concerning the epidemic of 1758: “On Oct.
24th, Whytt continues, the pestilence began to abate. He is not sure
whether this was due to a change in the weather, or because the disease
had already attacked most people, although the latter seems more
plausible to him, particularly as he says that ‘in Edinburgh and its
vicinity not one out of six or seven escaped,’ and in other localities
it is said to have been even worse. In the north of Scotland also, the
epidemic was greatly disseminated from the middle of October to the end
of November. A young physician wrote to Robert Whytt: ‘It was the most
universal epidemic I ever saw, and I am persuaded that more people were
seized with it than escaped.’ This same physician reported that ‘it was
not at all mortal here.’”
In the epidemic of 1762, we learn from Razoux, de Brest, Saillant,
Ehrmann, that the morbidity was great while the mortality was low.
According to Grimm, nine-tenths of the inhabitants of Eisenach
contracted the disease in 1767.
Daniel Rainy, of Dublin, in describing the invasion of an institution in
1775–76, tells us that from among 367 persons varying in age from 12 to
90 years, 200 were taken sick. Thomas Glass says: “There sickened in
Exeter Hospital all the inmates, one hundred and seventy-three in
number; one hundred and sixty-two had coughs. Two or three days after
the hospital was invaded the city workhouse was attacked; of the two
hundred paupers housed there only very few escaped the disease.”
Gilibert described an extraordinary morbidity in Russia in 1780–81.
Metzger says that in 1782 the Russian catarrh was so universal during
the month of March that in many houses all the inhabitants were
attacked. During this period, “in St. Petersburg, 30,000, and in
Königsberg, 1,000 persons fell ill each day;” in Rome two-thirds of the
inhabitants were attacked; in Munich, three-fourths; and in Vienna the
severity of the epidemic compelled the authorities to close the theaters
for eight days.
The epidemics of 1788–89, 1799–1800 and of 1802–1803 were characterized
by a relatively lower morbidity than that of 1830–32, in which the
morbidity was again enormous. Likewise in 1833, the morbidity was very
great. In Prague “scarcely a house was spared by the plague.” In
Petrograd, 10,000 persons were attacked; in Berlin at least 50,000.
These are the figures of Hufeland. The Gazette Médicale records the
morbidity as being four-fifths of the total number of inhabitants of
Paris.
In 1836, according to Gluge, 40,000 persons suffered from the disease in
Berlin alone.
In London, in the 1847 epidemic, it has been calculated that at least
250,000 individuals took sick, and in Paris, according to Marc d’Espine,
between one-fourth and one-half of the population developed the disease,
and in Geneva not less than one-third.
Leichtenstern informs us that in 1890 the early reports were made by
clinical men and were mere presumptions. They were almost universally
higher than the later statistical findings. The early estimates for the
morbidity in several German cities were from 40–50 per cent. On the
other hand, one of the highest statistical reports recorded by
Leichtenstern was for Strasbourg in which 36.5 per cent. of the
individuals became sick. The average morbidity reported by him ran
between 20 and 30 per cent. The difference is accounted for in part by
the fact that some of the very mild cases were not recorded in the
statistics, and in part by the tendency in giving estimates, to
exaggerate.
Auerbach has collected the statistics of 200 families distributed
throughout the city of Cologne. He found that 149 of these families (75
per cent.) were attacked. In these, 235 were ill—59 men, 95 women, and
81 children. The larger number of women was explained as due to the
illness of the female servants. He estimates each family as consisting
on an average of six individuals, and concludes that 20 per cent. were
taken with the disease.
Following the 1889 epidemic, Abbott concluded, on a basis of
questionaires sent out to various individuals and institutions in the
State of Massachusetts, that 39 per cent. of the entire population had
been attacked, in all about 850,000 persons.
Moody and Capps, in December, 1915, and January, 1916, made a survey of
the personnel and inmates of four institutions in Chicago, the Michael
Reese Hospital, the Illinois Training School for Nurses, the Old Men’s
Home, and St. Luke’s Hospital Nurses Training School, making a total of
677 persons surveyed, of whom 144 developed influenza, making a
percentage morbidity of 21. They remarked that there were many others
with colds who remained on duty and were not included in the table and
were not diagnosed as influenza.
We have already described the relatively low morbidity and mortality in
the early spring epidemic in the United States. According to Soper, the
total number affected in March, 1918, at Camp Forrest and the Reserve
Officers Training Camp in the Oglethorpe Camps was estimated at 2,900.
The total strength at that time was 28,586. The percentage morbidity
then was probably a little over 10 per cent. Dunlop, in describing the
May, 1918, epidemic in Glasgow, says that it was more limited in extent,
as well as milder, than the later epidemic.
It has been estimated that in the autumn epidemic in the United States
Army Camps one out of every four men had influenza, and one out of every
twenty-four men encamped in this country had pneumonia. During the four
autumn months of 1918, 338,343 cases of influenza were reported to the
Surgeon General’s Office; there were 61,691 cases of pneumonia.
Woolley reports that among the soldiers at Camp Devens, Mass. 30 per
cent. of the population was affected.
At Camp Humphreys, 16 per cent. of the entire personnel developed the
disease. The camp had an average strength of 26,600 individuals.
Fifty-two per cent. of the entire number of cases occurred during the
peak week, which ended October 4th. The outbreak began September 13th
and ended October 18th.
Hirsch and McKinney report that an epidemic of unusual virulence swept
with great rapidity through several organizations in Camp Grant between
September 21, 1918, and October 18, 1918. During this time 9,037
patients were admitted to the Base Hospital, representing about
one-fourth of the strength of the camp, and of these, 26 per cent.
developed pneumonia. About 11 per cent. of the total admissions or 43
per cent. of the total cases of pneumonia died.
Referring to the report of Howard and Love, we quote as follows: “It is
probable that practically all susceptible human material in infected
camps suffered from an attack of the disease during the continuance of
the epidemic. The records from various camps indicate that from 15 to 40
per cent. of commands suffered from an attack of the disease. These
records, as previously stated, do not indicate in full the true
incidence of the disease. Certain good results were accomplished in some
camps by the application of effective and early isolation of patients
and suspects and other measures generally recognized as of value. It was
sometimes possible to retard the progress of the epidemic and cause it
to be spread over a longer period of time. The epidemic thus became less
explosive in character, and fewer people were under treatment at the
same time. It was possible to take better care of the sick and thus
reduce the incidence of and deaths from complicating pneumonia. It has
not been shown that such measures accomplished reduction in the absolute
number of cases of influenza occurring in one command as compared with
another.
“The ‘cantonment’ group of camps gave a much higher death rate from
influenza and its complications than the ‘tent’ camp or ‘departmental’
group. At first glance it would appear that the different housing
conditions and the more marked overcrowding in cantonments at the time
would fully account for this divergence. Closer study, however, leads to
the conclusion that geographical location was a factor of equal or
greater importance. It is well known that the disease was most virulent
and fatal in the northern, eastern and middle west states, a district in
which cantonments predominated. In the southern and Pacific coast
states, where the most of the tent camps were located, a milder type of
the disease prevailed, with fewer resultant fatalities. Camp Lewis,
Washington, and Camp Gordon, Georgia (both cantonments), had relatively
low death rates, approximating those in nearby tent camps. On the other
hand, Camp Syracuse, New York, and Camp Colt, Pennsylvania (both tent
camps), suffered severely and reported death rates approximating those
of cantonments in the same geographical district.”
Three waves of influenza are reported by Stanley at San Quentin Prison.
During the early wave it was estimated that over 500 of the 1,900 men in
the prison population were ill. The wave lasted for a little over two
weeks. In the second epidemic there were 69 cases in all, ten per cent.
of which developed pneumonia, with two deaths. There were fewer
ambulatory cases than in the first. Three and seven-tenths per cent. of
the population was attacked in the second epidemic, as compared with 27
per cent. in the first. In the third epidemic there were 59 cases, with
no pneumonia and no deaths.
Hernando estimates that in the Philippine Islands, 40 per cent. of the
total population of 7,000,000 was stricken with the disease. The
epidemic began in June, although it did not become severe until October.
The group of ages that suffered most were those between ten and
twenty-nine years. Hernando does not believe that the disease was
imported because cases were reported before ships arrived from infected
countries. After the importation of cases from elsewhere the disease
assumed the more severe form.
Armstrong, in reporting a survey of 700 influenza convalescents in
Framingham, Mass., remarked that 16 per cent. of the entire population
were infected with influenza. Reeks, in a house survey in New Britain,
Connecticut, found from among 2,757 persons that the morbidity rate
reached 234 per thousand. Dr. Niven found in his block census in
Manchester, England, that of 4,721 individuals, 1,108 (25 per cent.) had
developed the disease. Fourteen and eight-tenths per cent. of the
population were attacked in the summer and 10.4 per cent. during the
autumn and winter.
Frost found in his survey of 130,033 individuals that the percentage of
the population attacked varied from 15 per cent. in Louisville, Ky., to
53.3 per cent. in San Antonio, Texas, the aggregate for the whole group
being about 28 per cent. He remarks that this agrees with scattered
observations in the first phase of the 1889–1890 epidemic, when the
attack rate seems to have varied within these limits. In five of the
localities studied, geographically widely separated, the incidence rate
varied only within a narrow limit, from 200 to 250 per thousand.
Variations in attack rate showed no apparent consistent relation to
geographic location or size of community, or to the rapidity of
development of the epidemic.
In a house-to-house survey of 10,000 individuals in Boston the author
found that in the winter of 1918–19, 19.71 per cent., or one-fifth of
the entire population had developed the disease. It should be pointed
out that while the standards used in this survey are entirely comparable
to those used by Frost, the author has, contrary to Frost’s method, not
included in his group of positive cases those classified as “doubtful.”
This would raise the total incidence to a certain extent, but we feel
convinced that by omitting the doubtful cases we have approached nearer
to a correct picture of the epidemic as it actually occurred. As will be
seen from Chart XVI there was no great variation in the different
districts studied, with the exception of Districts IV and V. Districts
I, II and III were in the tenement section of the city, while District
VI was in one of the finest residential parts of Brookline. Districts IV
and V were midway between these two extremes as regards economic and
sanitary status, as well as extent of crowding. The lowest incidence was
in the Irish tenement district. The highest in a middle class Jewish
population.
CHART XV.
[Illustration: 1 and 2 Influenza incidence in 10,000 individuals [both
epidemics]]
CHART XVI.
[Illustration: 1918 Incidence of Influenza by sex in Districts surveyed
1920 Incidence of Influenza by sex in Districts surveyed
Individuals having Influenza in both Epidemics by sex]
In the 1920 recurrence we found that 9.55 per cent., or one-tenth of the
entire population, suffered from the disease, and the arrangement of
districts in order of incidence was very little changed. The Irish
community suffered least; the two middle class communities most. The
well-to-do district in Brookline had the next lowest incidence in 1920.
That the high recorded incidence in middle class districts was not due
to more accurate or more thorough work on the part of the inspectors is
indicated by the fact that a great part of the work on Districts IV and
V was done by the same individuals who inspected Districts II and III.
One-fifth of the population studied developed the influenza in 1918–19,
and one-tenth of the same population suffered in 1920.
We may agree with Winslow and Rogers, who conclude that the proportion
of the population actually affected by the influenza epidemic in 1918
varied between 200 and 400 per thousand.
_Relation of sex to morbidity._—Abbott concluded from his studies in
1890, that the weight of testimony appears to favor the statement that
persons of the male sex were attacked in greater number and with greater
severity than females. Leichtenstern reached similar conclusions. In the
epidemic of 1889, the males were attacked more frequently than the
females. He attributes this to two causes: first, the greater exposure
to infection, and; second, the fact that strong, robust individuals are
more frequently attacked.
It is amusing to compare this explanation with another found in the
Medical Supplement to the Review of the Foreign Press for March, 1919.
“A Spanish mission composed of Maranon, Pittaluga and Falco visited
Paris last October to collect information as to the identity of the
Spanish epidemic with the world pandemic of influenza. They found that
the epidemics in France and Spain were absolutely identical from the
epidemiologic, bacteriologic and clinical standpoint. The great majority
of the severe cases in both countries occurred between the ages of 16
and 40. Both in France and Spain more females than males were attacked,
which was possibly explained by the greater tendency of the former to
lead an indoor existence.”
Jordan, Reed and Fink, working in Chicago, found very different results.
They could discover no noteworthy difference among the pupils in high
school and elementary school. The attack rate was 230 for the boys and
231 for girls. One sex was presumably as much exposed as the other.
Among the employees of the Chicago Telephone Company, on the other hand,
the men were affected in considerably lighter proportion than the women
(151 per 1,000 as compared with 233 per 1,000 for women). Jordan
believes that the age factor was largely responsible for the difference
as the women employees are as a rule of much lower average age than the
men.
Frost found that with few exceptions the attack rate at all ages was
somewhat higher in females than in males. The total excess of incidence
in females was six per cent., which ranged from an excess of nineteen
per cent. in the highest locality to a deficiency of two per cent. in
the lowest. Only two of the eleven localities surveyed showed a lower
incidence among females than among males.
When the sexes were compared in different age groups, the female was
found to be higher than the male in each age period except under 5, 10
to 14, 40 to 44, and 70 to 74. The excess of incidence in males in these
groups is relatively small, and is hardly significant in the highest age
groups, where the rates are computed from small figures. Frost found the
most striking excess of incidence in females occurring between the ages
of fifteen and forty, the difference between the sexes being relatively
slight in age periods above and below these limits. Females over the age
of fifteen and especially between the ages of 15 and 45 were either more
susceptible to infection, or more generally and more intimately exposed
than males of corresponding age.
Our own records by the different age groups were remarkably similar. We
have found an excess among the females in every age except under five
years, 10 to 14, 50 to 54, and 60 to 64. In 1920 we found a slight
excess among the males up to the age of 15, and again at the ages 55 to
65. Females predominated in all other ages (Chart XVII). Among those
individuals who had attacks of influenza during both epidemics females
again predominated except in the ages under 5 years, 10 to 14 and 55 to
59. In our own results we find that ages above 65 show a predominance of
females.
After considering both series of results it is safe to generalize in
saying that above the age of 15 the female sex tends to acquire the
disease in slightly greater proportion than the male sex.
Chart XV shows the predominance of the female incidence in both
epidemics.
CHART XVII.
[Illustration: Influenza 1918–19 Case Rate per 100 persons by age
periods
Influenza 1920 Case Rate per 100 persons by age periods
Influenza 1918–19 Case Rate per 100 persons by sex and age
Influenza 1920 Case Rate per 100 persons by sex and age]
CHART XVIII.
[Illustration: Distribution of 1918–19 cases according to severity
Distribution of 1920 cases according to severity
Changes in 1920 severity distribution as compared with 1918 [both
sexes]]
CHART XIX.
[Illustration: District 1 Influenza 1918–19 Case Rate per 100 persons by
age periods
District 2 Influenza 1918–19 Case Rate per 100 persons by age periods
District 3 Influenza 1918–19 Case Rate per 100 persons by age periods]
[Illustration: District 4 Influenza 1918–19 Case Rate per 100 persons by
age periods
District 5 Influenza 1918–19 Case Rate per 100 persons by age periods
District 6 Influenza 1918–19 Case Rate per 100 persons by age periods]
CHART XX.
[Illustration: District 1 Influenza 1918–19 Case Rate per 100 persons by
sex and age
District 2 Influenza 1918–19 Case Rate per 100 persons by sex and age
District 3 Influenza 1918–19 Case Rate per 100 persons by sex and age]
[Illustration: District 4 Influenza 1918–19 Case Rate per 100 persons by
sex and age
District 5 Influenza 1918–19 Case Rate per 100 persons by sex and age
District 6 Influenza 1918–19 Case Rate per 100 persons by sex and age]
CHART XXI.
[Illustration: District 1 Influenza 1920 Case Rate per 100 persons by
age periods
District 2 Influenza 1920 Case Rate per 100 persons by age periods
District 3 Influenza 1920 Case Rate per 100 persons by age periods]
[Illustration: District 4 Influenza 1920 Case Rate per 100 persons by
age periods
District 5 Influenza 1920 Case Rate per 100 persons by age periods
District 6 Influenza 1920 Case Rate per 100 persons by age periods]
_Relationship of sex to severity._—In classifying cases as to severity,
we have followed the standard previously described. Our results have
shown that the 1920 recurrence in our group of individuals has been
decidedly milder than the earlier 1918 spread. The proportion of mild
cases in 1920 is nearly twice that of mild attacks in 1918–19. The
proportion of severe cases was twice as great in 1918 as in 1920. The
actual severity in 1918 was even greater than would be indicated by
these figures. The last column in Chart XVIII is a combination of the
two preceding, and while the 1920 column includes all classed as severe,
pneumonia, and fatal, that for 1918 only includes the severe and
pneumonia cases, but does not include the fatal cases for that year,
because those who died during the 1918–19 epidemics are not counted in
our 10,000 individuals surveyed. If these were included the percentage
of total severe, or average severity would be greater than 42.70.
We find that in 1918 the female sex had a higher proportion of severe
cases according to our standard than did the male. This was equally true
in 1920. We should emphasize here that we are not comparing only the
fatal cases in the two sexes, but all classified as severe, and
including fatal in 1920.
Not only was the female sex attacked in slightly greater proportion, but
also the individual cases appear to have been on the aggregate somewhat
more severe in that sex.
_Morbidity by age._—Before discussing the incidence of influenza in the
various age periods we should explain that the charts for 1920 are based
on the ages given by the individuals, and those for 1918 upon these
ages, corrected by the subtraction of 15 months from the age as given.
In our study of cases recurring during both epidemics the age used in
the calculations is that of 1920. It is for this reason that in all of
our age charts we have a first age period from zero to 15 months.
Infants of less than 15 months at the time of our survey were born
subsequent to the peak of the 1918–19 epidemic, and are not included in
computations for that time.
The general similarity of the age incidence in the six districts studied
(Charts XIX and XX) is evident. As a rule two peaks can be discerned,
one falling somewhere between 15 months and 9 years, and the other
between 20 and 39 years. There are individual variations in the
different districts, and in Districts IV, V and VI there is a tendency
toward a peak in the period 55 to 64. This, however, disappears when the
total 10,000 is tabulated, when the two peaks, 15 months to 9 years, and
20 to 39, show out clearly for the year 1918 (Chart XVII).
Frost found for the same epidemic that the attack rate was highest in
the age group 5 to 9, declining with almost unbroken regularity in each
successive higher age group, with the exception of the groups 25 to 34,
in which the attack rates were higher than in the age groups 15 to 24,
but not as high as that of 5 to 9.
Both series of observations agree in finding relatively high incidence
in early childhood and in early adult life.
For 1920 (Chart XVII) we find that these peaks, although present, have
become decidedly less prominent, and that there is a relatively higher
incidence in individuals past the age of 40 (Charts XXI and XXII). There
is some tendency toward straightening out of the curve; age appears to
have played a less important part, and those higher ages which were
relatively insusceptible in 1918 have become more susceptible in 1920.
We cannot generalize in the statement that all ages which were lightly
attacked in the first epidemic were more severely attacked in the 1920
spread, because the ages from 10 to 19 are found to be relatively lower
during both epidemics.
Other observations have been made regarding the age incidence
particularly during the 1918 pandemic. Jordan’s figures for the October
epidemic show a higher incidence among school children of ages 4–13 than
among those of higher school age, 14–18. The teachers in these schools
had a lower attack rate than the pupils. The pupils in both school
groups were from the same section of the city and to a large extent from
the same families and were presumably exposed in similar degree.
Lynch and Cumming found that of 49,140 children in public institutions
the influenza rate was 412 per 1,000, while among 703,006 adults in
similar institutions the rate was 263 per 1,000. These figures include
children in a large number of institutions scattered throughout the
United States, and would indicate that in childhood the susceptibility
is much greater than in adults.
Many writers agree that nursing infants show a relative
insusceptibility. However Abt records a case of an expectant mother who,
within two weeks of term, developed influenza, and during the course of
her illness gave birth to a baby boy, who at birth was found to be
suffering from bronchitis and bronchopneumonia, but who lived for three
days, finally dying of bronchopneumonia. Abt concludes from a review of
all of the facts that the newly born infant had influenza and that the
baby had become infected before birth.
CHART XXII.
[Illustration: District 1 Influenza 1920 Case Rate per 100 persons by
sex and age
District 2 Influenza 1920 Case Rate per 100 persons by sex and age
District 3 Influenza 1920 Case Rate per 100 persons by sex and age]
[Illustration: District 4 Influenza 1920 Case Rate per 100 persons by
sex and age
District 5 Influenza 1920 Case Rate per 100 persons by sex and age
District 6 Influenza 1920 Case Rate per 100 persons by sex and age]
According to Carnwath, the age incidence showed curious changes. During
the 1918 summer wave the ages most affected were 15 to 45. In the winter
of 1918–19 there was a considerable shifting toward the extremes of life
and particularly toward the younger years. The susceptibility of young
children was the subject of a special inquiry in London. Though the
attack rate was below the average, the chances of recovery were less
than in other age groups. Of breast-fed infants, 30 per cent. contracted
the disease; of artificially-fed 54 per cent. The opposite, however,
occurred in lying-in homes. An inquiry in Cheshire revealed that 25.4
per cent. of expectant mothers affected died.
Renon and Mignot have made a report on the 1920 recurrence. According to
them the grip of 1920 attacked all ages, in contradistinction to the
1918 epidemic, which attacked especially the young and vigorous.
One-third of their group were over 40 years of age, while some were 70
and 80 years old. In spite of this the disease remained relatively mild.
_Age morbidity in previous epidemics._—Previous to the epidemic of
1889–93, the various recorded observations regarding morbidity, and
particularly regarding age morbidity, have consisted often of records
made by practising physicians, and are merely estimates based upon their
clinical experience and varying with the type of individual treated by
them. Or else they have been records made by non-medical historians.
During the 19th century, the tendency toward statistical enumeration
becomes more and more prominent, but the first statistical studies of
real value to the epidemiologist were made in the epidemic of thirty
years ago. Statistical study must begin with this last epidemic.
Observations of the earlier epidemics, while very interesting for
reference and comparison, are no longer acceptable as unquestioned
statements of fact. Even at the present time and with all of the
emphasis that is now being laid upon statistical procedure the records
are far from perfect, and it is to be hoped that in years to come the
improvement will be so decided that the records even of the 1918–20
epidemics will appear crude.
Buoninsegni remarks of the 1387 epidemic that many individuals of all
ages died, but the deaths were particularly prevalent among the aged.
Jacob, of Königshofen, writes that “there came a general pestilence in
the whole country, with cough and influenza, so that hardly one among
ten remained healthy,” and that old and debilitated persons were
frequently the victims.
Balioanus tells us that the epidemic of 1404 let not rank, age nor sex
escape its effect.
In 1557, according to Valleriola, the disease appeared with pestilential
rapidity, and spared neither sex, nor any age, nor rank, neither
children nor old persons, rich nor poor, but that it was not as a
general rule dangerous; children only, who could not freely cough out
the phlegm, dying.
The same story is told by Molineux, for 1693, “All conditions of persons
were attacked, those residing in the country as well as those in the
city; those who lived in the fresh air and those who kept to their
rooms; those who were very strong and hardy were taken in the same
manner as the weak and spoiled; men, women and children, persons of all
ranks and stations in life, the youngest as well as the oldest.”
Molineux, however, added that, “it rather favored the very old who
seldom were attacked with it.”
These observations are but broad generalizations; if we pause to study
the psychology of the historian we are tempted to conclude that his
primary object was to impress his readers with an idea of the
enormousness of the dissemination of the disease during his period. That
being the main endeavor, a tendency to exaggerate for the sake of
rhetoric and yet remain within the limits of truth may be considered
excusable. But during the 1889–93 epidemic there was ample opportunity
to compare the estimates made by the practising physicians with the
later statistical tabulations. As a rule the former were higher both as
regards morbidity and mortality.
In the 1830–32 epidemic an interesting observation has been made. While
Kahlert says that no distinction between age, sex nor rank occurred,
Leberscht stated that persons of middle age, especially women in the
climacteric period, were attacked with special frequency. This is of
interest in view of the findings in the 1918 epidemic. Krimer states for
the same epidemic that children under 14 years of age and adults over 45
years were spared by the epidemic.
For the 1836–37 epidemic Finkler records the following: “Most of the
patients were adults from 20 to 40 years of age, and of these more women
than men were attacked. Curiously, however, the physicians of Würtenberg
speak of the great dissemination of the disease among children.”
In 1847–48, among the adult influenza patients, there are said to have
been more women than men. According to Canstatt, there were
proportionately more children than adults attacked.
In 1889–90, according to Finkler, no age was spared, but persons between
20 and 50 years of age were attacked by preference. No trade was a sure
protection. The course of the disease in general was favorable and also
quite rapid, unfavorable only in many children during the first few
years of life, in many old people, in many debilitated persons, and
especially in those suffering from chest affections.
An interesting table of this kind is given us by Leichtenstern. His
hospital material included 439 influenza patients, and these he
carefully grouped according to age.
Age. Influenza admissions, General average of
per cent. admissions, per cent.
Under 10 years 0.9 0.7
10–20 years 14.7 8.8
20–30 years 40.3 27.5
30–40 years 19.1 23.3
40–50 years 10.1 15.7
50–60 years 7.4 12.3
60–70 years 5.3 8.9
70–80 years 1.7 2.6
Above 80 years 0.4 0.2
Comby found that in Paris only the new-born were noticeably
insusceptible to influenza, that children up to 15 years were attacked
in the proportion of 40 per cent., and adults in the proportion of 60
per cent. Danchez believed that in families in which all the adults
became ill, the little children usually escaped.
Finkler states that in the schools at Bordeaux the older children were
first and most frequently attacked. Of the 248 male and female teachers
in 41 schools, 153 (61.7 per cent.) developed the disease. Children up
to five or six years of age at any rate seem to have been very little
affected, while older children were no less susceptible than adults.
Among 47,000 cases of influenza treated by physicians in Bavaria in
1889, the various ages were as follows:
1 year 1.5 per cent.
2–5 5.4 per cent.
6–10 6.6 per cent.
11–15 7.2 per cent.
16–20 11.4 per cent.
21–30 22.2 per cent.
31–40 19.3 per cent.
41–50 12.6 per cent.
51–60 7.7 per cent.
61–70 3.6 per cent.
71–80 2.0 per cent.
Above 80 0.5 per cent.
Leubuscher recorded that in Jena the proportion of cases in the
individual age classes did not correspond with the figures reported from
other localities. Children, and especially very young children, suffered
relatively less than adults.
The following statistics of the 1889–90 incidence of influenza among
school children in Cologne were collected by Lent:
Attendance. Ill of influenza.
Class I–13 to 14 years of age 3,002 1,015 33.8 per cent.
Class II–11 to 12 years of age 5,737 1,835 31.9 per cent.
Class III–10 years of age 3,701 1,130 30.5 per cent.
Class IV– 9 years of age 3,590 930 25.9 per cent.
Class V– 8 years of age 2,929 822 28.0 per cent.
Class VI– 7 years of age 3,388 758 22.3 per cent.
These may be compared with figures for the public schools in the suburbs
of Cologne:
Attendance. Ill of influenza.
Class I–13 to 14 years of age 1,609 689 42.9 per cent.
Class II–11 to 12 years of age 2,885 1,094 37.9 per cent.
Class III–10 years of age 1,683 626 37.1 per cent.
Class IV– 9 years of age 1,758 552 31.4 per cent.
Class V– 8 years of age 1,771 502 28.2 per cent.
Class VI– 7 years of age 1,938 510 26.3 per cent.
The increase of disease incidence with age is apparent. Finkler’s
explanation for the higher incidence among the children of the suburbs,
“that the children in the country had usually to walk a greater distance
to school” does not appear to be complete.
Comby found that out of 3,411 school children in Lausanne 1,840
contracted influenza. This shows a relatively high incidence in children
of school age in that city.
Concerning age distribution in 1889–90 Leichtenstern remarks that the
greatest morbidity incidence was in school children, adolescents and
young adults, especially the last. Nursing infants were attacked in
considerably less degree than any of these other ages. Also in the
higher ages those above sixty were attacked in lesser degree. The
greatest morbidity frequently was between the ages of twenty and forty.
Abbott concluded on the basis of estimates furnished him from various
institutions and individuals in the State that people of all ages were
attacked but the ratio of adults was greatest, of old people next, and
of children and infants least.
_Relationship of occupation to morbidity incidence._—Leichtenstern found
that the only apparent influence of occupation on the incidence of
influenza depended upon the liability to exposure in the various
occupations. He remarks particularly on the large incidence of influenza
among physicians. In contrast was the low incidence in lighthouse
keepers. In 1889–90 among 415 dwellers on 51 lightships and 20 isolated
lighthouses on the English coast only 8 persons developed influenza and
these in four localities, and in every instance there was traceable
direct communication from some other source. There is contradictory
evidence as to whether individuals working out of doors are more apt to
develop influenza. Certain statistics show that postmen and individuals
working on railroads were attacked more frequently and earlier than
others, while other statistics show that in railroads the office
personnel was attacked earlier than individuals on the trains and those
working on the tracks.
Abbott concluded that special occupations did not appear to have had a
marked effect in modifying the severity of the epidemic. At the Boston
Post Office in 1889–90, of the indoor employees, 475 in number, 25 per
cent. were attacked. Of the carriers, 450 in number, 11 per cent. were
affected with the disease. But there were other reports of the same
period which stated that the ratio of the persons employed at outdoor
occupations who were attacked was greater than that of indoor
occupation.
Finkler has discussed the influence of occupation at some length:
“When we compare the statistics of the last pandemic concerning the
influence of vocation, we see in the first place that those first and
chiefly were attacked whose occupation compelled them to remain in the
open air. This was shown especially by Neidhardt, who studied the
influenza epidemic in the Grand Duchy of Hesse. His conclusions,
however, were disputed by others. Thus, the prejudicial influence of
exposure to the open air was not supported by the statistics of railroad
employees in Saxony. Of those who were employed in the outdoor service,
32 per cent. became ill; of those employed in office work, on the other
hand, 40 per cent. The statistics of the local benefit societies in
Plauen show that the percentage of the sick among farm hands and
builders was not greater than that among the members of other benefit
societies who worked indoors. In Schwarzenberg the laborers in the
forest who were working in the open air all day were affected less than
others, and there was no sickness whatever in some forest districts.
Lancereaux, of Paris, states that most of the railroad employees who
suffered from influenza were those engaged in office work and not those
who worked in the open air. The preponderance of influenza patients
among the factory hands may be seen from a table prepared by Ripperger:
_A. In the open air._
Occupation. Per cent. attacked.
Workmen and laborers of Niederbayern 7
Railway officials in Amberg 9
Peasants in Niederbayern 11.7
Workmen in the Salzach-Correction 20
_B. In closed rooms._
Slag mills in St. Jugbert 15
Cotton mill in Bamberg 20
Cotton mill in Bayreuth 33
Sugar factory in Bayreuth 36
Aniline works in Ludwigshafen 38.8
Cotton mill in Zweibrücken 50
Tinware factory in Amberg 60
Factory in Schweinfurth 62
Gun factory in Amberg 70
Gold beaters in Stockach 80
“Many peculiar records of how individual classes of occupation have
fared are obviously to be explained by the fact that the infection
manifested its action in very different degrees. Thus, among the workmen
on the Baltic ship-canal only those became ill who lived in the town of
Rendsburg; those who had been housed in barracks outside of the city
were not affected. Of the 438 lead workers of Rockhope, which is
situated in a lonely valley in Durham, all remained perfectly free from
the disease during the three epidemics of 1889–92.
“Some occupations are said to afford protection against influenza. Thus
workmen in tanneries, chloride of lime, tar, cement, sulphuric acid,
glass, and coke works, are said to have escaped the disease with
extraordinary frequency.
“We shall be compelled perhaps to agree with Leichtenstern in his
conclusion that occupation and social position only in so far exert an
influence on the frequency of the disease as certain occupations in life
lead to more or less contact with travellers.
“Very remarkable is the proportionately small number of soldiers
affected, at least in the Prussian army, where, according to the
official record, the epidemic from its beginning to its end attacked
only 101.5 per thousand of the entire forces.”
Comparison of morbidity by occupation necessarily includes so many
variables and so many factors other than occupation that the results are
decidedly unsatisfactory. An example is found in Jordan, Reed and Fink’s
report of the incidence among troops in the Student Army Training Camps
in Chicago. They found a strikingly different attack rate in the various
groups studied. In the Chicago Telephone Exchange they ranged from 30 to
270 per 1,000, although the working conditions in the various exchanges
were not materially different. In the Student Army Training Corps at the
University of Chicago the lowest was 39 and the highest 398 per 1,000.
The higher rate group was particularly exposed to infection while the
lower, although composed of men of similar ages, living under similar
conditions, were guarded to a considerable extent against contact with
beginning cases.
Woolley has made an interesting observation on the effect of occupation:
“The disease was no respecter of persons except that it was more severe
in those who were hard workers. Those who tried to ‘buck the game’ and
‘stay with it’ showed the highest mortality rates. So, the
non-commissioned officers and the nurses suffered more severely than the
commissioned officers and privates.
“The annual morbidity rate per 1,000 was as follows:
For commissioned officers 261
Non-commissioned officers 208
Nurses 416
White enlisted men 568
Black enlisted men 1,130
“The annual mortality rate per 1,000 was:
For commissioned officers 69
Non-commissioned officers 83
Nurses 77
White enlisted men 145
Black enlisted men 253
“The case mortalities were:
Per cent.
For commissioned officers 26.8
Non-commissioned officers 40.0
Nurses 33.3
White enlisted men 26.0
Black enlisted men 22.5
“The above figures are for the period of five weeks from August 28th to
October 1st, 1918, and cover the most active portion of the epidemic,
but are obviously incomplete. They are given for purposes of
comparison.”
Woolley makes the observation that the organizations which spent most of
the time in the open and which were therefore most exposed to the
weather suffered least during the epidemic. This was particularly true
in the Remount Depot.
In our work we have attempted to classify our population according to
occupation along very broad lines.
“_Infant_” includes all individuals up to the age of two years. In these
the exposure is limited by the fact that they are either relatively
isolated at home, or when abroad, are still under relative isolation in
a perambulator or under the eye of a nurse. There is relatively little
commingling with the older age groups.
“_Child_,” refers to all children up to the age of school years. There
is relatively much greater commingling, particularly with other
individuals of the same age.
“_School_” refers to all children and adolescents who were reported as
attending school.
“_Home_” includes not only the housewife, the housekeeper, but also
servants and invalids; all who in their daily routine spend the greater
part of the time in the home.
“_Manual Indoors_” refers chiefly to laborers in factories and includes
all manufacturing occupations in which the work is of a manual character
no matter what the particular branch.
“_Manual Outdoors_” refers to such occupations as ditch diggers, street
cleaners, conductors and motormen, longshoremen, trucksters and
teamsters, telephone and telegraph linemen, etc.
“_Retail Sales Indoors_” refers to clerks in stores and all other
individuals who, working indoors, come into about the same degree of
contact with the public-at-large.
“_Retail Sales Outdoors_” includes sales agents, life insurance agents,
traveling salesman, pedlers, newsboys, etc.
“_Office_,” officials, secretaries, stenographers, telephone operators,
telegraph operators, etc.
We have observed that in 1918 infants presented the lowest incidence and
school children the highest. Occupations designated Home and Office were
surprisingly high. Children also showed a high incidence, one out of
every five developing the disease. The records show that manual labor,
both indoors and outdoors, was associated with a higher incidence than
less strenuous work, as retail sales, indoors and outdoors (Chart
XXIII).
The attack rates in most of the occupations are so nearly the same as to
lead to no certain conclusions. It would appear from our records that
individuals working out of doors were less frequently attacked than
those whose occupation kept them in doors. The groups at the two
extremes of incidence correspond to what we should expect when
considering opportunities for contract. The infant has least direct
contact. His contact is only with one or a few individuals, the mother
or the nurse. This group developed the disease in 5.8 per cent. The
school child not only has the same degree of contact as do adults, but
also in the tussle and scramble of play the contact becomes much closer.
The factor of age plays a large part in the occupational distribution
and the apparent occupational susceptibility is influenced by the age
susceptibility.
When we consider the occupational incidence in the various districts we
find that the only constant feature in the relatively small groups is
the low incidence among infants (Chart XXIV).
CHART XXIII.
[Illustration: Influenza 1918–19 Case rate per 100 persons by Occupation
Influenza 1918–19 Case Rate per 100 male persons by occupation
Influenza 1918–19 Case Rate per 100 female persons by occupation]
CHART XXIV.
[Illustration: District 1 Influenza 1918–19 Case Rate per 100 persons by
occupation
District 2 Influenza 1918–19 Case Rate per 100 persons by occupation
District 3 Influenza 1918–19 Case Rate per 100 persons by occupation]
[Illustration: District 4 Influenza 1918–19 Case Rate per 100 persons by
occupation
District 5 Influenza 1918–19 Case rate per 100 persons by occupation
District 6 Influenza 1918–19 Case rate per 100 persons by occupation]
CHART XXV.
[Illustration: Influenza 1920 Case rate per 100 persons by occupation
Influenza 1920 Case Rate per 100 male persons by occupation
Influenza 1920 Case Rate per 100 female persons by occupation]
CHART XXVI.
[Illustration: 1918 Incidence of Influenza in the Various Districts
surveyed
1920 Incidence of Influenza in the Various Districts surveyed
Individuals having Influenza in both Epidemics]
The first fact gained from a study of the 1920 occupational case rate is
that just as was the case in age incidence there is less variation
between the highest and the lowest than in 1918–19. While in the first
epidemic the highest occupational rate was five times the lowest, in the
second it was only twice the lowest (Chart XXV). But at the extremes of
the two charts we see some tendency to an inversion of the order. In
1918–19 those occupied in “retail sales” outdoors showed a low
incidence, while in 1920 they were the highest. So also, the incidence
in the school group changed from highest in 1918 to lowest in 1920. The
incidence in infants increased; that in the office workers decreased. No
general conclusions are warranted from these results.
In comparing the sex incidence by age groups we have found that females
as a rule showed a slightly greater incidence than males. That this is
not due fundamentally to occupational differences is suggested by a
comparison of the sex incidence in the two epidemics studied. In 1918
the distribution is practically the same in the two sexes in all
occupations except “Home,” “Manual Outdoors,” “Retail Sales Indoors,”
“Retail Sales Outdoors” (Chart XXVI). In the first the number of males
is so small and in the second and fourth the number of females is so
small that these cannot justly be compared. The group, “Retail Sales,”
consists in 1918–19 of 69 males and 27 females, out of a total
distribution in the population of 426 males and 107 females. This is the
only occupation that showed a definite higher incidence among the
females, and even here the number is too small for accuracy. In 1920
this difference has practically disappeared.
_Effect of race stock._—Leichtenstern remarks in his monograph that the
reported differences in influenza morbidity among different races, such
for instance as European and other nationalities, doubtless are due to
factors other than genetic racial differences, such as different modes
of living, commerce, etc. The work of the last two years calls for a
reconsideration of this idea.
Frost in his valuable work found that “in the seven localities with
considerable colored population the incidence rates among the colored
were uniformly lower than among the whites, the difference persisting
after adjustment of the rate to a uniform basis of sex and age
distribution. The extent of the difference varied, being relatively
great in Baltimore, Augusta and Louisville, and very small in Little
Rock. This relatively low incidence in the colored race is quite
contrary to what would have been expected a priori, in view of the fact
that the death rate from pneumonia and influenza is normally higher in
the colored than in the white, and that the colored population lived
generally under conditions presumably more favorable to the spread of
contact infection.”
Brewer, in his study of influenza in September, 1918, at Camp Humphreys,
finds that the colored troops showed a decidedly lower rate than the
white troops throughout the epidemic. He finds that the incidence among
colored troops was only 43 per cent. of that among whites. The
difference between colored and white organizations was probably not due
to difference in housing. Most of the colored troops were in tents and
the white troops were all in barracks. But the 42d Company composed of
negroes was housed in barracks under the same conditions as the white
troops of other organizations and they had next to the lowest incidence
of all organizations. Brewer concludes that the colored race when living
under good hygienic conditions is not as susceptible to influenza as the
white race under the same conditions. The age distribution was the same
in both groups.
Armstrong concluded from figures based on reported cases of influenza
that in the autumn of 1918 proportionately four times as much influenza
and pneumonia was reported among the Italians as was reported for the
rest of the Framingham community, made up largely of Irish or
Irish-American stock. On the contrary, an examination of a large
proportion of the population of that town showed a tuberculosis
incidence among the Italian race stock of .48, in contrast to an
incidence among the Irish of 4.85 per cent. and of 2.16 per cent. in the
entire population. Armstrong contrasts the relative insusceptibility of
Italian stock to tuberculosis, with the apparent marked susceptibility
to acute disease of the respiratory tract, such as influenza and
pneumonia; and the high susceptibility of the Irish to tuberculosis,
with their low susceptibility to acute respiratory infection.
With regard to our work it is sufficient to state that the lowest
incidence in both epidemics, as well as in recurrent cases, was in the
Irish tenement districts. Both the Jewish and the Italian tenement
districts were slightly higher in both epidemics (Charts XIX and XXI).
The age distribution of the entire population of each of these three
districts was about the same, so it does not appear that the slightly
lower incidence among the Irish is due to a variation in the age
distribution of the population.
The subject of race in relation to influenza will be discussed further
under mortality.
MORTALITY.
According to Marchese, in 1387 at Forli in Italy, not a person escaped
the disease, but only a few died. Gassar says that during the same
epidemic in Germany the patients suffered four, or at most five, days
with the most disagreeable catarrhal symptoms and delirium, but
recovered, and only very few were removed by death.
Pasquier remarks concerning an epidemic in 1411 that an infinitude of
individuals were attacked but that none died.
Concerning the epidemic of 1414 in France, Lobineau relates that the
disease was fatal only for the aged. Mezeray also speaks of the high
mortality of the old in this epidemic.
Regarding the pandemic of 1510, Thomas Short remarks that none died
except some children. Mezeray, on the other hand, says that the disease
had claimed many victims.
Pasquier and Valleriola both write of the epidemic of 1557, in France,
as being distinctly mild in character. Children only who could not
freely cough out the phlegm died. Coyttar speaks of the absence of death
except in tuberculous patients.
In the pandemic of 1580 individual observers report enormous death
rates. Thus, according to Schenkius, the disease killed 9,000 persons in
Rome, while Madrid, Barcelona and other Spanish cities were said to have
been nearly depopulated by the disease. This high mortality was,
however, even at that time attributed by some physicians to the
injudicious employment of venesection. Throughout the more recent
history of pandemic influenza opinion seems to have been nearly
unanimous that blood letting has had very bad results in the outcome of
influenza cases. Remarks to this effect have been made by the
contemporaries of nearly every epidemic since 1580.
According to Rayger and others during the epidemic of 1675, nobody died
of the disease itself with the exception of debilitated persons,
although it spared neither the weak nor the strong.
Concerning the epidemic of 1688, Thomas Short writes for England that
though not one of fifteen escaped it, yet not one of a thousand that had
it died.
In 1712, Slevogt writes that in Germany “Fear soon vanished when it was
seen that although it had spread all over the city, it left the sick
with equal rapidity.”
Finkler remarks, concerning 1729–30, that, “The great mortality which
attended the epidemic in England and Italy seems somewhat remarkable.
Thus Hahn states that in London in the month of September one thousand
persons died each week, and in Mayence forty persons daily. Most likely,
however, other diseases which were present at the same time added their
quota to the mortality, especially as the disease in other places, for
example in Germany, ran a benign course.”
Perkins, Huxham, Pelargus, Carl and others, concerning the epidemic of
1732–33, all testify that the disease was of very low fatality.
In 1742 the epidemic was evidenced by an enormous morbidity but the
disease was not dangerous as a general rule although Huxham occasionally
speaks of the virulent character of the disease in England, and Cohansen
says that in January, 1743, over 8,000 persons died from influenza in
Rome and 5,000 in Mayence.
We have the testimony of Robert Whytt, for 1758, and that of Razoux and
Saillant and Ehrman for 1762, as to the low mortality of the epidemic
for those years.
According to Heberden the same was true for 1775, while Webster tells us
for 1780 that the disease was not dangerous but its effects were seen
the following year in the increased number of cases of phthisis.
Finkler remarks concerning the epidemic of 1802, “The mortality in this
epidemic was small, only the abuse of venesection brought many to the
grave. Thus, so many farmers are said to have died in Russia from it
that venesection was forbidden by an imperial ukase. Jonas says that
many patients were bled either on the advice of a simple village barber
or by their own wish, and most of them died. In Prussia also bleeding
was declared detrimental by the Government.”
He continues regarding 1836–37, that, “In London there died, during the
week ending January 24, 1837, a total of 871 persons, and among these
deaths there were 295 from disease of the respiratory organs; during the
week ending January 31st, out of a total of 860 deaths there were 309
from diseases of the respiratory organs.”
Watson, in describing the epidemic of 1847, discusses the mortality:
“The absolute mortality has been enormous; yet the relative mortality
has been small. You will hear people comparing the ravages of the
influenza with those of the cholera, and inferring that the latter is
the less dangerous complaint of the two; but this is plainly a great
misapprehension. Less dangerous to the community at large (in this
country at least) it certainly has been; but infinitely more dangerous
to the individuals attacked by it. More persons have died of the
influenza in the present year than died of the cholera when it raged in
1832; but then a vastly greater number have been affected with the one
disease than with the other. I suppose that nearly one-half of those who
were seized with the cholera perished; while but a very small fraction,
indeed, not more probably than two per cent. of those who suffered
influenza have sunk under it.”
Leichtenstern remarks on the very low mortality of 1889–90. In Munich
0.6 per cent. died; in Rostock 0.8 per cent.; in Leipzig 0.5 per cent.;
in fifteen Swiss cities 0.1 per cent.; in Karlsruhe 0.075 per cent.; in
Mecklenburg-Schwerin 1.2 per cent. This does not, however, include the
numerous deaths from complications, as from pneumonia, and does not
express the true mortality.
Newsholme gives the following table for mortality from influenza,
bronchitis and pneumonia, in England and Wales during the epidemic years
and the years immediately preceding them. The figures express annual
death rate per million of population. The highest rate was reached in
1891. The table does not include deaths registered as from other
diseases, but due directly or indirectly to influenza. Respiratory
diseases in general show a greatly increased death rate in years in
which influenza is epidemic. Such is also true to some extent with
diseases of the nervous and the circulatory systems.
═══════════╤═════════════════════════════╤═════════════════════════════
Death rate │ │
per million│ │
of │ Non-epidemic years. │ Epidemic years.
population │ │
from │ │
───────────┼─────────┬─────────┬─────────┼─────────┬─────────┬─────────
„ │ 1887│ 1888│ 1889│ 1890│ 1891│ 1892
───────────┼─────────┼─────────┼─────────┼─────────┼─────────┼─────────
Influenza │ 3│ 3│ 2│ 157│ 574│ 533
Bronchitis │ 2,117│ 2,041│ 1,957│ 2,333│ 2,593│ 2,266
Pneumonia │ 1,113│ 1,093│ 1,022│ 1,404│ 1,471│ 1,250
───────────┴─────────┴─────────┴─────────┴─────────┴─────────┴─────────
In a report by the United States Public Health Service early in 1919 the
death rates from all causes in twelve large cities of this country were
compared for 1889–90 and for 1918–19. It was found that while
considerable irregularity in the curves was evident, the curves of the
two epidemics manifested on the whole quite a striking similarity for
the same cities considered individually and for the group as a whole.
The death rate rose to a much higher point during the autumn wave of the
1918 epidemic than in the epidemic of 1889–90 in nine out of the twelve
cities. During both epidemics the rate was relatively low in St. Louis,
Milwaukee and Minneapolis. The mortality in all of these cities was 26.7
in 1889, as against 35.2 for 1918. In the peak week the rate rose to
55.6 in 1918 as against 35.4 in 1889.
The influenza deaths in Massachusetts in the year 1890 during a period
of fifty days were estimated by Abbott to have been 2,500. In 1918
Jordan estimates the mortality for the same state to have been six times
as great. The population of the state had not doubled in the interval.
The highest mortality from influenza in Massachusetts during the 1889–93
epidemic occurred in January, 1892, during which month the total deaths
amounted to 6,309 which was greater by 2,246 than the mean monthly
mortality of the year, and greater by more than 1,000 than the mortality
of any month in the ten year period 1883–92.
A comprehensive comparison of the damage done by influenza in 1918 with
the deaths from other plagues has been made by Vaughan and Palmer.
“The pandemic of 1918, when compared with that of 1889–90 is estimated
to have caused _six times as many deaths_.
“During the four autumn months of 1918, 338,343 cases of influenza were
reported to the Surgeon General. This means that in the camps of this
country _one out of every four men had influenza_.
“The combination between influenza and pneumonia during the fall of 1918
seems to have been closer and more destructive than in any previous
pandemic. During the autumn season there were reported to the Surgeon
General 61,691 cases of pneumonia. This means that _one out of every
twenty-four men encamped in this country had pneumonia_.
“During the same period 22,186 men were reported to have died from the
combined effects of influenza and pneumonia. This means that among the
troops in this country _one out of every sixty-seven died_.
“This fatality has been unparallelled in recent times. The influenza
epidemic of 1918 ranks well up with the epidemics famous in history.
Epidemiologists have regarded the dissemination of cholera from the
Broad Street Well in London as a catastrophe. The typhoid epidemic of
Plymouth, Pa., of 1885, is another illustration of the damage that can
be done by epidemic disease once let loose. Yet the accompanying table
shows that the fatality from influenza and pneumonia at Camp Sherman was
greater than either of these. Compared with epidemics for which we have
fairly accurate statistics the death rate at Camp Sherman in the fall of
1918 is surpassed only by that of plague in London in 1665 and that of
yellow fever in Philadelphia in 1793.
“The plague killed 14 per cent. of London’s population in seven months’
time. Yellow fever destroyed 10 per cent. of the population of
Philadelphia in four months. In seven weeks influenza and pneumonia
killed 3.1 per cent. of the strength at Camp Sherman. If we consider the
time factor, these three instances are not unlike in their lethality.
The plague killed 2 per cent. of the population in a month, yellow fever
2.5 per cent. and influenza and pneumonia 1.9 per cent.
“In four months typhoid fever killed 1.5 per cent. of the soldiers
encamped in this country during the war with Spain. Influenza and
pneumonia killed 1.4 per cent. of the soldiers in our camps in 1918 and
it also covered a period of four months.”
The Bureau of the Census has made the following report concerning
influenza deaths in the United States:
“In forty-six American cities, having a combined population of only a
little more than one-fifth the total for the country, the mortality
resulting from the influenza epidemic during the nine weeks period ended
November 9th was nearly double that in the A. E. F. from the time the
first contingent landed in France until the cessation of hostilities.”
The mortality, even as the morbidity, has varied in different localities
and at different periods. The low morbidity and mortality in the spring
of 1918 has been frequently mentioned. Among the Esquimaux in Alaska the
death toll was terrific. Whole villages of Esquimaux lost their entire
adult population. It has been estimated that in British India the death
roll totalled 5,000,000. “The central, northern and western portions of
India were the worst sufferers. The hospitals in the Punjab were choked
so that it was impossible to move the dead quickly enough to make room
for the dying. The streets and lanes of the cities were littered with
dead and dying people. The postal and telegraph services were completely
disorganized; the train service continued, but at all principal stations
dead and dying people were being removed from the trains. The burning
ghats and burial grounds were literally swamped with corpses, while an
even greater number awaited removal. The depleted medical service,
itself sorely stricken by the epidemic, was incapable of dealing with
more than a minute fraction of the sickness requiring attention. Nearly
every household was lamenting death, and everywhere terror and confusion
reigned. No part of the Punjab escaped.”
The Bureau of the Census estimates that 445,000 deaths from the epidemic
of influenza occurred in the United States in the period between
September 1st and December 31st, 1918. There is no doubt but that the
total death toll for that epidemic exceeded 500,000 individuals.
According to Winslow and Rogers, the two highest annual death rates on
record in Connecticut are both rates of 19.4 per 1,000 and these two
rates are for the influenza epidemic years of 1892 and 1918. In the
earlier of these two the normal general death rate was several points
higher than it is today, so that the effect of the recent epidemic was
much more serious than was that of its predecessor. For a single month
the death toll of October, 1918, was absolutely unprecedented in
Connecticut. They estimate that the epidemic between September, 1918,
and January, 1919, cost the State 5.5 lives per 1,000 population, or, in
all, 7,700 lives.
In the United States Army there was a total of 688,869 admissions for
influenza. The total deaths ascribed to the disease are 39,731, which
gives a rate of 15.64 per 1,000 for the acute respiratory diseases out
of the total disease death rate of 18.81 for the year. In 1915 the per
cent. of deaths from this group of infections was under 18 per cent. of
the total from all diseases. During the last four months of 1918, 11,670
deaths from influenza and pneumonia occurred in the American
Expeditionary Forces in France. There were approximately 1,600,000
officers and men in the United States and an equal number in France.
Carnwath gives the following comparison of the number of deaths in
London and in certain American cities from influenza and all forms of
pneumonia during the eight weeks of the 1918–19 epidemic.
_Deaths in London and in American cities._
Number of deaths. Rate eight weeks per 100,000
of population.
London 13,744 341
New York 20,681 360
Chicago 8,785 343
Philadelphia 12,806 749
Boston 4,211 548
The cause of death in the vast majority of cases is some form of
pneumonia. In fact it has been questioned whether influenza
uncomplicated can cause a fatal issue. Postinfluenzal meningitis has
been the cause of death in an appreciable number of cases. More remotely
the disease has caused many deaths by hastening the fatal outcome of
what were otherwise subacute or chronic conditions of the respiratory,
cardiovascular, or renal systems.
Vaughan and Palmer record that, “The pandemic of influenza in 1918 seems
to have been more closely associated with the pneumonias than appears in
any previous pandemic. From the reports as sent to the Surgeon General’s
Office, it appears that uncomplicated influenza was not by any means a
fatal disease and that the high death rate was due to the pneumonias
which followed. Pneumonia is a serious disease at all times. Recent
records for the United States Army show that the case mortality rate for
this disease has been as follows during the different periods of the
last two years:
Per cent.
The year 1917 11.2
6 winter months, 1917–18 23.1
5 summer months, 1918 18.8
4 autumn months, 1918 (Influenza period) 34.4
“It is not strange that once pneumonia has secured a foothold in
patients already weakened by influenza their chances of recovery were
lessened.”
Woolley reports that for the troops stationed at Camp Devens, Mass.
there were no fatalities from uncomplicated influenza. In every fatal
case but two a diagnosis of pneumonia was made, and in these two cases
pure cultures of pneumococcus were obtained from the blood after death,
so it appears that they were cases of pneumococcus septicemia. Up to
October 29, 1918, 19 per cent. of the total number of influenza cases
reported developed pneumonia and of these there was a case mortality of
27.9 per cent. The mortality rate among the influenza cases was 5.4 per
cent.
At Camp Humphreys, Virginia, 16 per cent. of the camp was attacked by
the disease; 28 per cent. of influenza cases had pneumonia; 10 per cent.
of influenza cases died; and 35 per cent. of pneumonia cases died. One
and six tenths per cent. of the population of the camp died from
influenza. The camp had an average strength of 26,600 individuals.
Fifty-two per cent. of the entire number of cases occurred during the
peak week which ended October 4th.
Between September 21st and October 18th, 1918, 9,037 patients were
admitted to the Base Hospital at Camp Grant. This represented about
one-fourth of the strength of the camp. Of these 26 per cent. developed
pneumonia and 43 per cent. of the pneumonia cases died. Death occurred
to about 11 per cent. of the total admissions.
The death rate at Camps Devens, Sherman and Grant were among the highest
of all of the camps in this country. The annual death rate from all
causes per 1,000 for the four last months of 1918 were 132 for Camp
Cody, 123 for Syracuse, 116 for Camp Sherman, 102 for Camp Beauregard,
97.3 for Camp Grant, 75.0 for Camp Dix, 67.0 for Camp Devens. These
seven camps stood out high above the majority. By far the majority, 28
camps, had an annual rate between 61.9 and 25.5 per 1,000. Only four
camps recorded lower rates than the latter figure.
The Municipal Statistics of Paris showed that during the first half of
October, 1918, the average weekly mortality was from two to three times
that of nonepidemic years. The returns for the Departments of France
also showed a mortality three times above the average for previous
years, though not uniformly so. In the Departments the mortality from
influenza did not exceed 10 per cent. and in many cases it was below 5
per cent. On the other hand cases admitted to hospital, which consisted
of the worst forms of the disease, showed a mortality varying between 12
and 30 per cent. Returns received from Italy were similar. The disease
in that country was especially severe in the northern part and in the
provinces bordering on Switzerland. Marcus, of Stockholm, reported in
September, 1918, that the epidemic in Sweden was running a very severe
course, more than 1,000 deaths having occurred up to the time of his
report. According to Weber, 2,770 deaths occurred in Berlin during
October, 1918, from influenza and pneumonia alone. In Vienna there died
from influenza between September 1st and October 19th, 1918, 3,125
persons. The deaths in Vienna from influenza and pneumonia normally
total 40 to 50 per week. At the highest point of the epidemic this
number had increased to 1,468. Böhm estimates the total influenza
incidence in Vienna as 180,000 cases, with a probable mortality around
1.7 per cent. Dunlop estimates that the total number of influenza deaths
in Scotland in the winter of 1918–19 may be assessed at 20,000.
A. Giltay has compared the epidemics of 1890 and 1900 with that of 1918
as regards mortality, in Amsterdam. He has studied figures for seven
consecutive weeks in each of the three periods under observation and
found that the maximum figures for mortality were 61.5 in 1890, 41.2 in
1900, and 52.7 in 1918, but if these figures are compared with the
average mortality for the year it is found that the increase of
mortality as the result of influenza alone is 39.3 for 1890, 24.5 for
1900, and 40.3 for 1918. Thus the present epidemic is more severe than
that of 1890.
Many reported mortality figures are without value because they are
either death rates in selected groups such as those in a hospital, or,
because the report does not state the status of the individual. Thus,
Hoppe-Seyler stated at a meeting of the Kiel Medical Society that of 577
cases treated in the Municipal Hospital, nearly all of which were
severe, 28.9 per cent. died. This was reduced to 18 per cent. after
deducting the cases admitted in a moribund condition. Again, Rondopoulos
reports that the October wave in Greece resulted in a mortality of from
15 to 24 per cent, in different localities.
Just as current vital statistics are of little value in determining the
morbidity rate, so also they cannot be relied upon in obtaining fatality
percentages. In organizations such as the Army, where all cases are
reported, we may get some idea of the fatality rate. The deaths in the
United States Army have already been discussed. Marcus, of Stockholm,
reports that the military records showed that there had been 34,000
cases in the Swedish Army, with 444 deaths, making a mortality of 1.3
per cent, in that Army.
House surveys also give a fair idea of the mortality. Winslow and Rogers
conclude that the fatality rate was as a rule somewhere between two and
four deaths per 100 cases, the lower being more likely to be correct.
Reeks found in his house census that there had been 3.9 deaths per 100
cases in the autumn of 1918. Carnwath reports that Dr. Niven, in his
census, discovered that out of 1,108 cases in the spring and autumn of
1918 there were but 15 deaths, which would give a fatality rate of 1.3
per 100 cases.
Frost has found from his large survey that the ratio of deaths to total
cases of influenza varied in the localities surveyed from 3.1 per cent.
in New London as a high point to 2.8 per cent. in San Antonio, Texas.
There was some apparent relationship between fatality rate and
geographic distribution, the higher rates being in San Francisco on the
Pacific Coast, and in the localities studied on the north half of the
Atlantic Seaboard, and the lower rates being in the central and southern
states. The fatality rate on the Pacific Coast was 2.33, on the Atlantic
Seaboard 2.05, and in the last district 1.08 per cent.
Our own figures correspond very closely with those of Frost. Among the
10,000 living individuals surveyed in 1920 there were 1,970 cases of
influenza in 1918. Add to this the 50 deaths for 1918, which were not
included in the 10,000 living individuals, which makes a total incidence
of 2,021. This case fatality rate of 2.47 per 100, corresponds closely
to Frost’s rate for the North Atlantic Seaboard.
The relative mildness of the 1920 recurrence is indicated in the lower
case fatality rate. Fourteen out of 955 cases died, giving a rate of
1.47 per 100 cases.
_Mortality by sex._—There is not a uniformity of opinion as to which
sex suffered the higher fatality rate during the 1918–19 spread.
Winslow and Rogers found for Connecticut a distinctly heavier
mortality among males for the last four months of 1918, 58 per cent.
of the influenza-pneumonia deaths being among this sex. They believe
that this is probably due to a greater exposure to the original
infection.
Fränkel and Dublin point out that in a study of 70,729 policy holders of
the Industrial Department of the Metropolitan Life Insurance Company in
the period from October 1, 1918, to June, 1919, the death rates for
males and females were practically the same for both white and colored
individuals.
The excess of males over females among the whites is only three per
cent., and there was no excess among colored. In contrast, the
respiratory diseases, including influenza-pneumonia, under normal
conditions, show a higher mortality incidence among males than among
females. In the seven year period from 1911 to 1917 the mortality rate
showed an excess of 18 per cent. males over females, among whites, and
of 30 per cent. among colored. This would seem to indicate that the
effect of the epidemic was not much, if any, greater on males than on
females, and suggests that the excess mortality caused by the epidemic
did not operate on the sexes as the normal mortality from
influenza-pneumonia had in previous years.
Dunlop finds that in a study of 10,797 deaths registered in Scotland up
until the end of December, 1918, 52.44 per cent. were females and 47.56
were males. These were for deaths reported as due only to influenza.
Apert and Flipo found a decided predominance among the female deaths in
Paris. In both of these observations the absence from the civilian
population of male inhabitants of military age obscured correct
comparative statistics.
Once again, Frost gives the most comprehensive discussion of the
subject. He found, as we have stated, that the influenza case incidence
in persons over fifteen years of age was higher in females than in
males, and that in persons under fifteen the relative incidence as
between males and females is variable, but with very slight excess in
males for the localities studied, combined. On the other hand, the case
fatality, the per cent. of influenza cases dying, under fifteen years of
age, was higher in females than in males. Over sixty years of age it was
considerably higher among the females, but between the ages of fifteen
and sixty the general tendency was to a much higher case fatality among
the males. The difference was greatest between the ages of 20 and 40.
The case fatality between the ages of 15 and 45 in the group of southern
and central states was in decided contrast to that in the Northern
Atlantic and Pacific groups, the case fatality in the former being
remarkably low in both sections and slightly higher in females than in
males. He suggests that in the south and middle west where the epidemic
was generally milder in respect to mortality than in the northeast and
far west, the essential difference was not in case incidence, but in
case fatality, especially in persons from 15 to 45 years of age, and in
the relatively low case fatality among young male adults. Frost makes
the important point that the relative mortality is determined more
accurately by case fatality than by case incidence, and that without a
full and exact knowledge of the variations in case fatality, statistics
of mortality are by no means translatable to terms of relative
morbidity. The fact that certain cities showed, as described by Pearl,
relatively high mortality rates, does not give conclusive evidence that
the morbidity was higher in these cities than elsewhere. The lower
influenza case fatality in females from 15 to 60 years of age appears to
be accounted for in part at least: first, by a decreased incidence of
pneumonia as compared with the males; and, second, by a lower fatality
in those cases which did develop pneumonia.
The relatively small number of fatalities in our own records do not
warrant a classification by age groups. We found that for all ages in
1918 7.9 per cent. of females developed pneumonia as contrasted with 6.8
per cent. males. This does not include those who died. In 1920, 1.87 per
cent. of the male cases died, while only 0.37 per cent. of the females
died. Five and fifteen-hundredths per cent. of all male cases developed
pneumonia and recovered, and 3.56 of the females did likewise. In 1920 a
higher proportion of males than females developed pneumonia, and
likewise a higher proportion died.
_Relationship of age._—Leichtenstern has summarized the results for the
epidemic of thirty years ago, in saying that the death rate for children
under one year was little disturbed by the influenza epidemic; that
there was very little increase in mortality in the other ages of
childhood; that the higher age periods showed the greatest relative
mortality for the disease. On the contrary, the records for England and
for Switzerland showed during those periods a higher death rate in
children up to five years of age.
Percentages.
Ages. 1847–8 1890
1–5 10.5 5.2
5–20 13.1 4.3
20–40 3.8 4.7
40–60 18.5 36.2
60–80 16.9 22.4
Above 80 8.6 2.5
Giltay has compared the age mortality in Amsterdam in 1890, 1900 and
1918 as shown in the following table:
═══════╤═══════╤═══════╤═══════╤═══════╤═══════╤═══════╤═══════╤═══════
│ Under │ │ │ │ │ │ │
│ one │ 1–4 │ 5–13 │ 14–19 │ 20–49 │ 50–64 │Over 64│Total.
│ year. │ │ │ │ │ │ │
───────┼───────┼───────┼───────┼───────┼───────┼───────┼───────┼───────
1890│ 8.4│ 8.1│ 2.3│ 3.0│ 30.7│ 19.3│ 28.1│ 100
1900│ 9.7│ 8.8│ 1.6│ 3.2│ 17.6│ 18.3│ 40.8│ 100
1918│ 3.0│ 13.0│ 8.7│ 8.3│ 51.9│ 8.7│ 6.4│ 100
───────┴───────┴───────┴───────┴───────┴───────┴───────┴───────┴───────
Evans has studied the records for the city of Chicago in the epidemic of
the year 1890, and found that the number of deaths was highest among
persons from 20 to 40 years of age. The greater increase above the
expected was in deaths of persons over 60 years of age. Children of
school age seemed to enjoy some relative immunity, as shown in the
mortality reports.
This latter age grouping for 30 years ago corresponds with those of
1918. Frost found that the death rate per 1,000 was notably high in
children under one year of age, in adults from 20 to 40, and in persons
over 60. The case fatality from pneumonia in his series tended to be
fairly constant, around 30 per cent., except in San Antonio, Texas,
where it was only 18.5 per cent. Case fatality was also higher in the
following age groups: Under one year, 20 to 40, and over sixty.
This age distribution was probably the same in all countries. Filtzos,
describing the epidemic in Greece, said that the ages that suffered most
and had the most fatal cases were between 20 and 45. In Spain in May and
June of 1918 the mortality was much lower among children and the aged
than it was among the adults, especially between 20 and 39 years of age.
The disease appeared fatal almost exclusively in these ages. In Vienna,
29.5 per cent. of all the fatal cases were between the ages of 20 and
30. Hoppe-Seyler stated that the ages of most of the cases were between
20 and 40 and the majority between 30 and 40, but that the mortality was
highest among the older patients.
Dunlop found that in Scotland the most frequent ages at death were
between 25 and 35, 25.28 per cent. of the total being between these two
ages. 53.85 per cent. of the total deaths were between 15 and 45 years.
The highest age group death rates occurred in age groups 75 and over,
and 25 to 35, the former being 7.87 per 1,000, and the latter 7.12. High
rates also occurred in age groups under one, and 65 to 75, the former
being 6.49, and the latter 5.33. The lowest age group death rates were
found in the groups which included children of school age, 5 to 15,
being 2.20 per cent., and the age group 10 to 15, being 1.80 per cent.
Dunlop has apparently only included those cases in which influenza was
diagnosed as the cause of death, and has omitted all in which the
diagnosis was bronchitis or pneumonia.
The Bureau of the Census has issued a report based on the mortality in
Indiana, Kansas and Philadelphia, for the period September 1st to
December 31st, 1918. It shows that the highest rate occurred in the age
period from 30 to 34 years, with the period from 25 to 29 second. Of all
the deaths tabulated more than half occurred between the period of 20 to
40, although this age group represents only 33 per cent. of the total
population concerned.
Age mortality has been studied thoroughly by Winslow and Rogers in
Connecticut:
“The four last months of 1917 show a normal age distribution with one
quarter of all deaths occurring under five years of age, one quarter
between 5 and 40 years, and one-half over 40 years, the proportion of
the infant deaths decreasing and the proportion of deaths in old age
increasing as one passes from the season of intestinal disturbances to
the season of respiratory diseases. In 1918 the distribution of deaths
from all causes is strikingly different. Instead of less than a quarter
of all deaths occurring between the ages of 5 and 40 years, this period
included 49 per cent. of all deaths in 1918; and the two decades between
20 and 40 included 40 per cent. of all deaths (as against only 14 per
cent. in 1917).
“Considering influenza and pneumonia alone, these two decades included
56 per cent. of the deaths, while only nine per cent. occurred at ages
over 49. The decade between 20 and 29 was most severely affected,
including 30 per cent. of all deaths, while the decade between 30 and 39
was a close second with 26 per cent. An even higher incidence occurred
at ages under five years, as has been brought out in other
investigations, since this age period contributed 16 per cent. of all
the influenza-pneumonia deaths. The proportion of deaths from all causes
in infancy did not rise even to normal, but with the enormous rise in
total deaths the maintenance of a nearly normal ratio, of course, means
a heavy influenza mortality.”
Jordan observes in his analysis a low pneumonia incidence among the
pupils of elementary and high schools. There were no deaths in 188
cases.
Wollstein and Goldbloom report that in a series of 36 children with
influenza and bronchopneumonia at the Babies Hospital in the City of New
York, 66.6 per cent. died. Achard and his co-workers review a similar
series of 32 infants in Paris with influenza. Eight of the 32 died. In
both of these studies we are dealing with selected groups of hospital
cases and the mortality rates are of little value for this type of
study.
Fränkel and Dublin in a study of 70,729 deaths from influenza-pneumonia
among the policyholders of the Industrial Department of the Metropolitan
Life Insurance Company, find that during the normal period between 1911
and 1917, influenza-pneumonia attacked primarily the first age period of
life, ages one to four years, and the period of late middle life and old
age. The rates are normally minimal between 5 and 30 years. In the last
quarter of 1918, on the other hand, the highest rate among the whites is
in the period of early adult life, between the ages of 25 and 34. There
appear three modal points instead of the two at the extremes. They find
that the excess over normal was most marked in infancy and early
childhood, and particularly in early adult life, culminating between the
ages of 25 and 34. The period of old age shows no significant _excess_
during the period of the epidemic.
If the deaths among the white males of the age period of active adult
life had continued throughout the whole year as they did during the last
quarter of 1918, approximately four per cent. of the population of that
age would have died.
Fränkel and Dublin are of the opinion that this change in the age
incidence of influenza mortality between epidemic and endemic periods
suggests strongly that the two diseases are different; that endemic
influenza is not the same disease as epidemic influenza. Or perhaps they
should say more correctly that the diseases occurring in interepidemic
times which are reported to them as deaths due to influenza-pneumonia
are not the same as the epidemic influenza. They draw similar
conclusions from the different manner in which the white and black races
are affected during the interepidemic and epidemic periods, from
so-called influenza-pneumonia. We have seen from Frost’s results that it
is hazardous to compare mortality rates of different localities and
different times with the idea of comparing the disease, influenza,
itself.
The ages showing highest mortality in the autumn of 1918 appear to have
been essentially the same as those which predominated thirty years ago.
There appears to be nothing in the age distribution that could be
explained by an immunity persisting over from the epidemic of 1889–93.
The age group 30 to 40 has almost universally a higher mortality than
the groups below 20, which would by this theory be non-immune and would
be expected to have a higher rate. The drop in rate is nearer the age
group of 40 than 30. The presence of smaller or larger influenza
epidemics in the course of the thirty years would further complicate
such an hypothesis.
_Relationship to occupation._—Dublin found in a study of 4,700 miners
that the death rate was unusually high from influenza in these
individuals for the last quarter of 1918. In fact in the age period 45
to 65 the rate among bituminous coal miners is close to four times as
high as among all occupied males. The annual death rate per thousand for
all ages among the former is 50.1; among all industrial white males,
22.3. The increase is apparent in all age groups from 15 to 65
inclusive. These results are based on the records of the Metropolitan
Life Insurance Company.
_Density of population._ _Rural and urban environment._—There have been
few reports which have like the above described clearly variations due
apparently only to occupational differences. Some attention has been
paid to a comparison of the rural incidence with that in large cities.
Although other factors play a part here, we may consider this under the
general subject of occupation. Statistics for the fall of 1918 from the
Netherlands show that with the exception of men over 80 years of age the
mortality was remarkably increased for both sexes in communities of less
than 20,000 inhabitants.
Winslow and Rogers have studied the variations in the urban and rural
incidence and find that in Connecticut with the single exception of
Tolland County, in which the small towns were severely hit, the rates
were in every case _higher_ in the large communities. In New Haven
County, for instance, among nine towns which were purely agricultural,
the combined death rate from influenza and pneumonia for the three
months of September to November, inclusive, was 9.2 on an annual basis.
For six towns in the same county in which there were manufacturing
plants the corresponding rate was 15.6. In Litchfield County the twelve
purely agricultural towns had a combined rate of 6.5, whereas among
eleven partly manufacturing towns the rate was 18.3. This was true for
other counties. The figures quoted are for influenza-pneumonia rates
only up to December 1st, but study of the records during the early
months of 1919 did not show any change in the figures. The rates for the
entire state for January, 1919, was 19.8, and that for the towns under
5,000, only 17.5.
These observations differ somewhat from those reported by Pearl, who
studied 39 large cities of the United States in an attempt to find a
correlation between the explosiveness of the influenza outbreak and the
density of population. He concluded that there was no such correlation.
Pearl, however, was dealing with cities which were all sufficiently
large to offer practically complete opportunities for contact infection,
and the two reports, therefore, cannot be justly compared. Winslow and
Rogers suggest as possible causes for lessened incidence in rural
communities either diminished opportunities for contact infection or
differences in age distribution and racial composition of the different
populations.
Let us consider in greater detail the fate of both rural and urban
individuals who had been recently drafted into the military forces of
this country. Almost universally the raw recruit was found more
susceptible to disease than was the seasoned soldier. A report by
Lieutenant W. D. Wallis from Camp Lee “shows that while those who had
been in the service less than one month constituted only 9.19 per cent.
of the total strength, they furnished 30.11 per cent. of the total
deaths from influenza and consequent pneumonia. Furthermore, it is shown
that while those who had been in the service from one to three months
constituted 45.18 per cent. of the camp, they furnished 46.24 per cent.
of deaths. On the other hand, those who had been in the service more
than three months constituted 46.63 per cent. of the population and
furnished only 23.69 per cent. of deaths.
Lieutenant Wallis says: “These figures show a much greater percentage of
deaths for the first month in camp than the corresponding proportion of
the population would warrant; while in the period of three months or
more of service the percentage is less than half of that of the camp
population having this length of service. The only approach to a
correspondence is in the period from one to three months where the
respective percentages differ but little. The increase in length of
service is accompanied by a progressive decrease in the percentage of
deaths from 30.11 per cent. to 27.41 per cent. to 18.87 per cent.,
although only 9.19 per cent. of the population in the camp falls within
the class of less than one month’s service.
“The incidence of mortality is in the first month’s service more than
three-fold the percentage of the number of men; and in the period of
three months or more of service is scarcely more than half of the
percentage of the number of men of the camp in that group.
“The fact that the case mortality is higher among those who came from
rural homes than among those who came from cities seems to hold even
after three month’s of service, or more.”
Vaughan and Palmer found that the case fatality at Camp Dix among those
who came from cities with a population of 10,000 or more was 10.8; while
among those who came from more rural homes the rate was 15.8, although
the average service of both groups was the same.
The Camp Surgeon of Camp Grant concluded from his records that the new
recruit is more susceptible to influenza and is more apt to succumb than
is the man who has been trained and is accustomed to Army life.
Wooley reports data collected from four Infantry organizations at Camp
Devens comprising 15,502 men. Of 9,559 men who had been in camp less
than five months, 3,575 or 37.5 per cent. developed influenza, whereas
of 5,943 men who had seen more than five months service in the army,
1,033 or 17.5 per cent. developed the disease. He concludes that the
large number of recruits in the camp certainly was a factor in
increasing the disease incidence. It should be remarked that Camp Devens
appears not to have had any influenza epidemic in the spring of 1918.
It is to be regretted that we have not several reports dealing with the
same subject from camps where the disease was definitely recognized in
the spring. Fortunately we have one such. Opie and his co-workers have
observed that the epidemic at Camp Funston, which occurred between March
4th and March 29th, 1918, and which attacked 1,127 out of a total of
29,000 men, involved chiefly the organizations which had been at Camp
Funston during six months or more. At that time it seems to have
infected all susceptible individuals, and to have spent itself.
Subsequent waves of influenza, four in number, and coming at a little
less than one month intervals, occurred when newly drafted men were
brought into the camp in April and May. In these latter cases the
disease affected the men newly arrived in camp.
At Camp Funston, at least, the higher incidence in the raw recruit
appears to be explained in part by a relative immunity of those who had
been in camp a month or more, existing as a result of an earlier
prevalence of the disease. More abundant evidence would, however, be
necessary before we could deny a diminution of natural immunity in the
recruits, caused by the exposure, overwork, fatigue, and change of daily
routine. As V. C. Vaughan has remarked: “It appears that natural
immunity gives way before exposure, overwork and fatigue, as was
demonstrated years ago by Pasteur in his experiments on birds with
anthrax. Likewise, it is possible for human beings to have their
resistance lowered by exposure to unaccustomed environment, so that
although naturally immune, the standard of immunity is reduced to the
point where the influenza virus gains admittance and overcomes the
lowered resistance.”
_Race stock and mortality._—The relationship of morbidity to race stock
has already been considered and should be borne in mind in a discussion
of mortality by race.
We have seen how the natives of India suffered unusually from the
influenza, the total deaths being estimated at over 5,000,000
individuals. A preliminary report from the Department of the Interior on
the mortality from influenza among American Indians showed that during
the six months period from October 1, 1918, to March 31, 1919, over two
per cent. of the Indian population died of influenza. The mortality
among Indians in the Mountain States, especially in Colorado, Utah and
New Mexico, was very high. For the Indian population as a whole the
annual mortality rate from influenza alone during the six months period
was according to the U. S. Public Health Reports 41.2 per 1,000, which
is above that for the larger cities in the United States during the same
epidemic period.
In both of the above races we cannot say that it was not factors other
than race, particularly living conditions, that resulted in the high
mortality.
Winslow and Rogers found in Connecticut that the proportion of
influenza-pneumonia deaths was lower than would be expected among
persons of native Irish, English and German stock, but higher than would
be expected among Russian, Austrian, Canadian and Polish stock, and
enormously high among Italians. They suggest that this marked difference
in racial incidence may be very largely due to the differences in age
distribution of the various race stocks, the races showing the highest
ratios being those which have arrived more recently in the country and
which are made up more largely of young adults at the ages which suffer
most severely from influenza. They further refer to the work done by
Armstrong in Framingham, and state that their results tend to confirm
his conclusions in regard to the Italians, as do the figures presented
by Greenberg from the records of the Visiting Nurse Association of New
Haven. “It appears that Italy suffered very severely from the influenza
epidemic in Europe, and Dublin has shown that the normal pneumonia rate
of this race is a very high one.”
We have rather more abundant comparison of the white and black races in
this country. Frost found in his extensive survey that the case fatality
was generally higher among the colored than among the white population.
A similar observation was made by Howard and Love, who found that the
case mortality for influenza and its complications in the United States
and in the American Expeditionary Forces, in 1918, was for colored
troops 4.3 per cent. and for white troops 3.3.
These two series of observations are of great importance, for they are
about all we have describing case fatality rate. The majority of other
reports describe mortality rate only, and are therefore not complete.
The death rate in the Army was higher among colored troops, but the
incidence of influenza, the rate per 1,000, was lower for the colored
race. “Considering only the southern states, the nativity rate for
influenza for the white was 247.11 and for the colored, 154.58. For
lobar pneumonia it was 10.77 for the white and 28.31 for the colored;
for bronchopneumonia and unclassified pneumonia 7.26 for the whites and
11.43 for the colored. It seems probable that the negro is less
susceptible to influenza than the southern whites, but that he is much
more susceptible to pneumonic infections, either primary or secondary.”
Fränkel and Dublin have studied the racial distribution of 70,729 deaths
among policy holders of the Industrial Department of the Metropolitan
Life Insurance Company, particularly with respect to incidence among
white and black. Normally the mortality from respiratory diseases is
higher among colored persons than among whites. In the seven year period
from 1911 to 1917, influenza-pneumonia death rates showed an excess of
72 per cent. colored males over white males and of 56 per cent. colored
females over white females. During the period of the epidemic the
situation was reversed. The whites suffered from higher rates than the
colored. While the rate among white males during the period, October to
December, 1918, was nearly fifteen times as great as during the period
1911 to 1917; that of colored males was only seven times as great as the
rate during the same seven year period. White females during the height
of the epidemic showed a rate more than sixteen times as high as the
normal, while colored females experienced a rate only nine times as
high. After the first of January, 1919, the excess rate returned slowly
to the normal figures. These facts are based on death rate only.
Any comparison of race morbidity or mortality, to be of value, must be
based on observations of individuals living in the same climate, in the
same domestic environment, and in similar age distribution. It is
practically impossible to discover groups living under such conditions.
Howard and Love, perhaps, approached more nearly to such an ideal in
studying the white and black races in the Army, but even in the military
forces many factors are at play. Thus, the death rate among enlisted men
was highest among the American troops in the United States (12.02);
second in Europe (6.07); third in Panama (1.09); fourth in Hawaii
(0.55); fifth in the Philippine Islands (0.14). By race it was highest
for the colored troops (12.69); second for the white (8.83); third for
the Porto Ricans (7.80); fourth for the Filippinos (2.84); and fifth for
the Hawaiians (1.72). The authors point out that while the native troops
had higher admission rates than the whites, the death rates were lower,
which illustrates the point that the death rate for this type of disease
is lower in the summer and in the tropics.
SECTION IV.
AN INTENSIVE STUDY OF THE SPREAD OF INFLUENZA IN SMALL GROUPS OF CLOSELY
ASSOCIATED INDIVIDUALS.
We have been discussing the disease under consideration chiefly from the
viewpoint of the statistician. The statistician, possessing a wealth of
information of a general nature, and from all parts of the world, and
armed with fascinating complex mathematical instruments, is able to
dissect the information at his disposal, and to reconstruct therefrom
both facts and apparent facts of absorbing interest. To him we are
indebted for the bulk of our knowledge of the distribution and spread of
the influenza through metropolises, through countries, and through
continents.
Like the aviator flying over enemy territory he acquires a breadth of
vision and a general perspective which is to a great extent denied to
those remaining on the ground. But also like the aviator, from the very
fact of his high position he loses the ability to recognize detail. The
small subdivisions in the enemy lines are slightly blurred and he can
distinguish the front line trenches in which most of the action is
occurring no more clearly than the reserve and support trenches. An Army
depending entirely upon its aeroplane reconaissance would find itself
helpless in combating the enemy. The aeroplane is useful, yes, it could
not be dispensed with, but never an opportunity is lost for scouting
parties to explore the enemy front lines; it is these latter who bring
back information as to the local strength and distribution of the enemy,
as to what particular divisions are in action, as to the strength of the
entrenchments, the enemy distribution within the trenches, and finally
what is most important, information as to the weak points in the enemy’s
lines, places at which we may concentrate our attack with the hope of
driving the enemy from its stronghold. Occasionally a raiding party will
return with a prisoner. He will be examined thoroughly and may yield
some valuable information. All such prisoners are not dressed alike. We
recognize that some belong to one regiment and some to another. After we
have extracted what information we can from the prisoner he is
incarcerated, if we may extend our metaphor, in a test tube, and there
he remains for future reference. We do not believe that these individual
private soldiers are the cause of the war, but we do know that they are
doing their share of the killing—that they are doing most of the
killing.
It is characteristic of human enthusiasm and hopefulness that each
raiding party prays that it may bring back with it a general officer, a
field marshall, the one who is chiefly responsible for the enemy
offensive. In our own little battle with our invisible host we have long
since discovered that field marshalls here as elsewhere are difficult to
discover by raiding parties. But the raids are and should be made just
the same. They almost invariably bring back some new item of
information, and it is the experience of many wars that even though the
commanding general be never captured, repeated small or large attacks
following preliminary reconaissance, if diligently and valiantly
prosecuted under good leadership may win the war.
In studying the life and habits of the influenza virus and its army of
secondary invaders, and the results thereof in small groups composed of
individuals as the unit, instead of large groups with communities as a
unit, we will be able to discover a certain number of additional facts,
some of which may have considerable value.
In the study by the author of six selected districts in Boston a special
study was made of the occurrence and manner of spread of the influenza
in the household or family as a unit. The 10,000 individuals canvassed
were distributed through 2,117 families. Of these two thousand odd
families, 45.44 per cent. were visited with one or more cases of the
disease in the 1918–19 epidemic, and 27.25 per cent. in the winter of
1920. Of these, 14.31 per cent. had cases in both epidemics. In either
one or both of the two epidemics under consideration, 58.38 per cent. of
all families had influenza (see Table III).
TABLE III.
_Per cent. of families invaded by influenza._
═══════════════╤═════════════╤═════════════╤═════════════╤═════════════
Boston District│ 1918–19. │ 1920. │ 1918–19 and │ Total.
No. │ │ │ 1920. │
───────────────┼─────────────┼─────────────┼─────────────┼─────────────
1 │ 49.59│ 32.79│ 20.05│ 62.33
2 │ 36.04│ 17.36│ 7.25│ 46.15
3 │ 45.89│ 26.43│ 14.71│ 57.61
4 │ 48.48│ 32.20│ 14.39│ 66.29
5 │ 52.48│ 34.11│ 19.53│ 67.06
6 │ 43.16│ 24.21│ 11.23│ 56.14
All Districts │ 45.44│ 27.25│ 14.31│ 58.38
───────────────┴─────────────┴─────────────┴─────────────┴─────────────
Explanatory note: 45.44 per cent. of all families were invaded in 1918.
27.25 per cent. of all families were invaded in 1920.
14.31 per cent. of all families were invaded in both
epidemics.
58.38 per cent. of all families were invaded in one
or the other or both.
41.62 per cent. of all families remained free from
influenza throughout both epidemics.
In this discussion of family incidence, as in our work on the incidence
among individuals, the question naturally arises as to the reliability
of our information and the accuracy of our results. We have shown the
close correspondence between our own results and those of Frost, done on
a vastly larger number of individuals. The information for families was
obtained from the same sources and from the same individuals. The
thoroughness with which the inspectors did their work is indicated by
the fact that in addition to the 2,117 families on which we base our
results, only the records of 194 families have been discarded for
various reasons. In discarding the family records we also discarded the
individual records and such are, therefore, for individuals above our
total of 10,000. One hundred and fifty-four of these were for families
whose homes were in the districts surveyed, but who were not at home at
the time of the first survey. These were omitted during the second
survey, irrespective of whether individuals were at home. In this group
are also included a few in which children were at home, but were unable
to give reliable information. Fifteen of the 194 families gave
insufficient information, and 25 refused to co-operate. The small number
in this last group speaks well for the efficiency and methods of the
inspectors. All families accepted for tabulation co-operated to the best
of their ability, and we believe that the records are as accurate as
this type of work may be made.
Dr. Niven, in the work referred to by Carnwath, made an inquiry covering
1,021 houses, with a population of 4,721. Five hundred and three
households or almost exactly one-half, were invaded in either the summer
1918, or the autumn-winter 1918 epidemic. This proportion of families is
quite similar to our own, but it must be pointed out that Niven was not
studying the same two epidemics that we are discussing. Two hundred and
sixty-six of his total households, or 26.05 per cent. were invaded in
the autumn epidemic.
Previous to the present time the author has been unable to find records
of investigators having used this method of studying influenza to any
appreciable extent. Certainly there has been nothing done on the subject
previous to the last pandemic. Since then Frost has studied, as
indicated in his report, family incidence to the extent of determining
the relationship to overcrowding and to economic status, and Niven has
studied family incidence with special reference to immunity.
Thomas Sydenham, speaking of the epidemic of 1675, says that: “No one
escaped them whatever might be his age or temperament, and they ran
through whole families at once.”
According to Waldschmidt, during the epidemic of 1712, in Kiel, ten or
more persons were frequently taken ill in one house.
In 1732, Huxam tells us that, “not a house was free from it, the
beggar’s hut and the nobleman’s palace were alike subject to its attack,
scarce a person escaping either in town or country, old and young,
strong and infirm, shared the same fate.”
Metzger says that the influenza was so universal in March, 1782, that in
very many houses all of the inmates were attacked. On the other hand,
Mertens did not believe the influenza a contagion during the same
epidemic for the reason that according to his observations now only one,
and again all, of the members of a family, were stricken.
In 1833, in Königsberg, according to Hufeland, parents, children, and
servants were frequently smitten with the disease at the same time, so
that strange help had to be obtained for the family.
Parkes taught that, “Persons in overcrowded habitations have,
particularly in some epidemics, especially suffered, and several
instances are on record of a large school or a barrack for soldiers
being first attacked, and of the disease prevailing there for some days
before it began to prevail in the town around. Sometimes, on the other
hand, schools and prisons have escaped. A low, damp, ill-ventilated and
unhealthy situation appears to predispose to it, and in some instances,
in hospital patients, it has assumed a malignant character. In other
cases again, hospital patients have escaped; for example, the old people
in the Salpêtrière in 1837, when the younger attendants were attacked.”
_Effect of overcrowding._—The family or household forms a social unit in
which human intercourse is very close, and in which the opportunities
for contact infection either direct or indirect are manifold. In
addition to all of the opportunities which each individual has for
contracting the disease outside of the family every case in the family
exposes every other member many times during the day. One of the first
questions arising in a study of the disease in the family is, therefore,
whether the size of the family in and of itself exerts any predisposing
influence on the total incidence in any one family. Are large families
more likely to have a greater percentage of cases than small families?
We have endeavored to answer this question by grouping together all
families containing only one individual, all of those with two, three,
four, etc., and determining the percentage of individuals contracting
influenza in each of the groups. The standard for comparison is the
percentage of the total 10,000 who contracted the disease in either
year, or in both. 19.71 per cent. of all persons canvassed contracted
influenza in 1918–19. Reference to Table IV shows that of persons living
in families of one, 17.95 per cent. developed the disease; of those in
families of two, 18.46 per cent.; in families of three, 19.96 per cent.;
in families of four, 20.10 per cent.; and in families of from five to
seven, between 22 and 23 per cent. Families of over seven all showed
lower, but varying incidence of the disease. As is seen by the table,
they comprise only a small number of families.
TABLE IV.
_The incidence of influenza in families of different sizes._
(Influence of size of family).
═══════════╤═══════════╤═══════════╤═══════════════════════════════════
│ │ Total No. │
No. of │ │ of │
individuals│No. of such│individuals│ Number of these individuals who
in family. │ families. │included in│ developed influenza.
│ │ all such │
│ │ families. │
───────────┼───────────┼───────────┼───────────┬───────────┬───────────
„ │ „ │ „ │ 1918. │ 1920. │ Total.
───────────┼───────────┼───────────┼─────┬─────┼─────┬─────┼─────┬─────
„ │ „ │ „ │ No. │ Per │ No. │ Per │ No. │ Per
│ │ │ │cent.│ │cent.│ │cent.
───────────┼───────────┼───────────┼─────┼─────┼─────┼─────┼─────┼─────
1│ 39│ 39│ 7│17.95│ 3│ 7.69│ 10│24.42
2│ 260│ 520│ 96│18.46│ 55│10.58│ 151│29.04
3│ 359│ 1077│ 215│19.96│ 128│11.88│ 343│31.85
4│ 396│ 1584│ 319│20.10│ 169│10.67│ 488│30.81
5│ 375│ 1875│ 423│22.56│ 203│10.83│ 626│33.39
6│ 264│ 1584│ 361│22.79│ 151│ 9.53│ 512│32.32
7│ 179│ 1253│ 279│22.27│ 109│ 8.70│ 388│30.96
8│ 103│ 824│ 156│18.93│ 55│ 6.67│ 211│25.61
9│ 57│ 513│ 85│16.57│ 21│ 4.09│ 106│20.66
10│ 28│ 280│ 40│14.14│ 26│ 9.29│ 66│23.57
11│ 15│ 165│ 10│ 6.06│ 7│ 4.24│ 17│10.30
12│ 4│ 48│ 0│ 0.0│ 5│10.42│ 5│10.42
13│ 2│ 26│ 5│19.23│ 3│11.54│ 8│30.77
14│ 1│ 14│ 0│ 0.0│ 0│ 0.0│ 0│ 0.0
───────────┴───────────┴───────────┴─────┴─────┴─────┴─────┴─────┴─────
In 1920, 9.55 per cent. of the entire canvassed population contracted
the disease. The table shows that 7.69 per cent. of all individuals in
families of one contracted influenza, and between 10 and 12 per cent. in
families of from two to five individuals. Above the family of five the
incidence rates again are lower and varying within wide limits. The last
column shows the percentage of individuals by size of family contracting
the disease in either or both epidemics.
The average size of all families was 4.7 individuals.
If we consider only those family groups having over 1,000 individuals as
being sufficiently large to be representative, we may conclude that
families of from three to seven individuals show no progressive increase
in influenza incidence with increase in size of the family. But all the
available evidence indicates that other things being equal, the age
incidence is a very important factor. Its influence will be felt in the
subject under consideration, and it will modify the results. Thus,
families of one or two are almost invariably adults; families of three
are very frequently made up of two adults and a child or infant, while
families of from five to seven will be more likely to have a high
proportion of young adults—the age period more seriously affected.
The next question arising is whether those families, large or small,
which are living in crowded circumstances, are more likely to develop
the disease. Arbitrary standards must be chosen as indices of crowding.
We have chosen two in order that they may check each other. The first is
based upon the number of individuals sleeping in a bedroom. Families are
classified as follows: Maximum sleeping in a single bedroom, 1; maximum
sleeping in a single bedroom, 2; maximum per bedroom, 3, 4, etc.
The second standard of crowding is based upon the ratio of the number of
individuals in the family and the number of rooms occupied. One person
living in one room is not crowded; two in two rooms, three in three
rooms, four in four rooms, eight in eight rooms, twelve in twelve rooms,
are not crowded. Two people living in one room four in two rooms, six in
three rooms, twelve in six rooms, are decidedly more crowded. On the
contrary, one individual in two rooms, two in four, three in six, four
in eight, five in ten, etc. have an unusual amount of room.
The ratios ^P⁄_{R} are then throughout, ¹⁄₁, ²⁄₁, ½. These are used as
dividing lines. All families with ratios higher than ²⁄₁ are classed as
very crowded. Families with ratios above ¹⁄₁ up to and including ²⁄₁ are
classed as crowded. Families with ratios above ½ up to and including ¹⁄₁
are classed as roomy, and those with ratio of ½ or lower are classified
as very roomy.
Classifying all families in all six districts according to these last
four degrees of crowding, we find, as is shown by Table V, that there is
a progressive increase in the proportion of families with one or more
cases of the disease, with increase in the extent of crowding.
According to the standard first described we find as is shown in Table
VI that families with three, four and five individuals sleeping in a
single room show a progressive increase of incidence over those families
with but one or two per bedroom. This again is shown best in the total
for all families, but is borne out in a study of each district. These
statistics are however of little value for the study of the effect of
overcrowding, because crowded families are usually large families. With
an influenza incidence of 20 per cent. we would theoretically expect
every family of five or larger to have one or more cases. This would
amount to 100 per cent. infected families and such a state would not
only influence, but dominate the statistics regarding overcrowding.
TABLE V.
_Effect of crowding on development of influenza in families._
(A higher proportion of crowded households than roomy are invaded).
(Standard used: ratio of number individuals to number rooms).
══════════════╤══════════╤═════════════════════════════════════════════
Living │ No. of │ Proportion of these families visited by
conditions. │ such │ influenza.
│families. │
──────────────┼──────────┼──────────┬──────────┬────────────┬──────────
│ │ In │ │ In both │ Total
„ │ „ │ 1918–19. │ In 1920. │ epidemics │ families
│ │ │ │(Recurrent).│ invaded.
──────────────┼──────────┼────┬─────┼────┬─────┼─────┬──────┼────┬─────
„ │ „ │No. │ Per │No. │ Per │ No. │ Per │No. │ Per
│ │ │cent.│ │cent.│ │cent. │ │cent.
──────────────┼──────────┼────┼─────┼────┼─────┼─────┼──────┼────┼─────
District I. │ │ │ │ │ │ │ │ │
V. Cr. │ 53│ 30│56.61│ 15│28.31│ 12│ 22.64│ 31│58.49
Cr. │ 195│ 107│54.87│ 59│30.26│ 43│ 22.05│ 123│63.08
R. │ 79│ 36│45.57│ 24│30.38│ 18│ 22.78│ 42│53.16
V. R. │ 16│ 7│43.75│ 1│ 6.6│ 0│ 0.0│ 8│50.00
──────────────┼──────────┼────┼─────┼────┼─────┼─────┼──────┼────┼─────
District II. │ │ │ │ │ │ │ │ │
V. Cr. │ 4│ 1│25.00│ 1│25.00│ 1│ 25.00│ 1│25.00
Cr. │ 137│ 70│51.09│ 31│22.63│ 2│ 8.76│ 89│64.96
R. │ 208│ 70│33.65│ 39│18.75│ 7│ 8.17│ 92│44.23
V. R. │ 103│ 20│19.42│ 7│ 6.80│ 2│ 1.94│ 25│24.27
──────────────┼──────────┼────┼─────┼────┼─────┼─────┼──────┼────┼─────
District III. │ │ │ │ │ │ │ │ │
V. Cr. │ 13│ 9│69.23│ 2│15.38│ 1│ 7.69│ 10│76.92
Cr. │ 213│ 99│46.48│ 65│30.52│ 40│ 18.78│ 124│58.22
R. │ 143│ 62│43.36│ 35│24.48│ 15│ 10.49│ 82│57.34
V. R. │ 21│ 8│27.59│ 2│ 6.89│ 2│ 6.89│ 8│38.09
──────────────┼──────────┼────┼─────┼────┼─────┼─────┼──────┼────┼─────
District IV. │ │ │ │ │ │ │ │ │
V. Cr. │ 0│ 0│ │ 0│ │ 0│ │ 0│
Cr. │ 27│ 18│66.67│ 8│29.63│ 5│ 18.52│ 21│77.77
R. │ 137│ 72│52.55│ 50│36.49│ 21│ 15.33│ 101│73.72
V. R. │ 95│ 38│40.00│ 27│28.42│ 12│ 12.63│ 53│55.79
──────────────┼──────────┼────┼─────┼────┼─────┼─────┼──────┼────┼─────
District V. │ │ │ │ │ │ │ │ │
V. Cr. │ 6│ 2│33.33│ 4│66.67│ 2│ 33.33│ 4│66.67
Cr. │ 110│ 67│60.91│ 37│33.64│ 25│ 22.73│ 79│71.82
R. │ 209│ 104│49.76│ 70│33.49│ 38│ 18.18│ 146│69.86
V. R. │ 14│ 3│21.42│ 3│21.42│ 0│ │ 6│42.84
──────────────┼──────────┼────┼─────┼────┼─────┼─────┼──────┼────┼─────
District VI. │ │ │ │ │ │ │ │ │
V. Cr. │ 0│ 0│ │ 0│ │ 0│ │ 0│
Cr. │ 2│ 1│50.00│ 0│ 0.0│ 0│ 0.0│ 1│50.00
R. │ 92│ 57│61.96│ 23│25.00│ 14│ 15.22│ 66│71.74
V. R. │ 189│ 65│34.39│ 46│24.34│ 19│ 10.05│ 92│48.68
──────────────┴──────────┴────┴─────┴────┴─────┴─────┴──────┴────┴─────
═══════════╤══════════╤═════╤═════╤═════╤═════╤═════╤═════╤══════╤═════
Living │ No. of │ No. │ Per │ No. │ Per │ No. │ Per │ │ Per
conditions.│families. │1918.│cent.│1920.│cent.│both.│cent.│Total.│cent.
│ │ │1918.│ │1920.│ │both.│ │
───────────┼──────────┼─────┼─────┼─────┼─────┼─────┼─────┼──────┼─────
Very │ 80│ 43│53.75│ 25│31.25│ 18│22.50│ 50│62.50
crowded │ │ │ │ │ │ │ │ │
Crowded │ 693│ 372│53.68│ 201│29.00│ 126│18.18│ 447│64.50
Roomy │ 865│ 394│45.55│ 244│28.21│ 125│14.45│ 513│59.31
Very Roomy │ 443│ 143│32.28│ 87│19.64│ 36│ 8.13│ 194│43.79
───────────┼──────────┼─────┼─────┼─────┼─────┼─────┼─────┼──────┼─────
All │ Total │1918 │ Per │1920 │ Per │Both │ Per │Total │ Per
│ │ │cent.│ │cent.│ │cent.│ │cent.
───────────┼──────────┼─────┼─────┼─────┼─────┼─────┼─────┼──────┼─────
│ 2081│ 952│45.75│ 557│26.77│ 305│14.66│ 1204│57.86
───────────┴──────────┴─────┴─────┴─────┴─────┴─────┴─────┴──────┴─────
TABLE VI.
_Effect of crowding._
(Standard used: maximum number sleeping in one bed room.)
══════════════╤══════════╤═════════════════════════════════════════════
Maximum No. │ No. of │ Proportion of these families with cases of
sleeping per │ such │ influenza.
room. │families. │
──────────────┼──────────┼──────────┬──────────┬────────────┬──────────
│ │ In │ │ In both │ Total
„ │ „ │ 1918–19. │ In 1920. │ epidemics. │ families
│ │ │ │ │ invaded.
──────────────┼──────────┼────┬─────┼────┬─────┼─────┬──────┼────┬─────
„ │ „ │No. │ Per │No. │ Per │ No. │ Per │No. │ Per
│ │ │cent.│ │cent.│ │cent. │ │cent.
──────────────┼──────────┼────┼─────┼────┼─────┼─────┼──────┼────┼─────
District I. │ │ │ │ │ │ │ │ │
1 │ 16│ 6│37.50│ 4│25.00│ 3│ 18.75│ 7│93.75
2 │ 93│ 52│55.91│ 31│33.33│ 20│ 21.51│ 63│67.74
3 │ 145│ 65│44.83│ 47│32.41│ 27│ 18.62│ 85│58.62
4 │ 79│ 43│54.43│ 25│31.65│ 17│ 21.52│ 51│64.56
5 │ 24│ 11│45.83│ 11│45.83│ 6│ 25.00│ 16│66.67
6 │ 10│ 3│30.00│ 3│30.00│ 1│ 10.00│ 5│50.00
──────────────┼──────────┼────┼─────┼────┼─────┼─────┼──────┼────┼─────
District II. │ │ │ │ │ │ │ │ │
1 │ 90│ 15│16.67│ 7│ 7.77│ 2│ 2.22│ 20│22.22
2 │ 211│ 68│32.23│ 36│17.06│ 14│ 6.64│ 90│42.65
3 │ 115│ 59│51.30│ 23│20.00│ 10│ 8.69│ 72│66.61
4 │ 33│ 20│60.60│ 11│33.33│ 6│ 18.18│ 25│75.76
5 │ 3│ 1│33.33│ 2│66.67│ 1│ 33.33│ 2│66.67
6 │ 0│ 0│ │ 0│ │ 0│ │ 0│
──────────────┼──────────┼────┼─────┼────┼─────┼─────┼──────┼────┼─────
District III. │ │ │ │ │ │ │ │ │
1 │ 26│ 10│38.46│ 3│11.54│ 2│ 7.69│ 11│42.31
2 │ 179│ 73│40.78│ 47│26.26│ 23│ 12.85│ 97│54.19
3 │ 145│ 72│49.66│ 37│25.52│ 23│ 15.86│ 86│59.31
4 │ 39│ 20│51.28│ 15│38.46│ 8│ 20.51│ 27│69.23
5 │ 8│ 5│62.50│ 2│25.00│ 1│ 12.50│ 6│75.00
6 │ 0│ 0│ │ 0│ │ 0│ │ 0│
──────────────┼──────────┼────┼─────┼────┼─────┼─────┼──────┼────┼─────
District IV. │ │ │ │ │ │ │ │ │
1 │ 53│ 15│28.30│ 15│28.30│ 6│ 11.32│ 24│45.28
2 │ 165│ 80│48.48│ 56│33.94│ 22│ 13.33│ 114│69.09
3 │ 42│ 29│69.05│ 15│35.71│ 10│ 23.81│ 34│80.95
4 │ 5│ 4│80.00│ 0│ 0.0│ 0│ 0.0│ 4│80.00
5 │ 0│ 0│ │ 0│ 0.0│ 0│ │ 0│
6 │ 0│ 0│ │ 0│ │ 0│ │ 0│
──────────────┼──────────┼────┼─────┼────┼─────┼─────┼──────┼────┼─────
District V. │ │ │ │ │ │ │ │ │
1 │ 23│ 8│34.77│ 6│26.08│ 1│ 4.35│ 13│56.52
2 │ 156│ 70│44.37│ 48│30.77│ 24│ 15.38│ 94│60.26
3 │ 130│ 81│62.31│ 44│33.84│ 27│ 20.77│ 98│75.38
4 │ 27│ 18│66.66│ 14│51.85│ 12│ 44.44│ 20│74.07
5 │ 6│ 3│50.00│ 4│66.67│ 3│ 50.00│ 4│66.67
6 │ 1│ 0│ 0.00│ 0│ 0.00│ 0│ 0.00│ 0│ 0.00
──────────────┼──────────┼────┼─────┼────┼─────┼─────┼──────┼────┼─────
District VI. │ │ │ │ │ │ │ │ │
1 │ 120│ 42│35.00│ 24│20.00│ 10│ 8.33│ 56│46.67
2 │ 146│ 77│52.74│ 34│23.29│ 22│ 15.07│ 89│60.96
3 │ 10│ 5│50.00│ 5│50.00│ 1│ 10.00│ 6│60.00
4 │ 0│ 0│ │ 0│ │ 0│ │ 0│
5 │ 0│ 0│ │ 0│ │ 0│ │ 0│
6 │ 0│ 0│ │ 0│ │ 0│ │ 0│
──────────────┼──────────┼────┼─────┼────┼─────┼─────┼──────┼────┼─────
Total │ │ │ │ │ │ │ │ │
1 │ 328│ 96│29.27│ 59│17.99│ 24│ 7.32│ 131│39.94
2 │ 450│ 420│44.21│ 252│26.53│ 125│ 13.16│ 547│57.57
3 │ 587│ 311│52.98│ 171│29.13│ 98│ 16.69│ 381│64.91
4 │ 183│ 105│57.38│ 65│35.52│ 43│ 23.50│ 127│69.39
5 │ 41│ 20│48.78│ 19│46.34│ 11│ 26.83│ 28│68.29
6 │ 11│ 3│27.27│ 3│27.27│ 1│ 9.09│ 5│45.45
──────────────┴──────────┴────┴─────┴────┴─────┴─────┴──────┴────┴─────
An objection will be raised, and justly so, that we have up to this
point been studying influenza in families irrespective of how many cases
there are in each family. Until now the family with one case was
classified exactly the same as the family with eight cases. In the
following classification we have taken first all families with a maximum
of one sleeping in one room, and sub-divided these into families with no
influenza, those with one case, two cases, etc. We have likewise
classified families with maxima from two to six per bedroom. For the
sake of brevity we will consider only the last column of Table VII,
influenza incidence among the individuals of the various classes of
families for both epidemics. Study of the table will show a
correspondence in the other columns. Solitary cases were more numerous
in families with but one or two per bedroom (27 per cent.) and less
frequent in families with three, four and five per bedroom, (23 per
cent., 18 per cent., and 20 per cent., respectively). The families of
six per bedroom form such a small group that here again they should not
be considered. Multiple cases become progressively more numerous as the
number of individuals per bedroom increases (14 per cent. in families of
one per bedroom, 29 per cent. in two per bedroom, 41 per cent. in three,
51 to 52 per cent. in four, and 45 per cent. in five). Fifty-eight per
cent. of families with a maximum of one per bedroom, 43 per cent. with
two per bedroom, 35 per cent. with three, 31 per cent. with four and 35
per cent. with five had no influenza at all.
But here again, the fact that crowded families are usually large
families interferes with drawing any conclusions. A family with four per
bed room would generally be larger than one with two per bed room.
Frost observed that, considering the ratio of incidence in total white
populations irrespective of housing as 100, and after adjusting all
groups to a uniform sex and age distribution, the ratio where there were
more than 1.5 rooms per person was 77, from 1 to 1.5 rooms per person
the ratio was 94, and for individuals averaging less than one room per
person it was 117. _The attack rate showed a consistent increase as the
number of rooms per person decreased._
Woolley observed, “Housing, if one includes in the term overcrowding,
has surely been an important factor in spreading the epidemic. Whether
it has had any appreciable effect upon the incidence of complications is
a question. The epidemic has certainly gone faster and was over sooner
because of the crowding; the hospital was filled sooner than it should
have been as a result of the rapidity of spread of the disease, and
overcrowding of the hospital occurred when with a less rapid spread it
would not have occurred; but whether the number of fatalities or the
number of pneumonias was greater than they should have been with less
crowded conditions may be doubted.”
TABLE VII.
_Relationship between crowding and number of cases in the family._
(Influenza appeared more frequently in crowded households and such
families more frequently had multiple cases.)
══════════════════════════════════════════════════════════════════════
Families with maximum per bed room of one.
(58.23 per cent. of these had no influenza.)
──────────┬──────────┬─────────┬─────────┬──────────┬─────────┬───────
Cases │Total such│ Invaded │ Invaded │Invaded in│ Total │Two or
developing│families. │ in │in 1920. │ both │families │ more
in family.│ │1918–19. │ │epidemics.│invaded. │cases.
──────────┼──────────┼───┬─────┼───┬─────┼────┬─────┼───┬─────┼───────
„ │ „ │No.│ Per │No.│ Per │No. │ Per │No.│ Per │ Per
│ │ │cent.│ │cent.│ │cent.│ │cent.│ cent.
──────────┼──────────┼───┼─────┼───┼─────┼────┼─────┼───┼─────┼───────
1│ 85│ 55│17.68│ 37│11.89│ 7│ 2.25│311│27.33│
2│ 32│ 26│ 8.36│ 16│ 5.14│ 10│ 3.22│ │10.28│} 14.44
3│ 9│ 8│ 2.57│ 2│ 0.64│ 1│ 0.32│ │ 2.88│ „
4│ 4│ 3│ 0.96│ 4│ 1.28│ 3│ 0.96│ │ 1.28│ „
5│ 0│ 0│ │ │ │ │ │ │ │
6│ 0│ │ │ │ │ │ │ │ │
7│ 0│ │ │ │ │ │ │ │ │
8│ 0│ │ │ │ │ │ │ │ │
──────────┴──────────┴───┴─────┴───┴─────┴────┴─────┴───┴─────┴───────
2 per bed room.
(43.35 per cent. of these had no influenza.)
──────────┬──────────┬───┬─────┬───┬─────┬────┬─────┬───┬─────┬───────
1│ 254│169│18.27│112│12.11│ 27│ 2.92│925│27.46│
2│ 135│112│12.11│ 64│ 6.92│ 41│ 4.43│ │14.59│} 29.17
3│ 79│ 65│ 7.03│ 38│ 4.11│ 24│ 2.59│ │ 8.54│ „
4│ 40│ 35│ 3.78│ 16│ 1.73│ 11│ 1.18│ │ 4.32│ „
5│ 11│ 9│ 0.97│ 8│ 0.81│ 6│ 0.64│ │ 1.18│ „
6│ 3│ 3│ 0.32│ 0│ 0.0│ 0│ 0.0│ │ 0.32│ „
7│ 2│ 2│ 0.22│ 1│ 0.11│ 1│ 0.11│ │ 0.22│ „
8│ 0│ 0│ │ │ │ │ │ │ │
──────────┴──────────┴───┴─────┴───┴─────┴────┴─────┴───┴─────┴───────
3 per bed room.
(35.34 per cent. of these had no influenza.)
──────────┬──────────┬───┬─────┬───┬─────┬────┬─────┬───┬─────┬───────
1│ 136│104│17.84│ 50│ 8.58│ 18│ 3.08│583│23.33│
2│ 103│ 77│13.21│ 55│ 9.43│ 29│ 4.97│ │17.67│} 41.33
3│ 59│ 51│ 8.75│ 29│ 4.97│ 21│ 3.60│ │10.12│ „
4│ 43│ 40│ 6.86│ 16│ 2.76│ 13│ 2.23│ │ 7.37│ „
5│ 22│ 22│ 3.77│ 9│ 1.54│ 9│ 1.54│ │ 3.77│ „
6│ 12│ 12│ 2.06│ 5│ 0.86│ 5│ 0.86│ │ 2.06│ „
7│ 2│ 2│ 0.34│ 0│ │ 0│ │ │ 0.34│ „
8│ 0│ │ │ │ │ │ │ │ │
──────────┴──────────┴───┴─────┴───┴─────┴────┴─────┴───┴─────┴───────
4 per bed room.
(30.79 per cent. of these had no influenza.)
──────────┬──────────┬───┬─────┬───┬─────┬────┬─────┬───┬─────┬───────
1│ 31│ 24│13.64│ 10│ 5.68│ 3│ 1.70│176│17.61│
2│ 22│ 19│10.80│ 13│ 7.39│ 10│ 5.68│ │12.50│} 51.60
3│ 37│ 32│18.18│ 25│14.20│ 20│11.36│ │20.92│ „
4│ 14│ 11│ 6.25│ 6│ 3.41│ 3│ 1.70│ │ 9.09│ „
5│ 9│ 9│ 5.12│ 4│ 2.27│ 4│ 2.27│ │ 5.12│ „
6│ 4│ 3│ 1.70│ 2│ 1.19│ 1│ 0.59│ │ 2.27│ „
7│ 3│ 3│ 1.70│ 0│ │ 0│ │ │ 1.70│ „
8│ 0│ │ │ │ │ │ │ │ │
──────────┴──────────┴───┴─────┴───┴─────┴────┴─────┴───┴─────┴───────
5 per bed room.
(35 per cent. had none.)
──────────┬──────────┬───┬─────┬───┬─────┬────┬─────┬───┬─────┬───────
1│ 8│ 6│15.00│ 4│10.00│ 2│ 5.00│ 40│20.00│
2│ 6│ 5│12.50│ 4│10.00│ 3│ 7.25│ │15.00│} 45.00
3│ 3│ 2│ 5.00│ 2│ 5.00│ 1│ 2.50│ │ 7.50│ „
4│ 2│ 1│ 2.50│ 2│ 5.00│ 1│ 2.50│ │ 5.00│ „
5│ 4│ 2│ 5.00│ 3│ 7.50│ 1│ 2.50│ │10.00│ „
6│ 2│ 2│ 5.00│ 2│ 5.00│ 2│ 5.00│ │ 5.00│ „
7│ 0│ │ │ │ │ │ │ │ │ „
8│ 1│ 0│ 0.0│ 1│ 2.50│ 0│ 0.0│ │ 2.50│ „
──────────┴──────────┴───┴─────┴───┴─────┴────┴─────┴───┴─────┴───────
6 per bed room.
(50 per cent. had none.)
──────────┬──────────┬───┬─────┬───┬─────┬────┬─────┬───┬─────┬───────
1│ 2│ 1│10.00│ 1│10.00│ 0│ 0.0│ 10│20.00│
2│ 1│ 1│10.00│ 1│10.00│ 1│10.00│ │10.00│} 30.00
3│ 2│ 1│10.00│ 1│10.00│ 0│ 0.0│ │20.00│ „
4│ 0│ │ │ │ │ │ │ │ │
5│ 0│ │ │ │ │ │ │ │ │
6│ 0│ │ │ │ │ │ │ │ │
7│ 0│ │ │ │ │ │ │ │ │
8│ 0│ │ │ │ │ │ │ │ │
──────────┴──────────┴───┴─────┴───┴─────┴────┴─────┴───┴─────┴───────
The housing methods in the cantonments and even in the tent camps
resulted in a degree of congestion and close physical contact among
individuals that was attained in no civil communities with the possible
exception of some institutions. In cantonments the number of men in
individual rooms ranged from 30 to 100 and even under the best
circumstances there was very evident close crowding. An individual in
any of these large rooms contracting a contagious disease had
opportunities to spread it by contact and by droplet infection not only
to one or two others, as in the case of the average family, but to a
large group of the men in the same room. A vicious circle was thus
formed which tended to propagate the disease throughout any camp with
utmost rapidity. Brewer has compared the influenza incidence rate in the
principal white organizations at Camp Humphreys with the floor space
allowed each man in the respective organizations, and concludes that,
“It is not proper or just to attribute the differences shown, alone to
the amount of floor space allowed each organization, but it certainly
points very strongly to the fact that the incidence of the disease
varied with the density of the population, although not with
mathematical regularity.” Brewer cites regiments which although housed
alike showed definite variation in the influenza incidence. This merely
shows that other factors also play a part. Thus, in one instance, the
difference in the two regiments was in length of service. Brewer also
found that among the white troops the incidence of pneumonia appears to
vary with the density of the population.
V. C. Vaughan has reported on the relationship between incidence in
tents and in barracks at Camp Custer. From this one observation it would
appear that the incidence is little changed under the two conditions.
“During September and October, 1918, a study was made on the
relationship, if any, of influenza to methods of living. Of the command,
3,633 were in tents. The morbidity per thousand in these was 129. There
were in barracks 36,055. The morbidity per thousand among those was 275.
At first glance the lower morbidity of those in tents is striking, but
going further into the matter it was found that the entire morbidity of
the Quartermaster Corps was very low. Of the Depot Brigade 2,881 were in
tents, with a morbidity of 128 per thousand, while 3,824 were in
barracks, with a morbidity of 134 per thousand.”
Howard and Love offer three reasons why during the last four months of
1918 the deaths from influenza and pneumonia in the Army in the United
States ran at a rate nearly three times as high as that among our troops
in France: First, that the troops in the United States were recent
recruits and therefore more susceptible to disease; second, that
probably many of the troops in France who had seen much longer service
had had the disease in mild form in the early spring; and, third, that
the method of housing was entirely different in France. There the men
were spread over a wide territory and whenever in rest area they were
billeted in houses rather than crowded into barracks. Furthermore, they
were living much more in the open. It was found that in commands of the
Service of Supply, where troops were housed in barracks with a large
number of men to a single room, the epidemic ran much the same course
with high mortality, as it did in the cantonments in the United States.
The percentage of infection and the fatalities from influenza and
pneumonia in France were much greater among troops of the S. O. S. than
among troops at the front.
_Domestic cleanliness._—We have studied the relationship between
influenza incidence and the cleanliness of the household by the same
method used in studying overcrowding. In Table VIII we have classified
according to cleanliness and according to the number of cases developing
in each family. We have had four subdivisions, “very clean,” “clean,”
“dirty,” and “very dirty.” There is greater opportunity for erroneous
results in this table than in the one preceding because the standards of
cleanliness are difficult to define. As a matter of fact we are guided
entirely by the inspector’s own impression of each household, as she
examined it during her visits. The following is an excerpt from the
instructions given each inspector on this subject:
“A few words on this subject may describe much. State of cleanliness
of the individual, slovenly condition, dust and dirt, foulness of air
noticed on first entering, condition of children, of kitchen sink,
etc., should be noticed, and good or bad features recorded. In the
poorer districts not a few families will be found in which the
cleanliness, considering the surroundings, is quite laudable. Of
particular importance are amount of daylight, ventilation, care of
bathroom and toilet, garbage, whether windows are kept open at night.”
On the basis of these returns we have classified the families as
indicated, but each inspector was governed to a certain extent by the
average cleanliness of her district, and it is difficult to compare the
cleanest tenement with any of the districts of well-to-do individuals.
We will therefore probably find it more profitable and more nearly
accurate to combine the groups and classify them only as “clean” and
“dirty.”
TABLE VIII.
_Relationship between cleanliness and number of cases in family._
(Clean families were invaded less frequently and had solitary cases more
often than did dirty households.)
══════════════════════════════════════════════════════════════════════════
Very clean.
(47.62 per cent. had none.)
─────────┬─────────┬────┬─────┬────┬─────┬─────┬─────┬──────┬─────────────
Cases in │ Total │’18.│ Per │’20.│ Per │Both.│ Per │Total.│ Per cent.
families.│families.│ │cent.│ │cent.│ │cent.│ │
─────────┼─────────┼────┼─────┼────┼─────┼─────┼─────┼──────┼─────┬───────
1│ 124│ 72│15.65│ 50│10.87│ 8│ 1.74│ 460│26.96│
2│ 53│ 41│ 8.91│ 27│ 5.87│ 15│ 3.25│ │11.52│} 25.42
3│ 37│ 33│ 7.17│ 13│ 2.82│ 9│ 1.95│ │ 8.04│ „
4│ 18│ 16│ 3.48│ 8│ 1.74│ 6│ 1.30│ │ 3.91│ „
5│ 4│ 3│ 0.65│ 2│ 0.43│ 1│ 0.21│ │ 0.87│ „
6│ 3│ 3│ 0.65│ 0│ 0.0│ 0│ 0.0│ │ 0.65│ „
7│ 2│ 2│ 0.43│ 1│ 0.21│ 1│ 0.21│ │ 0.43│ „
8│ 0│ 0│ │ 0│ │ 0│ │ │ │
─────────┴─────────┴────┴─────┴────┴─────┴─────┴─────┴──────┴─────┴───────
Clean.
(41.52 per cent. had none.)
─────────┬─────────┬────┬─────┬────┬─────┬─────┬─────┬──────┬─────────────
Cases. │Families.│’18.│ Per │’20.│ Per │Both.│ Per │Total.│ Per cent.
│ │ │cent.│ │cent.│ │cent.│ │
─────────┼─────────┼────┼─────┼────┼─────┼─────┼─────┼──────┼─────┬───────
1│ 301│ 212│18.45│ 120│10.44│ 31│ 2.70│ 1149│26.19│
2│ 177│ 143│12.45│ 91│ 7.92│ 57│ 4.96│ │15.40│} 32.29
3│ 101│ 83│ 7.22│ 52│ 4.53│ 34│ 2.96│ │ 8.79│ „
4│ 52│ 47│ 4.09│ 20│ 1.74│ 15│ 1.26│ │ 4.53│ „
5│ 30│ 29│ 2.52│ 17│ 1.48│ 16│ 1.22│ │ 2.61│ „
6│ 8│ 7│ 0.61│ 3│ 0.26│ 2│ 0.17│ │ 0.70│ „
7│ 3│ 3│ 0.26│ 0│ 0.0│ 0│ 0.0│ │ 0.26│ „
8│ 0│ 0│ │ 0│ │ 0│ │ │ │
─────────┴─────────┴────┴─────┴────┴─────┴─────┴─────┴──────┴─────┴───────
Dirty.
(36.89 per cent. had none.)
─────────┬─────────┬────┬─────┬────┬─────┬─────┬─────┬──────┬─────────────
Cases in │ Total │’18.│ Per │’20.│ Per │Both.│ Per │Total.│ Per cent.
families.│families.│ │cent.│ │cent.│ │cent.│ │
─────────┼─────────┼────┼─────┼────┼─────┼─────┼─────┼──────┼─────┬───────
1│ 79│ 59│17.40│ 36│10.62│ 16│ 4.72│ 339│23.30│
2│ 58│ 48│14.16│ 29│ 8.55│ 19│ 5.61│ │17.11│} 39.81
3│ 37│ 31│ 9.14│ 22│ 6.49│ 17│ 5.01│ │10.91│ „
4│ 26│ 22│ 6.49│ 12│ 3.54│ 8│ 2.36│ │ 7.67│ „
5│ 6│ 5│ 1.79│ 4│ 1.18│ 3│ 0.94│ │ 1.77│ „
6│ 7│ 7│ 2.06│ 4│ 1.18│ 4│ 1.18│ │ 2.06│ „
7│ 0│ 0│ │ 0│ │ 0│ │ │ │ „
8│ 1│ 0│ 0.0│ 1│ 0.29│ 0│ 0.0│ │ 0.29│ „
─────────┴─────────┴────┴─────┴────┴─────┴─────┴─────┴──────┴─────┴───────
Very dirty.
(39.26 per cent. had none.)
─────────┬─────────┬────┬─────┬────┬─────┬─────┬─────┬──────┬─────┬───────
1│ 22│ 16│14.95│ 8│ 7.47│ 2│ 1.85│ 107│20.56│
2│ 11│ 8│ 7.47│ 6│ 5.10│ 3│ 2.80│ │10.28│} 40.18
3│ 14│ 12│11.21│ 10│ 9.35│ 7│ 6.54│ │13.08│ „
4│ 7│ 5│ 4.67│ 4│ 3.73│ 2│ 1.85│ │ 6.54│ „
5│ 6│ 6│ 5.10│ 1│ 0.93│ 0│ 0.0│ │ 5.61│ „
6│ 3│ 3│ 2.80│ 2│ 1.85│ 2│ 1.85│ │ 2.80│ „
7│ 2│ 2│ 1.85│ 0│ 0.0│ 0│ 0.0│ │ 1.87│ „
8│ 0│ 0│ │ 0│ │ 0│ │ │ │
─────────┴─────────┴────┴─────┴────┴─────┴─────┴─────┴──────┴─────┴───────
But even without combining in this way, the table shows us that for both
years 27 per cent. of the very clean families, 26 per cent. of the
clean, 23 per cent. of the dirty and 21 per cent. of the very dirty, had
but one case, while 25 per cent. of the very clean, 32 per cent. of the
clean, 40 per cent. of the dirty, and 40 per cent. of the very dirty,
had multiple cases.
The cleaner the family the less is the likelihood of multiple cases.
It is rather difficult to find concrete examples of the influence of
domestic habits and environment in the 1918 pandemic. The remarkably
high incidence among the natives of India and among the American Indians
might by some be attributed to unfavorable environment. Lynch and
Cumming obtained records from a large number of institutions and from
business concerns having their own records, and discovered that the
influenza incidence was higher in those institutions where dish washing
was done manually than in those in which mechanical washing was
performed. They appear to conclude that the difference in the two
methods of washing dishes was the cause for the greater incidence in
influenza, thus bearing out their theory of the propagation of influenza
chiefly through eating utensils. On the contrary it is possible that the
presence of the mechanical washer is an indication of advanced methods,
greater care in the kitchen, and better hygiene probably not only in the
kitchen and dining room, but throughout the institution.
_Economic status._—Although in our survey information has been obtained
regarding the economic status of the various families we would not
stress this phase of our subject. Obviously the amount of money an
individual has in his bank will not directly influence the amount of
influenza he will have in his home. As nearly an accurate classification
by wealth is by the separation into the districts, Districts I and III
being very poor, District II poor, Districts IV and V moderate, and VI
well-to-do. From Chart XXVI we see no definite relationship between
influenza incidence and economic status.
Dr. Niven has had similar experiences. He remarks that the disease does
not appear to have affected especially any class or section of the
community. Rich and poor suffered alike. Inquiry in some towns shows
that the epidemic not infrequently started in the well-to-do districts
and only later involved the poorer and less prosperous areas.
We cannot state with any degree of accuracy in what section of Boston
the 1920 recurrence first began. The sections studied are for relatively
small portions of the city, and it is possible or probable that the
original increase was in some area outside of our districts. In the
districts studied the earliest increase in reported cases was from the
section of the city known as Dorchester (Districts IV and V), where
there was some increase in December, 1919. The latest definite increase
was in the Irish district of South Boston. Geographically these two
areas are quite near. The relative insusceptibility of the Irish
population is probably a much more important factor in the difference.
Frost found after classifying the white population canvassed in Little
Rock and San Antonio according to economic status, and adjusting the
incidence rate in each group to a uniform sex and age distribution, that
the ratios of incidence in each economic group to incidence in total
white population did show an increase with increasing poverty.
“Notwithstanding that the classification according to economic status is
a very loose one, based solely on the judgment of inspectors with widely
different standards, a considerably higher incidence is shown in the
lower as compared to the higher economic group.”
Parsons, in 1891, discussed the influence of poverty, but believed that
it is the concomitants of poverty which were the cause of the higher
incidence among the poor.
“Sanitary conditions do not seem to have had any influence in
determining the occurrence of influenza, and what share they have had in
determining its extent or fatality cannot yet be decided. On the
occasion of the last great epidemic, Dr. Peacock concluded, ‘The more
common predisponents to disease, _e.g._, defective drainage, want of
cleanliness, overcrowding, impure air, deficient clothing, innutritious
or too scanty food, powerfully conduce to the prevalence and fatality of
influenza.’ And Dr. Farr showed that in the last six weeks of 1847,
while in the least unhealthy districts of London the annual rate of
mortality was raised from a mean rate of twenty per 1,000 to
thirty-eight, in the unhealthiest districts it was raised from a mean
rate of twenty-seven to sixty-one.
“That overcrowding and impure air must have a powerful influence in
aiding the development of the epidemic follows from what we have seen of
its greater prevalence among persons associated together in a confined
space; and though rich and poor have alike been sufferers from the
epidemic, and even royal personages have been fatally attacked by it, it
cannot be doubted that poverty must have in many cases conduced to a
fatal issue in persons, who, if placed under more favorable
circumstances, might have recovered, seeing that it often involves not
only inferior conditions of lodgment, but also want of appropriate food,
of sufficient warmth and clothing, and of ability to take the needed
rest.”
_Distribution of the disease through the household._—During the autumn
and winter epidemic of 1918 there was considerable discussion, and
particularly were there popular newspaper reports of entire families
being taken ill with influenza, sometimes all on the same day. This was
less true of 1920. But few of us are personally acquainted with such
instances and at best they must have been relatively rare.
Among 1,236 families with influenza in either epidemic we found only 94
or 7.6 per cent. in which the entire family contracted the disease. No
family consisting of over seven individuals was reported as having all
the members of the family sick in either epidemic. Over two-thirds of
the families with even numbers of individuals (464 out of 605) suffered
the illness of less than half of the household. One quarter of all
families of more than one (539 out of 2,107) had but one case per
family. Over a third of all families of over two individuals (745 out of
2,006) had two or less cases per household. _As a rule there were at
least one and usually several individuals in each household who did not
contract influenza._
That as a rule the disease did not appear explosively in a family; but
that cases developed successively, is indicated by the fact that out of
577 families contracting influenza in the epidemic of 1920 the cases
were all of simultaneous development in but fifteen. In thirteen of
these, two individuals fell ill on the same day and no subsequent cases
developed. In the other two families three individuals came down on the
first day and no other cases developed. In addition there were, out of
the 577 families, fourteen in which there were two or more cases
developing on the first day of the invasion, but which were followed on
subsequent days by later cases in the same family. Again, there were
eleven families in which two or more cases occurred simultaneously at an
interval of one or more days after the development of a single prior
case.
We may say that _as a rule in the 1920 epidemic, cases of influenza
developed in families successively and not simultaneously_. In only 29,
or 5 per cent. of the families contracting the disease in 1920, did more
than one case develop on the first day of the appearance of the disease
in the family.
A certain difficulty in determining the date of onset is that we must
rely upon the patient’s statement. One individual may have been sick for
hours or days before a second member coming down with the disease called
forth recognition of the fact that they both had it.
Unfortunately we are not able to give similar statistics for the 1918–19
epidemic. Our investigation occurred so long after the epidemic that
specific dates of onset of the disease would have been entirely
unreliable. The nearest date we have attempted to obtain was the month
of the attack.
Dr. A. L. Mason states that 63 cases came under his observation in the
epidemic of 1889 as occurring in groups in families. In but six
instances were two persons attacked on the same day. The average
interval between cases in the same household was four days. Sometimes a
week or more elapsed. Whole families were never stricken at once.
Parsons in 1891 concluded from the results of questionaires sent to
physicians that in the first spread, 1889–90, there was an interval
between cases in individual households just as we have described. Among
the replies to his questionaires nine described intervals of one day and
under, six described intervals of two days, three of three days, three
of four days, and four replies described intervals of more than four
days.
Leichtenstern observed likewise: “In large families the contagious
character of influenza is evidenced by the fact that the other members
of the family become sick one after the other following the first case.
This rule of succession is most easily seen in the early or late period
of an epidemic and is less noticeable at the height, where the
opportunity for all the members of the family to acquire the influenza
outside the home is enormous. This latter fact explains why, when all
sicken at once, the disease appears to be miasmatic in origin. There are
many examples where other members of a family living with a sick
individual remained unaffected. Parsons reports such cases, and this was
so frequently the case that some British physicians state that it is the
rule that there is but one case in a family or that the cases are widely
separated in time. This was only partly true during the period of the
pandemic and was very frequent in the epidemic following it. In this
respect influenza acts like the common contagious diseases, diphtheria,
scarlet fever, measles, etc., while the difference lies in the short
incubation period and the very high contagiousness of the disease.”
That West, in England, had observed the same phenomenon is indicated by
the following quotation: “How is it, for instance, that one member of a
household may be picked out and the others escape, though they are
susceptible, as is shown by their acquiring the disease shortly after in
some other way?”
Again Leichtenstern wrote: “It is noteworthy that influenza on ships
usually did not occur explosively, but spread gradually, and on ships
usually lasted several weeks, as on the Bellerophon, from the 27th of
March to the 30th of April; on the Canada from the 11th of April to the
24th of May; on the Comus from the 10th of April to the 3d of May.
“The German Marine Report states, ‘Everywhere on the ships the disease
began not suddenly but gradually.’ The frigate Schwalbe first had a
large number of cases only on the 6th day after the beginning of the
epidemic. There are, however, some exceptions, where the disease has
begun suddenly with the greatest violence on ships as on land. Such was
true of the frigate Stag which on the 3d of April, 1833, neared the
influenza infected coast of Devonshire, and as it came under the land
wind the epidemic suddenly broke out with great violence. Within two
hours forty men took sick. Within six hours the number had increased to
sixty. Within twenty-four hours 160 men were sick. As Parkes has
remarked the evidence is insufficient that there had been no
communication with the coast. There have been other examples of sudden
outbreaks on ships, as on a Dutch frigate in the harbor of Mangkassar,
where 144 men out of 340 took sick in a few days (1856); on the Canopus
(1837) in the harbor of Plymouth, where on the 15th of February
three-fourths of the men took sick with influenza.”
Garvie, in reporting his personal experiences with influenza in 1918 in
an industrial area in England, experiences not based on statistical
study, concludes that there are two types of cases, the sporadic case
which occurs mainly among the wage-earning members of the family and has
little tendency to affect other members of the household, and second,
the type of case where a large number of individuals in the household
are affected. He called this the “household wave.” If we interpret him
aright he really means that there are either single or multiple cases,
and that the single cases are more apt to occur in the wage-earner, the
individual who is more exposed on the outside of the household. He also
believes that the household wave is more severe in character than the
so-called sporadic case, and is accompanied by a greater number of
complications.
Armstrong, in his survey in Framingham, examined influenza
convalescents. He found that of these 10 per cent. were in families in
which no other cases had developed, and 87 per cent. were in families
where one or more additional cases had occurred. In three per cent.
information was lacking.
It is important in studying the literature on this subject to
distinguish between definitely established fact and less definite
description. Thus one is still left in some doubt when one reads in a
London letter in the Journal of the American Medical Association for
1915 concerning the epidemic in London at that time that, “whenever it
has seized an individual it has usually run through the entire
household. Whole offices have succumbed.”
_The first case in the family._—Chart XXVII shows clearly that in both
epidemics in our experience the wage-earner was much more frequently the
first case in a family than was any other occupation. The individuals
whose occupations kept them at home were second. Infants, as was to be
expected, were recorded as being “first case” in the smallest number of
instances.
In 1889 the distribution was practically the same. Parsons found that
out of 125 households the first case was a bread-winner in 96; a
housekeeper in nine; a child at school in thirteen; a child not at
school in two families. In the last five families the first case was in
adults, occupation not given. This order is identical with our own.
Neither our own observations nor those of Parsons consider the relative
proportions of wage earners in the population as a whole. The results
are nevertheless suggestive.
H. F. Vaughan reached comparable results for the 1920 epidemic in
Detroit. During the first few weeks the age groups from 20 to 29 showed
a relatively much more frequent influenza incidence than did children up
to ten years. In later weeks of the epidemic there was a relative
increase in the incidence among children and decrease among young
adults. He concluded that the disease first attacks the young adult and
from this group it extends into the home.
In the Local Government Board Report for 1891, H. H. Murphy
distinguishes three groups or ways in which the disease may be brought
into the family. The examples will be found to be characteristic for any
epidemic and for any country:
_Group A._—Cases of single exposure.
“Household 1.—Mr. Q. goes to London daily. Was ill with influenza on
December 25th. No other case in this house till January 15th.
“Household 2.—Mrs. A. called on Mr. Q. on December 31st, and had a few
minutes’ conversation with him. She was taken ill on January 3d. There
was a Christmas family gathering at this house, and this is how the
other members were affected: Mr. B., January 6th; Miss C., Mrs. D., and
Master D., January 8th; Mr. J., January 10th; Mr. H., January 11th.
CHART XXVII.
[Illustration: Occupational distribution of first cases in each
household]
“Household 3.—Miss M. went to a party January 3d. She had a few minutes’
conversation with a young lady who said she was suffering from
influenza. Miss M. had a characteristic attack on the 6th of January.
“Household 4.—Mr. G. goes to London daily; taken ill January 5th. Mrs.
N. visited him for a short time on January 5th, and was taken ill
January 10th.”
_Group B._—Where disease was brought from a distance into a previously
healthy household.
“Household 8.—Mrs. R. G., living in the north of London, came here on a
visit December 17th. On the 19th she was taken ill with influenza, the
first case that I knew of in this neighborhood. Mr. C. G., on the 23d,
servant on the 26th, Mrs. G. 31st, and Mr. G. January 9th.
“Household 9.—Mr. I. lives at his business place in London, taken ill
December 20th with influenza. His family reside here. Boy C. visited his
father for a few days, and came back ill on January 4th. The other
members of the family were attacked as follows: Baby, 8th; Mrs. and boy,
12th; boy, 18th, girl, 22d; girl 25th.
“Household 10.—Master K. stayed a few days with some friends in London.
They had been ill with influenza. Returning home on December 31st he was
taken ill. Four brothers and sisters ill on the 2d January, Mr. K. on
3d, child and two servants on the 5th, Mrs. K. on the 7th.”
_Group C._—Where the source of infection could not be determined or was
local.
“Household 28.—Mrs. D. (who thinks she got it shopping) was taken ill 2d
January, her daughter on the 5th, and Mr. D. on 6th.
“Household 29.—Mrs. L. (who thinks she got it shopping), aged 80, had
influenza badly in 1847; similar symptoms, but much milder, on January
6, 1890; Miss L. was attacked on the 10th, and servant on the 17th.
_Note._—A former attack did not confer immunity after forty-three years.
“Household 30.—Mrs. B. (who thinks she got it out at work) taken ill 9th
January, and her child on the 11th.”
In Murphy’s complete list, one of the most frequent remarks is, Mr.
Blank goes to London daily. Or, Miss Blank, absent on a visit, was taken
ill with influenza and returned home.
Again, in 1890, Dr. Bruce Low studied the development of influenza at
East Keal, a town of 300 inhabitants. We quote in part his description:
“The following is believed to have been the commencement of the
outbreak, and for these facts I am indebted to Dr. Francis Walker,
Medical Officer of Health, Spilsby, R. S. D. Mrs. N., residing at East
Keal Hall, went to London (Forest Hill) on a visit on November 11th. She
visited Barnum’s Show on November 13th. She became ill on the night of
the 14th. Her symptoms were those of a cold, attended with sore throat.
No one else so far as she knew was ill in this way in the house before
her. She left Forest Hill on November 16th, still feeling very unwell,
and went to stay with friends at Kensington. She was too ill to return
home till November 23d, at which time she was still feeling very weak.
She heard from Forest Hill that, directly after she left one of the
inmates of the house where she had been visiting fell ill with symptoms
similar to her own. Within a few days, probably about the 27th of
November (the exact date is not fixed), of her return home, her son,
aged four, became unwell with what appeared to be an ordinary cold, but
the child had epistaxis; he soon recovered, but during the next
fortnight the four servants in the house were ill with what were said to
be ‘colds,’ one of them also had epistaxis. On January 2d another son,
aged six, was ill with ‘cold’ for a few days; he went out and had a
relapse, which compelled him to stay in the house for another week.
“On January 3d, Mrs. N. again fell ill with ‘a bad cold,’ attended with
headache, backache and epistaxis. She was in bed two days and felt
miserable and prostrate for more than a week after. On January 5th, Mr.
N., her husband, had headache, backache, and general soreness ‘all
over.’ On January 10th, the boy, aged four, who was first attacked after
his mother’s return from London, again became ill, his symptoms being
the same as before. The only other remaining member of the family who
had managed to escape an attack of ‘cold’ up to this date, was said to
have felt ill the day the boy had his second attack; but the illness of
this individual was slight, and only caused suffering for one night.
Thus between the return of the mother on November 23d and January 10th
all the inmates of this house, nine in number, had an attack of illness,
evidently of the same nature. A boy who works in Mr. N.’s yard was taken
ill with influenza about the end of November. He lives in the village.
After his illness his four brothers also were ill. Dr. Walker says that
‘about the end of November’ cases of like illness were beginning to crop
up in East Keal. Mrs. W., the wife of the village grocer and baker, who
waited on customers in the shop and never left the shop or house, was
taken ill on the afternoon of November 30th. Next morning, December 1st,
her husband and six children were all attacked in the same way with what
is now recognized to have been marked influenza. The only inmate of the
house who escaped was a youth employed to deliver bread and groceries in
a cart in the neighboring village.”
Leichtenstern relates that a physician traveling from Berlin on the 10th
of December became sick in his home town, Elgesburg, on the 8th of
December, but he made several visits and a few days later those people
seen by him fell sick, while otherwise there were no cases of influenza
in the town or its neighborhood. These cases would probably have fallen
in Group C., of Murphy’s classification.
_Intimacy of family contact._—We have been able to discover in a
representative number of families in which influenza has occurred, not
only what individuals slept in the various rooms of the household, but
also what individuals slept in the same bed with influenza cases. We
can, therefore, study for the 1920 epidemic three degrees of contact;
contact by sleeping with a case of influenza; by sleeping in the same
room but a different bed; and general contact by being in the family,
but sleeping in another room. For brevity we designate these,
“_sleeping_,” “_room_” and “_family_” _contact_. We have established
similar information for 1918, after eliminating families in which deaths
or births or other additions or losses had occurred during or subsequent
to the 1918 pandemic, in which there has been a change of address, in
which the cases are so widely separated that we have designated them
_unrelated_, and finally, those families in which the information has
been insufficient. With the remaining we have assumed that the
distribution within the household has been the same in both epidemics.
Statistics are available on 1,734 individuals who in 1918 were exposed
to a prior case in the family. Of these, 462 developed influenza and
1,272 did not. 26.6 per cent. of exposed individuals in families
contracted influenza, without respect to the degree of exposure.
═════════════════╤═════════════════╤═════════════════╤═════════════════
Intimacy of │ Number so │Number infected. │ Per cent.
contact. │ exposed. │ │ infected.
─────────────────┼─────────────────┼─────────────────┼─────────────────
“Sleeping” │ 360│ 166│ 45.2
“Room” │ 303│ 59│ 19.5
“Family” │ 1,064│ 273│ 22.3
─────────────────┴─────────────────┴─────────────────┴─────────────────
45.2 per cent. of individuals sleeping with cases of influenza in 1918
contracted the disease; 19.5 per cent. of those sleeping in the same
room, but different beds did so; 22.3 per cent. of those living in the
same family, but sleeping in other rooms contracted the disease.
_Sleeping contact is more productive of influenza than are the less
intimate forms._
Throughout this study the fact that there are multiple possible sources
of infection both outside and often within the family complicates the
picture.
The results for 1920 are similar. Here, 30.0 per cent. of all
individuals sleeping with cases of influenza contracted the disease,
17.7 per cent. of room exposures contracted it, while but 11.5 per cent.
of family exposures were attacked.
Four hundred and sixty-three or 29.1 per cent. of the total of 2,193
individuals exposed in 1920 had had the disease in the 1918 pandemic.
Did they show by reason of any immunity a lower attack rate for the same
degree of exposure than other individuals in 1920?
═══════════════════════╤═══════════════════════╤═══════════════════════
│ Per cent. of exposed │Per cent. of those who
Type of exposure in │individuals who had had│had not had a previous
1920. │ influenza in 1918–19 │ attack, and who on
│ and who contracted it │ exposure contracted
│ again, per cent. │ influenza, per cent.
───────────────────────┼───────────────────────┼───────────────────────
“Sleeping” │ 27.0│ 31.0
“Room” │ 18.3│ 17.6
“Family” │ 12.0│ 11.2
───────────────────────┴───────────────────────┴───────────────────────
_On the whole there is no evidence of protection afforded by a previous
attack._—Individuals who had had the disease before succumbed to a
second attack in the same proportion as those who had not previously had
influenza.
_Recurrent cases._—In certain families there were individuals who had
had influenza during both the 1918 and 1920 epidemics. Were these
recurrent cases the first ones to occur in the family, or did they, as a
rule, follow other cases in the same household? We have records of 236
recurrent cases in which we know the order of occurrence of the various
cases in the family. Out of this total number 57 were the initial cases
in the household. One hundred and nineteen were the only cases occurring
in the family. Therefore 176 or 74 per cent. of the total number of
recurrent cases were either the first or the only cases in the family.
Sixteen recurrent cases followed between other cases and 44 occurred as
the last of a series of two or more in the household.
SECTION V.
IMMUNITY.
Opinions of all observers who have studied in detail the question of
immunity in influenza are remarkedly in accord. The conclusions reached
by Parkes in 1876 are valid today, and form as excellent an abstract of
our present knowledge as any produced since his time. “There is some
discrepancy of evidence, but, on the whole, it seems clear that, while
persons seldom have a second attack in the same epidemic (though even
this may occur), an attack in one does not protect against a subsequent
epidemic. Indeed, it has been supposed rather to render the body more
liable.”
In 1890, Abbott wrote: “There is but little if any evidence in support
of the protective power of one attack to confer immunity against a
second; and hence adults are not exempt, as they usually are in
epidemics of scarlet fever or other exanthemata; so that the proportion
of adults to children attacked in an epidemic is necessarily greater
than that which is observed in epidemics of other infectious diseases.”
Parsons made somewhat similar observations: “One attack of influenza
does not seem to be protective against another; the disease in this
respect resembling diphtheria, erysipelas, and cholera rather than
smallpox, measles, or whooping cough. The duration of the epidemic in a
locality is so short that it is difficult to distinguish between second
attacks properly so-called, and relapses, which are frequent enough. A
case is recorded in the ‘British Medical Journal’ of February 15, 1890,
in which a patient who had suffered from influenza in France in
December, 1889, had another attack in England in January, 1890. It was
noticed in 1837 that many persons suffered from influenza who had had
the disease during the previous epidemic in 1834. The shortness of the
interval between these two epidemics, as compared with that between 1848
and 1889, seems to show that the periodical return of the disease in an
epidemic form does not depend upon the accumulation in the interval of
susceptible individuals unprotected against the disease by a previous
attack. If one attack afforded protection against another a large
proportion of the population in 1837 must have been protected, yet an
epidemic occurred, and on the other hand for many years before 1889 a
large majority of the population must have been unprotected by a
previous attack, yet the epidemic did not recur.
“The persons now living who passed through the disease in 1847 are of
course comparatively few, but such persons have not been exempt from the
present epidemic.
“I should be inclined to attribute the short duration of the influenza
epidemic in a locality to the establishment of a tolerance for the
specific poison among the persons exposed to it, similar to the
tolerance for dust possessed by workmen in rag factories, as mentioned,
but which is soon lost on their ceasing to be exposed to it, rather than
to a true immunity being established.
“Relapses in influenza are of frequent occurrence; they occurred in 9.2
per cent. of the cases at the Morningside Asylum, Edinburgh, and in some
cases indeed a second relapse has been recorded. The time at which the
relapse occurs is usually from a week to a fortnight after the primary
attack, and it can often be distinctly traced to an exposure to cold, or
return to work before complete recovery. The symptoms of the relapse are
similar to those of the primary attack, except that they are commonly
more severe.”
In his report of 1893, Parsons goes into the subject of recurrent
attacks in individuals in greater detail. He quotes several
communications received from various physicians and health officers.
These opinions differ, some believing that the disease predisposes to
another attack; others, that there is no effect on the incidence in
recurring epidemics; and still others believing that there is a small
amount of acquired immunity. The communications are not based upon
statistical evidence. He does find, however, an opportunity for
statistical study in the industrial schools at Swinton near Manchester:
“These schools were severely affected in March, 1890, 171 out of 589
children having suffered, or 29 per cent. In the first epidemic of 1891
they were again affected, but to a less extent, only 35 cases occurring.
At that time there were in the schools 449 children who had been there
at the time of the former epidemic. Of these 150 had had influenza in
1890 and 4 of them had it again, or 2.6 per cent.; 299 had escaped
influenza in 1890 and 17 of these had it now, or 5.7 per cent. Thus, so
far as these figures go, an attack of influenza confers a degree of
protection which after the lapse of a year diminishes by one-half the
liability to contract the disease.”
Leichtenstern, like Parsons, recognizes the importance of distinguishing
between relapses and recurrent cases. Relapses in influenza are not
common. They usually occur after the patient is up, and about when he is
ready to leave the house. These are not recurrent cases, but in the
epidemics in the years following 1889 there were plenty of well
substantiated cases of recurrent typical influenza in the same
individual and some times even in entire families. During the 1889
epidemic, as during the 1918 epidemic it has been suggested by various
observers that the apparent immunity among the very old was due to
immunity developed as the result of previous epidemics, such as that of
1837, 1847 and 1857. Leichtenstern has collected the statistics from
five different hospitals in which 8, 32, 35, 24, and 24 per cent. of
individuals attacked in 1891–92 had already had the disease in 1889.
Allbutt in 1905 remarked that whereas he had previously believed that
immunity to influenza usually persists as long as six months, many cases
had recently been brought to his notice where such an interval seemed
improbable, where the succeeding attack was probably not a relapse but a
new infection. He has seen two attacks apparently separate occurring in
the same individual within two months. In the same year Moore wrote that
influenza shows a decided tendency to relapse, a feature to which the
indirect fatality of the disease is in great measure due. “So far from
establishing immunity, an attack of this malady seems to render an
individual more liable to contract the disease upon any future exposure
to its contagion.”
Again West, in the same year wrote, “From our present experience we must
conclude that influenza is infectious in a very high degree indeed, and
that the protection afforded by an attack is imperfect, or of very short
duration. Indeed, one attack seems actually to predispose, after a time
to another, or, to put it differently, that the positive phase of
protection is followed by a negative phase, in which the individual
seems rather more than less liable to succumb to infection if exposed to
it. It seems more likely that an individual may never have influenza at
all than that, having had it once, he should never have it again. Some,
indeed, seem to offer so little resistance that they develop it
regularly once or twice a year.”
We have previously shown that the relatively low morbidity among the
older age groups in 1918 is not satisfactorily explained by an immunity
lasting over from the epidemic of 1889–93. If such were the case the
change in mortality rate in large groups of individuals would occur at
the age of 30.
During the autumn of 1918 many observations were made, particularly in
the armies, of light incidence in those groups or communities that had
had the disease in mild form in the spring of the same year.
Parsons quotes many similar observations for the period 1890–1893.
V. C. Vaughan relates that at Camp Shelby, Mississippi, “there was in
April a division of troops numbering about 26,000. An epidemic of mild
influenza struck this camp in April, 1918, and within ten days there
were about 2,000 cases. This included not only those who were sent to
the hospitals, but also those who were cared for in barracks.
“This was the only division that remained in this country without change
of station from April until the fall of 1918.
“During the summer this camp received 20,000 recruits. In October, 1918,
the virulent form of influenza struck this camp. It confined itself
almost exclusively to the recruits of the summer and scarcely touched
the men who had lived through the epidemic of April. Not only the 2,000
who had the disease in April, but the 24,000 who apparently were not
affected escaped the fall epidemic. It appears from this that the mild
form of influenza of April gave a marked degree of immunity against the
virulent form in October. There is another observation which points the
same way. Looking over the statistics of the fall epidemic in cities in
the United States we find that certain cities had a low death rate,
while others had a relatively high rate. Among those cities which had a
low death rate we will mention Atlanta, Ga.; Kansas City, Mo.; Detroit,
Mich., and Columbus, Ohio. Going to the spring records of these cities
we find that in all of them in March and April of 1918 there was an
unusually high death rate from pneumonia and undoubtedly in these cities
at that time there was a relatively mild epidemic of influenza. In this
way I am inclined to account for the relatively low death rate in these
cities in the fall of 1918. I make no claim that this and other
instances of a similar kind prove that the mild and virulent forms of
influenza are manifestations of the same disease, but I do hold that the
evidence points that way.”
Lemierre and Raymond report the following observation in favor of the
development of a certain degree of immunity in the French troops in
April, 1918. After an intervening period of quiescence there was a
manifest recrudescence at the end of August. Many military formations
were attacked during both periods. This was true especially in three
groups of an artillery regiment under their observation. In the first of
these groups there were three cases in April, while 114 men were
attacked in August. In the third group there were 100 cases in April and
only 3 in August. In the second group there were 20 cases in April and
59 in August. Their report does not state the total number of
individuals in each of the three groups.
Joltrain and Baufle discuss the flaring up of the epidemic in October,
and relate that a troop of soldiers from Indo-China nearly all had the
disease lightly in the spring, but when the disease appeared again it
spared this troop completely, while troops and civilians around
developed it in a severe form.
Gibbon writes: “During the last three waves of the epidemic I had to
deal with the sick of 2,000 troops, and during this time we treated in
hospital over 400 cases. No cases admitted in June, July or August were
re-admitted in October, November, or December, and no cases admitted in
either of these two periods were re-admitted in February this year.
Unfortunately I am unable to trace the cases into March as the troops
were changed.”
Dopter reports recurrent epidemics of influenza in a French Army
Division in 1918. The division, of which he was surgeon, was one of the
first to contract la grippe at the time of its first appearance in the
zone of the armies at the end of April, 1918. At this time nearly the
entire body of infantry troops was attacked. The disease was mild, and
without complications. The regiment of artillery escaped nearly
entirely. This epidemic subsided very rapidly, and by the end of May it
had entirely disappeared. Early in August a group of heavy artillery was
attached to the division, bringing influenza with it. Then a few cases
appeared in the regiment of light artillery which had hitherto escaped.
By the end of August all three groups of this regiment had been
attacked. In this second epidemic the men who had come through the first
unattacked were very severely ill in the second.
With rare exceptions those sick in the first did not contract it again.
Dopter notes that in the battery the most severely affected in August,
of which the effectives were reduced almost to none, only those men were
considered well enough for duty who had had influenza in the first
period. They escaped the second in spite of the close contact with their
comrades. The infantry regiments, which were in close association with
the artillery, remained unaffected.
Finally, toward the middle of September new troops were attached to the
division, in view of an imminent attack by the enemy. These troops,
coming from neighboring and distant formations were suffering at the
time from grip, and continued to have the disease in the new sector.
Again, those attacked in May passed without damage through this new
epidemic. Among them there were only rare isolated mild cases. The
recurrences made only 1.6 per cent. of the total incidence.
Opie and his associates found that at Camp Funston after the first wave
of influenza in March and April, 1918, the succeeding waves usually
affected only new recruits, who had not been in camp during previous
waves.
In Calcutta influenza appeared as an epidemic in July, 1918, and in
November, 1918. During the first quarter of 1919, at Calcutta as
elsewhere, many cases were still recurring. Malone investigated the
incidence of the disease in three institutions of Calcutta: He found
that in the Gourepore Jute Mills where the population was practically
stationary, those individuals who were attacked in July, 1918, passed
through two later epidemics, in December, 1918, and February, 1919,
without contracting the disease a second time, in spite of intimate
contact with infected persons. The same was true according to Malone in
the Alipore Central Jail and the Presidency Jail in Calcutta. He
believes that his evidence strongly suggests an immunity lasting for at
least nine months.
Dunlop found that Glasgow had a mild epidemic in the month of May, 1918,
in which the death rate rose from 14.1 to 20.1. There is no record of
any similar outbreak in Edinburgh. In the July epidemic the Glasgow
death rate rose from 11.7 to 15.9, while the Edinburgh death rate went
from 11.3 to 18.0, a higher increase. In the October-November epidemic
the Glasgow rate rose from 11.0 to 38.4, while the Edinburgh rate went
from 10.8 to 46.2. In the February-March epidemic the Glasgow rate rose
from 14.9 to 48.3, and the Edinburgh rate from 18.9 to 52.1 In the July
and October epidemics Edinburgh showed a greater increase in death rate,
while in February, 1919, the increase in the two cities was the same.
However, in this case probably other factors play a part. Also, we must
remember that here we are dealing with death rates, not with incidence
rates.
The Inspector General of Health, in Spain, reported in January, 1918,
that those cities which had the disease in May, 1918, suffered lightly
in the autumn of that year, while others of the large cities which had
been spared in the first invasion suffered most in the second.
Maillard and Brune report an epidemic of influenza in an epileptic
colony. There were 32 deaths among the 63 cases. None of the inmates of
the hospital who had influenza during the June epidemic contracted it
anew during the October wave.
Ovazza records that although a number of persons contracted the
influenza anew on its return in the fall after having had it in the
spring, yet the return cases were strikingly mild, and always free from
complications.
Barthélemy describes the successive waves of epidemic influenza at
Bizerte. He found that the doctors and nurses who had been through the
first epidemic did not develop influenza in the second one a few months
later, even though they came in the closest contact with the patients.
Hamilton and Leonard have studied two successive outbreaks due to lapses
in a rigid quarantine in an institution of 180 girls between 12 and 18
years of age. The girls were distributed through six cottages. In the
first epidemic November, 1918, 76 girls contracted the disease, at which
time it was entirely limited to the occupants of cottages 2, 3, and 4.
The second outbreak occurred in January, 1919, when 82 took ill. Only
five of these were located in cottages 2 and 4, the remainder being in
1, 5 and 6. No cases occurred in cottage 3 during the second spread.
Both epidemics lasted a little under two weeks. Those who had suffered
in the first spread appeared to be immune to the second. There were no
recurrences. The second epidemic was much milder in character. Twelve
per cent. of the total remained well throughout both epidemics.
Dr. Niven, in his study of 1,021 households previously described, found
that 105 families suffered in both the summer and autumn 1918 epidemics.
“They comprised a population of 565 persons, of whom 205 suffered in
summer and 360 escaped. In the autumn epidemic eighty-two (or 40 per
cent.) of the presumably ‘protected’ persons succumbed again, whereas
only 120 (or 33 per cent.) of the ‘unprotected’ suffered. Of the former,
however, only one died, while five of the latter terminated fatally.
These are interesting figures. If they are borne out by subsequent
inquiry, they are somewhat difficult of explanation. The persistent
susceptibility to the primary disease and yet comparative immunity from
the fatal sequel, would seem to suggest a dual infection, against one
element of which the body is able to produce protection, while it is
unable to do so against the other.”
Frost made a canvass of 33,776 individuals in Baltimore between November
20th and December 11th, 1918. The same population was again covered in
January, 1919, to determine the extent of the recrudescence reported in
December. Among 32,600 people, 724 cases of influenza had occurred in
the interval since the first survey. Of this number only 26 or 3.6 per
cent. were definitely cases of second attack in the same individual.
Even in these cases the diagnosis is necessarily uncertain. Frost says
that considering that 23 per cent. of the population had had influenza
prior to December 11th, the proportion of second attacks should have
been much greater if no immunity had been acquired. A second canvas in
San Francisco gave generally corresponding results.
Our own experience was quite similar. We have divided the whole period
from March, 1918 to March, 1920, into two portions separated at August
1, 1919. In the first portion we have knowledge of but four individuals
suffering from what the records would indicate to be two genuine attacks
of influenza. Similarly, five individuals appeared to have had two
attacks within the second interval. These are to be contrasted with a
total incidence in the fall and winter of 1918–1919 of 1,971 cases, and
in the winter of 1919–20, of 965 cases. Among the total nine individuals
the intervals between attacks varied from 26 days to five months. All
except one had an interval of one month or over. In two cases there was
an interval of one month, in one an interval of two months, in two an
interval of three months, in one of four months, and in one of five
months. None of the four individuals who had two attacks in the first
group of months had a subsequent attack in the second. On the contrary,
two of the five suffering two attacks in the second group of months had
one previous attack in the first. The second attack, following the first
by a relatively short interval tended to be milder than the first. In
five out of the entire nine the second attack was milder, in two it was
of the same degree of severity, and in only two was it more severe than
the first. The order of severity in the two individuals having three
attacks each was, in the first, severe, mild, severe; in the second,
severe, average, average.
Zinsser makes the following remark: “The writer himself believes that he
had three attacks during the last epidemic. The first and second were
mild ones and the third complicated and therefore severe; and
innumerable others with whom he has spoken have had similar
experiences.”
From a consideration of these reports by divers authorities it is
reasonable to conclude that for a period of a few months at least, one
attack of influenza protects against a second. As is to be expected,
this relative immunity is not of constant duration in all individuals.
If there were no lessened susceptibility following an attack we would be
faced with the phenomenon of individuals succumbing time and again to
rapidly successive attacks of the disease. Such a circumstance is very
rare.
It is difficult to determine how long even on an average this relative
protection or insusceptibility lasts. Evidence is fairly uniform in
indicating a protection of at least three months. Usually it is longer.
There seems to be some basis for the supposition that a group of
individuals exposed to an attack of influenza displays within the
succeeding three months, or slightly longer, a relative general group
immunity. If the group be considered as a whole those even who did not
develop the disease previously appear to have become less susceptible.
Whether we can ascribe this to the individual as a unit, or whether we
must explain it by some assumption with the community as a unit, is
uncertain. Is it because the exposed individuals in the group who did
not contract the disease have individually received some of the virus
into their systems and developed a certain immunity, or is it a much
more complex phenomenon depending on greater relative dispersion of
susceptibles and other communal factors?
We may place the minimum period of “immunity” at from three to five
months, rarely less. There is additional evidence by which we may
delimit fairly closely the other extreme, that time at which individuals
considered as a group no longer manifest increased resistance to the
disease.
The author found that 19.17 per cent. of his population contracted
influenza in 1918, and 9.55 per cent. contracted the disease in 1920.
Two hundred and forty individuals, or 2.4 per cent. of the entire
population developed the disease in both epidemics. Out of 1,971
individuals having the disease in the 1918 spread, 240, or 12.1 per
cent. recurred in 1920. This is to be compared with the total 1920
incidence of 9.55 per cent. More correctly we should separate the 1920
cases into two groups, those who had and who had not had influenza
previously. The former group, 240 individuals, constitute as just
stated, 12.1 per cent. of all who had had the disease previously. The
second group, 715 individuals, constitute 8.9 per cent. of the 8,034 who
had not had the disease in 1918–19.
From these results we must conclude that _a previous attack contracted
on an average of from 10 to 17 months before, conferred no protection
whatever against a second attack. On the contrary, the attack rate was
slightly higher in this group than in those who had not previously had
the disease._
Yet another evidence of the insignificant part played by any immunity in
the occurrence of influenza in individuals in 1920 is indicated by our
series of 319 infants living in 1920 but who had not been born during
the 1918 spread and who were presumably not immune to the disease. We
have not investigated whether the mothers had had the disease in 1918.
From among these 319 infants, thirty or 10 per cent., developed the
disease in 1920. This is practically the same percentage as for the
population at large.
These findings also correspond with our previously recorded conclusion
made after studying the disease incidence with three increasing degrees
of exposure, _sleep_, _room_ and _family_ (page 198).
TABLE IX.
_Comparison of the severity of the first and second attacks in
individuals contracting influenza in 1918–19 and again in 1920._
═════════════════════════════╤═════════════╤═════════════╤═════════════
Severity. │No. of cases.│ Comparison. │No. of cases.
──────────────┬──────────────┼─────────────┼─────────────┼─────────────
1918–19. │ 1920. │ „ │ „ │ „
──────────────┼──────────────┼─────────────┼─────────────┼─────────────
Average │Mild │ 43│Second attack│ 132
│ │ │ milder │
Severe │Mild │ 50│ „ │ „
Severe │Average │ 39│ „ │ „
──────────────┼──────────────┼─────────────┼─────────────┼─────────────
Mild │Mild │ 30│Both of equal│ 72
│ │ │ severity │
Average │Average │ 22│ „ │ „
Severe │Severe │ 20│ „ │ „
──────────────┼──────────────┼─────────────┼─────────────┼─────────────
Mild │Average │ 13│ Second more │ 36
│ │ │ severe │
Mild │Severe │ 5│ „ │ „
Average │Severe │ 18│ „ │ „
──────────────┴──────────────┴─────────────┴─────────────┴─────────────
Altho we find no conclusive evidence of protection against recurrent
attacks, we do find (Table IX) that the second attack in the same
individual was usually milder. However, the 1920 epidemic as a whole was
milder, (Chart XVIII).
Zinsser quotes a letter from Frost in which the latter states that in
Baltimore those persons who were attacked during the 1918–19 epidemic
showed no relative immunity during the epidemic of 1920. This is not a
contradiction to the earlier Baltimore studies, since in that case the
interval between the epidemic waves was not more than about three
months.
Jordan and Sharp have obtained statistics regarding approximately 4,000
men at the Great Lakes Naval Training Station. The men’s statement
regarding previous influenza was accepted whenever the attack was said
to have occurred during the influenza period of 1918–1919, _i.e._, in
September, October, November, December, January, February and March. The
great majority were reported for the period of September to December.
Only a few cases were reported as occurring in March, and perhaps these
actually occurred somewhat earlier than the men recalled. A few cases
were accepted as influenza when reported as occurring in Europe during
July and August, 1918.
They found that 28.5 per cent. of 3,905 men had had the disease in 1918,
and that 22.6 per cent. were attacked in 1920. Of those who had the
disease in 1918–19, 21.2 per cent. had a repeated attack in 1920, while
of those who had not had a previous attack, 23.1 per cent. were attacked
in 1920.
A similar study among 2,472 men at Camp Grant showed that 15.8 per cent.
had had influenza in 1918–19, and 11.7 per cent. in 1920. Of those with
previous influenza history 15.6 per cent. had a repeated attack, while
of the remainder without previous history of influenza 10.9 per cent.
were attacked in 1920. They conclude that no marked immunity to
influenza exists 12 to 15 months after a previous attack, but that the
results do not show that some degree of immunity may not obtain at an
earlier period.
It is interesting while considering the subject of immunity to pay
particular attention to those who _did not_ develop the disease as well
as to those who did. In our series 70 per cent. of all individuals
escaped the disease in both epidemics. With some variation this figure
will hold for all communities. Or, again, among those who had the
disease in 1920, 75 per cent. _had not had it_ in the preceding waves.
Hall states that in Copenhagen at the Bispebjaerg Hospital, among the
500 patients with influenza in the four weeks early in 1920, 91.8 per
cent. _had not had_ the influenza during the 1918–19 epidemic. H. F.
Vaughan found in a review of 2,500 cases occurring in Detroit in
January, 1920, that _84 per cent. had never had_ the influenza before.
The true significance of these figures cannot be recognized, because we
are not informed as to the per cent. of these populations attacked in
1918–19.
We observed such a universal distribution of influenza during the
epidemic period that it is frequently assumed that all individuals are
exposed to the disease, that the virus must enter the body of all or
nearly all, and that it is due chiefly to a relative natural immunity
that some do not fall victims. Is this the actual state, or is it true
that the distribution of the virus is limited to about one-third of the
population and that practically all of those who are actually exposed
develop the disease? These are the two extremes; more probably the
actual state is somewhere between.
This question cannot be definitely answered, and yet it is one of
extreme importance, particularly with regard to prevention and combat of
the disease. How universally is the influenza virus distributed during
pandemics? What proportion of the population is actually exposed by
invasion with the virus? What proportion of actually exposed individuals
develops the disease? We will refer to this again when comparing
influenza with other infectious diseases, but it is of particular
interest now to review our individuals who were exposed by sleeping with
cases of influenza. Fifty-five per cent. of all individuals sleeping in
the same bed with cases of influenza in 1918 _did not_ contract clinical
influenza. Seventy per cent. of all individuals sleeping with influenza
cases in 1920 _did not_ contract the disease, in recognizable form.
Sixty-nine per cent. of all individuals in 1920 who had not had the
disease previously and who slept with cases _did not_ develop evidences
of the disease.
It is difficult to conceive of a degree of exposure much closer than
that of sleeping in the same bed with a sick individual. And yet it is
equally conceivable that many individuals sleeping in the same bed with
a patient were not penetrated by the virus of influenza. This does not
aid us in answering our question. We do not know whether the more
important factor is that of a natural immunity or that of absence of
actual invasion by the virus.
These results with sleeping contacts form an interesting link in the
chain of evidence started during 1918 by the U. S. Navy and Public
Health Service, and reported by Rosenau and by McCoy and others. These
experimenters working in Boston and in San Francisco carried out
inoculation experiments on human volunteers. The work in Boston, as
reported by Rosenau, was carried on with 100 volunteers from the Navy
between the ages of eighteen and thirty, most of them between eighteen
and twenty-five; all of them entirely well, and with the exception of a
few controls, none having experienced known attacks of influenza
previously. First, suspensions of thirteen different strains of
influenza bacilli, all from cases of influenza during the epidemic, were
sprayed into the nose, eyes and throat of nineteen volunteers. None of
them took sick. Next, secretions from the mouth, nose and throat and
bronchi of acute cases of influenza were collected, pooled, and without
filtration sprayed into each nostril, into the throat during
inspiration, and onto the conjunctiva of each of ten volunteers. None of
them took sick. Some of this same material was filtered through a
porcelain filter and administered in the same manner, with similar
results. One cubic centimeter of each type was administered to each
individual. The interval between the time of collection and time of
inoculation was then decreased to one hour and forty minutes, the
minimum time in which the material could be transferred from hospital to
experiment station. The same results were obtained. This time six cubic
centimeters were administered to each individual. Finally, transfer was
made directly with swabs from the nose, throat and nasopharynx of one
individual to another in nineteen cases. None developed the disease.
The next series of experiments consisted in an attempt to inoculate
volunteers with influenza by injecting into them 10 cc. of citrated
blood, which was the pooled collection from five cases of acute
influenza. Ten volunteers were inoculated. None took sick. Next, the
secretions from the upper respiratory tract of acute cases were injected
subcutaneously into ten volunteers, each receiving 3.5 cc. This material
was first put through a porcelain filter. None took ill. In an attempt
to reproduce the disease in imitation of nature, ten individuals were
exposed to cases of acute influenza in hospital wards. Each volunteer
was placed very near to the patient, shook hands with him, talked and
chatted with him, for five minutes, after which he received the
patient’s breath full in his face five times while he inhaled, and
finally the patient coughed five times directly into the subject’s face.
Each volunteer did this with each of ten different patients, all of them
acutely ill, none more than three days sick. No volunteers developed the
disease. All cases of influenza used throughout the period of these
experiments were typical acute cases selected from a distinct focus or
outbreak of the disease. Sometimes, for example, they would select four
or five typical cases from an epidemic in a school with a hundred cases.
In February, 1919, the experiments were continued at Portsmouth, where
the secretions were transferred direct from individual to individual. In
about thirty-six hours half of the number came down with streptococcus
sore throat, but not with influenza. One of the medical officers,
however, who had been very active in the experiments, and who had come
into intimate contact with the disease since early in October, but who
had not been inoculated, developed, during this experiment, typical
influenza. The explanation for these failures is not certain. The
experiments were started rather late after the onset of the epidemic,
and the volunteers may have developed some immunity, although they had
not developed the disease. Or, they may never have been susceptible.
McCoy made a similar series of experiments in San Francisco, using
volunteers who so far as known had not even been exposed to the
outbreak, also with negative results. However, many of these latter had
been “vaccinated against influenza” with a mixed vaccine.
Wahl and his co-workers found that the nasal application of a filtrate
from the pneumonic lung of an individual dead with typical
influenza-bronchopneumonia failed to call forth any abnormal symptoms in
human subjects. The application to the mucous membrane of the nares and
nasopharynx of five healthy men, who had been inoculated from four to
six weeks previously against influenza with a polyvalent influenza
vaccine, and of one uninoculated, of freshly prepared suspensions of
four different live strains of Bacillus influenzae, even in massive
doses failed to produce any abnormal symptoms. The implantation of
living suspensions of Bacillus influenzae produced no material
alteration besides the addition of the influenza bacillus itself. When
experimentally introduced into the nasopharynx of men the influenza
bacillus exists and multiplies for a considerable length of time, two
weeks or more. It apparently shows much resistance to the action of
dichloramin T.
SECTION VI.
INFLUENZA AND OTHER DISEASES.
_Influenza and tuberculosis._—Following the 1918 and 1920 epidemics of
influenza, there has arisen in the literature some controversy regarding
the effect, if any, of influenza on tuberculous individuals. This has
centered particularly on the question whether tuberculosis produces some
degree of immunity to influenza, and whether the latter, on the other
hand, predisposes either to the lighting up of a latent tuberculosis, or
to a new infection with the tubercle bacillus. Keen observers in the
field of tuberculosis who have had apparently equal opportunities to
study the effects of the pandemic differ radically in their conclusions.
The first mention of consumption following influenza was made in 1580 by
Thomas Short.
After the 1889–1893 epidemics, Leichtenstern recorded that the mortality
tables of all countries agree in showing considerable rise in the
mortality from pulmonary tuberculosis in influenza periods. The
clinicians of that time made the frequent observation that the course of
tuberculosis in the lungs is markedly and unfavorably influenced by grip
and its pneumonic complications. Latent quiescent cases often became
active, and healed and healing foci broke out anew. Afebrile cases were
changed to the hectic type and frequently hemoptysis was induced. In
London, during the height of the 1889 epidemic, the weekly death reports
from phthisis rose to double the average. The increase in death rate
during the epidemic period was not limited entirely to tuberculosis, but
there was almost a doubling of deaths due to all acute respiratory
infections. After the cessation of the epidemic, however, there was some
decrease in the general mortality, as well as in the mortality from
respiratory infections. This was especially true of deaths from
pulmonary tuberculosis, which decreased to such an extent that the total
mortality rate for the year for this disease was little greater than for
preceding years.
Similar observations have been made following the 1918 pandemic. Jordan
remarks that in New York City in 1918 during the two weeks of maximum
epidemic mortality, the deaths reported from pulmonary tuberculosis
numbered 430, as compared with 264 for the corresponding weeks of 1917.
Vaughan and Palmer found that the deaths from tuberculosis in the army
were higher in the autumn of 1918 than in the two previous four months’
periods, the death rate rising from 18 per 100,000 during the summer to
46 per 100,000 in the autumn. The rate for the same time of the
preceding year had been 15 per 100,000. They assume that the most
plausible explanation for this increase in deaths is that dormant and
incipient cases introduced into the army during the preceding year had
accumulated and possibly were hastened into the acute stage, both by the
duties of camp life, and the prevalence of the epidemic of grip and
pneumonia. Quite naturally there had been from the time of the first
assembling of troops an accumulation of tuberculous individuals,
inasmuch as such men were not discharged, but were kept in the army and
under Government control and supervision. Sir Arthur Newsholme in
reviewing the relationship between influenza and tuberculosis in England
concludes that many deaths from tuberculosis are undoubtedly hastened
during an influenza epidemic. Abbott wrote of the epidemic of 1889 in
Massachusetts that the chief diseases which followed in its train and
were intimately associated with it were bronchitis and pneumonia, and
that phthisis when already existing in the victim of the attack was
undoubtedly aggravated, and in many cases a fatal termination was
hastened. Baldwin says that influenza is a frequent and important agent
in bringing latent tuberculosis to life. “Allowing for mistakes in
diagnosis, influenza must be classed as an important exciting cause, if
not a true predisposition.”
In frank opposition to the foregoing authorities, Fishberg claims that
influenza has had no effect whatever on the course of tuberculosis. He
says that a large proportion of tuberculous patients under treatment in
New York City in 1918–1919 contracted the disease and not a single one
succumbed. This appears as rather an inclusive statement. He goes on to
say that some were in far advanced stages of the disease, with large
cavities in the lungs, and yet they passed through the acute symptoms
and recovered, the tuberculous process then pursuing its course as if no
complicating disease had affected them. He believes that the prognosis
was, if anything, better in those who suffered from tuberculosis or any
other chronic pulmonary disease, such as asthma, bronchitis, emphysema,
bronchiectasis, than in those in whom the lungs and bronchi had been
apparently in healthy condition. Fishberg observes that, instead of
lighting up the tuberculosis, the influenza runs a milder course than
when attacking healthy persons, and the old lung lesion remains in about
the same condition as could be expected if no complicating process had
attacked the patient. He says that authors who have asserted the
contrary have based their arguments mainly on the facts first, that many
tuberculous patients date the onset of their tuberculosis as concurrent
with an attack of influenza; that many patients suffering from phthisis
state that ever since an intercurrent attack of influenza the symptoms
of tuberculosis have become more pronounced; that the Pfeiffer bacillus
has been found quite frequently in the sputum of tuberculous patients,
especially that derived from pulmonary cavities; and finally that in
some countries it has been noted that during and soon after an epidemic
of influenza the mortality from tuberculosis was increased.
He believes that many of the conditions diagnosed as influenza have been
no more than ordinary colds, and that the average patient will call any
upper respiratory tract infection grip during or around the time of an
epidemic. He further believes that a misdiagnosis of tuberculosis is
frequently made in influenza convalescents who show some signs of
moisture in their lungs which does not clear up for some time, causing
doubt in the mind of the examiner, but which is not truly tuberculous in
origin. Fishberg cites P. J. Murphy, Hawes, Armstrong, McRae, and
Dickinson, as well as Geiber and Schlesinger, in Vienna, and Rickmann
and Ladeck in Germany, as having observed the same phenomenon of
relative insusceptibility of tuberculous patients and failure of
influenza to hasten the progress of tuberculosis. He also calls
attention to the low incidence of influenza in tuberculosis sanatoria,
but apparently compares this incidence with the incidence for the public
at large, and not with that in similar institutions devoted to the care
of invalids with diseases other than tuberculosis, or with other
institutions in general.
Amberson and Peters, as well as Minor, take sharp exception to the
statement of Fishberg, and the former have collected the evidence
against Fishberg’s view. They first point out that a comparison of the
incidence of 5.4 per cent. among hospitalized tuberculous patients at
Chicago cannot be compared with a much higher incidence of the epidemic
in the various military camps. As Heiser has pointed out, the mere
quartering of men in barracks seems to have a tendency to increase the
risk from acute respiratory diseases. Furthermore, the incidence at some
sanatoria was low, while at others it was high, nearly as high as for
the community at large. In Hawes’ report of the epidemic among the
Massachusetts sanatoria, Lakeville had escaped entirely, while Rutland
which consisted chiefly of ambulatory cases, less easily controlled, had
an influenza incidence of 18.3 per cent. among the patients, and 21.3
per cent. among the employees. At Montefiore Home, the proportion of
tuberculous patients and employees contracting the infection was
practically the same as among the nontuberculous employees, and about
the same percentage of both groups developed evidence of
bronchopneumonia.
Still another fallacy in the comparison of incidence in institutions and
the like is proven by the work done by Jordan, Reed and Fink, who found
that in the various Chicago telephone exchanges the attack rate varied
from five per cent. to twenty-seven per cent., although the working
conditions were approximately the same. The attack rate in one section
of the students’ army training corps in Chicago was 3.9 per cent., while
in another section particularly exposed to infection it was 39.8 per
cent. Similarly Frost found the incidence in Louisville, Kentucky, to be
15 per cent., and in San Antonio, Texas, 53.3 per cent. All these
figures show the difficulty of comparing rates for various institutions
and various groups of individuals. Although Fishberg quoted Rickmann in
support of his contention that influenza has no effect whatever upon
tuberculosis, Amberson and Peters used his work in support of their
contention, and call attention to the fact that in thirty out of forty
tuberculous persons reported by him who had contracted the grip, the
attack did not produce any aggravation of the lung condition. Presumably
it did in the other ten. If even 25 per cent. of tuberculous patients
who contract influenza have their pulmonary condition aggravated, this
should be regarded as a notable number. According to Stivelman, 11.4 per
cent. of tuberculous influenza cases died at Montefiore Home. In a
survey of convalescents from the Loomis Sanatorium, Amberson and Peters
found that seventy had contracted influenza, or 5.7 per cent. of the
number surveyed, and that 11.4 per cent. of these had had relapses of
their pulmonary condition, apparently due to the acute disease, while
22.9 per cent. had died from the intercurrent infection. 2.8 per cent.
were deaths due to tuberculosis after convalescence from the influenza.
Tubercle bacilli have been found in the sputa of convalescent grip
patients, whose sputa had previously been negative, by Amberson and
Peters, as well as by Berghoff, at Camp Grant. The latter found that 50
per cent. of his cases showed a reactivation and a positive sputum after
an attack of influenza.
Amberson and Peters agree with Fishberg in the observation that there
has been no increase in the general mortality from tuberculosis within
the recent months, and suggest as an explanation the possibility that
during the epidemic enough of the old cases were carried off to account
for a temporary lull until new cases developed, or others had time to
reach later stages of the disease. As we have previously remarked,
Leichtenstern observed this same phenomenon following the 1889–1890
epidemic.
The state of our knowledge of influenza and tuberculosis is considerably
clouded by divergent opinions such as those quoted above. To further
complicate the picture, there are other authors who assume a middle
ground and believe that there is some truth in both lines of contention.
Thus, Amelung believes that the morbidity among patients with pulmonary
tuberculosis is slight, and that the grip takes a milder course in such
patients than in the nontuberculous, unless the disease is far advanced,
but that pulmonary tuberculosis may and sometimes does follow the
disease in patients whose lungs were previously sound, and that in the
last mentioned cases the prognosis is relatively bad. Peck finds that in
some tuberculous patients the disease has been aggravated, but in the
majority the intercurrent influenza did not appear to have been the
causative factor in the acute exacerbation of the tuberculosis.
Debré and Jacquet have reviewed the European literature on the subject
pro and con, and though they admit that there are exceptions, as at
l’hôpital Tenon, where, in a barracks reserved entirely for female
tuberculosis patients there was a veritable epidemic of grip, 29 per
cent. of the twenty-eight being attacked in a few days; and at the
sanatorium de La Tronche, where 83 per cent. took ill between the 25th
of September and the 20th of October; they conclude that as a rule
tuberculous individuals are less heavily attacked by the influenza than
are the nontuberculous. As they suggest, the first explanation that
comes to mind is that the tuberculous are isolated in the hospitals
where general hygienic conditions are good, but we have all seen other
institutions, hospitals, etc., in which the inmates were not spared as
they were in tuberculosis hospitals. Furthermore, in certain sanatoria,
such as the sanatorium of the Côte Saint-André, and Bligny, and several
German sanatoria, the proportion of tuberculous individuals attacked was
very much less than that of the professional attendants, the physicians
and nurses. Again, where cases have occurred in these hospitals, and
little precaution was taken to prevent its spread, very few other
individuals took sick. Finally, many have noted the infrequency of the
disease even in those tuberculous individuals who were living at home.
It has been suggested that rest in bed from the beginning of the attack
explained the mildness, or that the immunity resulting from the
infection with pneumococcus, streptococcus, etc., in tuberculous
individuals explained the absence of pulmonary complications. Marfan,
who observed this same phenomenon in 1890, suggested that it might be
due to a refractory state of the tubercle bacillus against the virus of
influenza. Debré and Jacquet conclude that none of these explanations is
satisfactory.
Having concluded that tuberculosis does protect in some measure against
influenza, Debré and Jacquet next discuss whether the latter has
increased the severity of tuberculosis in the subjects who were already
tuberculous. They review the literature and make their conclusions, not
from statistical records, but from general observations. They consider
first those cases of phthisis which are open cases when attacked, and
second, latent tuberculosis. Their conclusion concerning the first group
is that influenza does not have any effect on the rapidity of evolution
of the tuberculous process, except in very rare instances, such as an
occasional case of miliary tuberculosis following grip. As regards
latent tuberculosis, however, they do believe that the intercurrent
acute infection does cause in many cases a lighting up of a previously
entirely dormant tuberculosis. It seems rather difficult to reconcile
the two ideas. If one type of tuberculous individual is rendered more
susceptible to the ravages of consumption, it would seem reasonable to
expect that all types would be so affected.
The greatest difficulty in reaching a conclusion regarding the effects
of influenza on tuberculosis, and vice versa, is due to the fact that
the individuals studied are in all stages of the disease, and that each
individual reacts differently and in his own way. Opinions have been
based chiefly on clinical observations, and not on statistical study of
large series of cases, while from the nature of the conditions, even
statistical studies would not be without great fallacy.
Armstrong, found in a survey made in Framingham, Massachusetts, that 16
per cent. of the entire population was affected with influenza, but only
4 per cent. of the tuberculous group in the community. Most of these
latter were of the arrested type and were going about taking their part
in industry and exposed to the same degree of contact as was the case
with the normal population. The fatality rate was equally in contrast.
Armstrong concluded that there appeared to be a relative degree of
protection for the highly tubercularized. If we accept these figures at
their face value we must conclude then either that tuberculosis offers
some degree of protection against acute influenzal infection, or, that
the tuberculous of Framingham have been so well trained in sanitation
and personal hygiene, as a result of the Framingham demonstration, that
they have been able to protect themselves against the grip. In the
latter case we must look upon the result as a successful demonstration
of the principles of preventive medicine. Certainly this did play a
part, to the extent at least that individuals knowing themselves to be
infected with tuberculosis, and knowing themselves to be in the presence
of a pandemic, became more wary of crowd contact, and in case they did
become ill, they undoubtedly went to bed at the earliest opportunity.
If, on the other hand, this is a true demonstration of relative immunity
in a chronically infected individual, the explanation must be sought
elsewhere. Does a chronic respiratory infection confer a relative degree
of immunity to an acute respiratory disease? Do the germs already on the
premises exert, so to speak, “squatters’ rights?” Are we observing an
example of non-specific immunity due to local preceding infection? Still
another factor may play an important role, the factor of race stock. The
excess of tuberculosis in negroes, for instance, over that in whites, is
in some localities double or treble, while various observers, as Frost,
Brewer, and Fränkel and Dublin, report that the influenza incidence and
mortality among negroes was decidedly less than that among the whites.
Winslow and Rogers found that in Connecticut the proportion of
influenza-pneumonia deaths is lower than would be expected among persons
of native Irish, English and German stock, and higher than was to be
expected among Russian, Austrian, Canadian and Polish stock, while it
was enormously high among the Italian. Italians are notably
insusceptible to tuberculosis, while the Irish are much more prone to
infection with the disease. For example, in Framingham, where the
tuberculosis incidence rate for the entire population was 2.16 per
cent., the rate in the Italian race stock was 0.58 per cent., and in the
Irish, 4.80 per cent. In Framingham there was about four times as much
influenza among the Italians as among the Irish. Is this apparent
insusceptibility of certain race stocks an inherent condition, or is it
dependent chiefly on differences in living conditions and in age
prevalence in the different races? Probably it is chiefly the former.
Frost, for instance, found that among the negroes the incidence of
influenza was lower even though the living conditions were much poorer
than those among the whites.
Armstrong’s survey has also thrown some light on the effect of the
influenza on previously tubercularized individuals. In a survey of 700
individuals who had had the acute disease there were ten arrested cases
of tuberculosis, or 1.4 per cent. All these had been known to be
arrested cases previous to the epidemic, and in none of them did the
disease appear to have been actively and permanently lighted up. Some
had manifested a slight activity, but all seemed to be on the way to a
rearrest of the disease. On the other hand, thirteen cases, or 2 per
cent. of the 700, were found to have active tuberculosis which had
hitherto been undiagnosed, and an additional eight cases, with
indefinite broncho-pulmonary signs, were designated as incipient
tuberculosis cases. This is to be contrasted with an incidence of active
tuberculosis in the pre-epidemic examination of approximately one per
cent. These figures would indicate an increase in tuberculosis
incidence. How may this be explained? The accuracy of these results will
depend on how the 700 cases were selected. If, for example, individuals
who feared tuberculosis because of known exposure, requested
examination, the results might be influenced by their inclusion.
It has long been known that individuals with measles will not react to
tuberculin tests, even though they have been positive before developing
the measles, and though they will become positive again after recovery.
The same may be said of vaccination. Individuals vaccinated against
smallpox, who have measles, and are during their illness revaccinated,
will not show an immediate reaction. The test will remain entirely
negative, while after recovery, the immediate reaction may be obtained.
Normally, it will appear in 95 per cent. of cases, while among those
with measles the phenomenon remains absent in 90 per cent. The same
phenomenon is present in certain other acute illnesses, particularly
scarlet fever. It has been variously explained. von Pirquet, who was the
first to observe it in measles, believed that the acute disease created
a temporary inability to produce antibodies, and therefore designated
the condition by the name “anergie.” The same phenomenon of anergie has
been found recently to hold in the case of influenza. Debré and Jacquet,
Lereboullet, Bloomfield and Mateer, as well as Berliner and Schiffer,
have brought forth abundant evidence to this effect, following the 1918
pandemic. It has also been shown by Cayrel and others that there is a
diminution of typhoid agglutinins in the serum of influenza patients
vaccinated against typhoid. The agglutinin titer again increases after
recovery. It is true that the agglutinin titer is not a measure of
immunity, but it is frequently used as such and serves to give us some
information on the subject. If, then, influenza is an anergic disease, a
“maladie anergisante,” we have a theoretical explanation of the increase
in severity of tuberculosis following the acute infection. We have long
observed that tuberculosis frequently follows measles. We have recently
been thoroughly convinced that influenza lessens resistance to secondary
infection with streptococcus, pneumococcus, and other respiratory tract
organisms. Shall the tubercle bacillus be added to this list? During the
1918 epidemic we saw men in the army camps who passed through an attack
of influenza-pneumonia and died within a few weeks from tuberculous
pneumonia or miliary tuberculosis. These men had previously been so free
from signs of their tuberculosis, as to be accepted for military service
as healthy individuals. The number of these cases was small, to be sure,
but sufficiently large to convince us that there do exist instances in
which tuberculosis is tremendously fired by an intercurrent influenza.
If we may judge merely by the balance of evidence and risk any
conclusions from such conflicting testimony, we may sum up as follows:
1. Great variation in the interaction of tuberculosis and influenza must
be expected, because of the many stages at which the tuberculous may be
attacked, because of the altered mode of living of known consumptives,
and because of the protected life of most of them.
2. Phthisical patients as a group, may be _relatively_ insusceptible to
influenza infection. This may be due to the tuberculous process itself
or to some extrinsic, but nearly related cause.
3. But many individuals with pulmonary tuberculosis _do_ get influenza.
4. And the disease, having been contracted, in many cases hastens the
fatal termination of the tuberculous process.
5. It may be that this phthisical exacerbation occurs more frequently in
individuals with latent tuberculosis, individuals who are not at the
time mobilizing their protective antibodies.
_Other infectious diseases._—We have found diversity of opinion
regarding the relationship between influenza and tuberculosis, and yet
the latter, being as a rule very chronic and presenting very definite
signs which may easily be followed, should theoretically be a disease in
which the results of study would be quite definite. When it comes to a
study of other maladies we find the same difference of opinion
frequently present.
It has been the experience of many that during influenza epidemics other
acute specific infectious diseases appear to diminish, both in number of
cases and in extent. At Camp Sevier, for example, two measles wards had
been quite constantly full of patients up to the time of the fall
influenza epidemic, while during the time of the epidemic one ward
appeared sufficient to hold all cases of measles. In the stress of the
epidemic this difference was probably more apparent than real, and
certainly is not to be taken as of statistical value.
Vaughan and Palmer report for all troops in the United States that,
“Without exaggeration it may be said that for the time being at least,
influenza and pneumonia suppressed other infectious diseases. Typhoid
fever increased to a barely noticeable degree. The death rate from this
disease was somewhat higher, but the total number is so small as to
barely warrant comment, and not to justify any definite conclusion.
Scarlet fever and malaria were both lower than during the summer. In
fact, there was but one scarlet fever outbreak of any importance and
that occurred at Camp Hancock. Within two weeks over 300 cases were
reported and this marks the largest scarlet fever epidemic that occurred
in the camps in this country at any time. Meningitis increased although
it did not reach the prevalence of the previous winter. The weekly
incidence curve for all troops in this country suggests that meningitis
was in some instances a sequel to influenza. The greatest meningitis
incidence corresponds with the influenza peak. Diphtheria showed no
material increase. Deaths from tuberculosis were higher in the autumn
than in the two previous periods, the death rate rising from 18 per
100,000 during the summer to 46 in the autumn. The rate for the previous
winter was 15.”
In 1889 Abbott was unable to find satisfactory evidence of a connection
between influenza and other epidemic diseases, although as he mentions,
such connection had often been affirmed. Instances in support of each
position were to be found in the literature of the time.
P. Friedrich, after an exhaustive study of the literature, following the
1889 pandemic, concluded that there was no relationship whatever between
the incidence of influenza and other acute infections. Wutzdorff reached
the same view after studying the various diseases during the influenza
recrudescences and recurrences. Finally, Ripperger concluded likewise.
It may be remarked that following 1918 there have been several articles
written concerning the relationship between influenza and certain other
diseases. These are difficult to correlate and in most instances so many
additional factors play a part that the conclusions drawn are perhaps
not entirely well grounded. Sylvestri found that in his experience
malaria patients escaped the influenza during the pandemic. He believes
that it was the malaria rather than the quinine which was responsible
for the apparent immunity. On the contrary others have observed, if
anything, an increase in malarial patients.
Fränkel and Dublin found that during the pandemic period deaths from
whooping cough increased. The difficulty of differentiating between
whooping cough and influenza as a cause of death is apparent.
It seems quite certain that deaths from organic diseases of the heart
increase during and following influenza epidemics and are due probably
to the inability of the weakened patients to resist the added burden.
Fränkel and Dublin found an increase in deaths from this cause. This was
also observed to be true in Spain and other localities.
Jordan has compared the curves of influenza with those of acute coryza
among school children of Chicago and finds that the period of highest
incidence of colds in October, 1918, occurred in the second week of
school and that it preceded the corresponding period of influenza by
seven weeks. There were three peaks in the curve for colds and only two
in that for influenza. The period of highest incidence of colds follows
the first peak of the influenza curve by one week, while during the week
of greatest prevalence of influenza there is a sharp fall of the number
of cases of colds. The third peak for colds occurred one week after the
height of the influenza curve. As a rule the colds curve runs at a
higher level than that for influenza. A striking fact is that the
portion of the curve for influenza contained within the period November
23d to December 7th, is almost the exact opposite of the corresponding
portion in the curve for colds. How much of this is due to the factor of
diagnosis is difficult to say.
_Encephalitis lethargica._—It is not within the scope of our report to
discuss in detail this disease. Its apparent relationship with
influenza, in point of time, if not otherwise, calls for special
mention. In 1712 a disease followed a pandemic of influenza, occurring
particularly in Germany, where it was known under the name of “Tübingen
Sleeping Sickness.” In the spring of 1890, according to Netter, a
disease of similar character called “Nona” was distributed especially in
Northern Italy and Hungary and scattered more or less diffusely over a
large part of Europe. Preceding the last influenza pandemic the disease
was first reported in Vienna in the winter of 1916–17. Cases were seen
in Paris in February and March, 1918, and the first official report of
the disease in England seems to have been on January 26, 1918. In the
spring of 1918 there were 168 officially reported cases in England with
37 deaths. The disease seems to have disappeared there in June, 1918,
and reappeared in the autumn of the same year. The first cases in the
United States were reported by Pothier at Camp Lee, Va. Following the
great influenza pandemic cases of lethargic encephalitis have appeared
in all parts of the world. It has been present in England, France,
Belgium, Switzerland, Austria, Greece, Italy, and other countries of
Europe, South America, Mexico, the United States, Australia, Queensland,
New South Wales, and Algiers. There was an increase of encephalitis
lethargica concomitant with the increase of influenza in the early
months of 1920. Thus, in Switzerland 440 cases were reported during
February, 1920. The 1920 epidemic of influenza in that country had
almost ceased by the middle of March, while that of lethargic
encephalitis had greatly decreased. One hundred and forty-one cases of
the latter disease appeared in the canton of Zürich alone.
Is epidemic encephalitis a disease sui generis or is it a form of
influenza?
The consensus of opinion has been that it is a separate disease. There
is, however, no way of telling how close is the relationship to the
influenza itself. If lethargic encephalitis is a sequel to influenza, is
it caused by the same germ? Flexner points out that in 1916, when the
first cases of encephalitis appeared or at least were recognized in
Austria, the epidemic of influenza had not yet appeared. In England,
France and the United States the epidemics of the two diseases were more
or less coincidental. He believes that little weight can be given the
supposed coincidence of influenza and the “sleeping sickness” of 1712,
and that it is highly improbable that the semi-mysterious affection,
“nona,” which dates from 1890 was definitely a sequel of influenza. He
concludes that the outbreak of encephalitis either antedated the
pandemic of influenza of 1918, or that the two diseases more or less
overlapped; that is, although probably quite by accident, they prevailed
concurrently. He prefers for the time being at least to regard them as
independent diseases.
Crookshank believes that encephalitis lethargica is a distinct disease,
but that it occurs frequently as an antecedent of or coincident with
influenza, together with increase in the existence of poliomyelitis and
certain other diseases.
Nevertheless the association in point of time and place between
influenza and lethargic encephalitis cannot be lightly overlooked. As we
have seen, Flexner’s criticism that encephalitis antedated the influenza
is not valid, because the latter was present in 1916. We must await
fuller evidence on this subject.
SECTION VII.
COMPARISON OF INFLUENZA WITH OTHER EPIDEMIC DISEASES.
A certain amount of knowledge concerning the epidemiology of influenza
may be gained by a comparison of the epidemic features of that disease
with those of other epidemic diseases, particularly measles and the
exanthemata, meningitis, the plague, and certain diseases of the lower
animals. Influenza is described as a disease with distinctive
epidemiologic characteristics, the chief of which are found only in
epidemic spreads. Thus one of the fundamental characteristics of these
epidemics is supposed to be the primary type of wave, the wave
characterized by rapid rise, quasi-symmetrical evolution, and a
concentration closely grouped around the maximum. “This is found in no
other disease. In no other type of epidemic does the curve rise as
rapidly to a peak or fall as swiftly, nor is the epidemic completed in
as short a time.”
The secondary type of curve, that which is more frequently found in
recurring influenza epidemics, characterized by a more gradual ascent, a
still more gradual decline and a longer duration, is found frequently in
the curves for other diseases; it is much less characteristic. We shall
attempt by a comparison of epidemic influenza with these other diseases
to explain the cause for this characteristic primary curve, so as to
gain a further insight into the epidemic features of the disease.
There are certain characteristics held by epidemic influenza in common
with other diseases. There are certain resemblances between it and
epidemic meningitis; in certain ways it resembles measles and there are
some points of similarity to the pneumonic form of plague. The fact that
it cannot be compared with one of these diseases to the exclusion of the
others renders deductions more complicated.
_Epizootics._—Soper has written at some length on a comparison of
influenza in man with the so-called influenza among horses. The close
resemblance in many features is striking.
Epizootics of a disease apparently resembling influenza have been
described among horses from before the Christian Era. A disease believed
to have been influenza was recorded as having occurred B.C. among horses
in Sicily. According to Parkes the epidemic which attacked the army of
Charlemagne in 876 attacked at the same time dogs and birds. Finkler
describes an epizootic among horses in 1404 A.D. There were other
epizootics in 1301, 1711 and 1870 to 1873. In 1901 a severe outbreak
occurred in America, and one has also been described by Mathers as
occurring in Chicago in the winter of 1915–16. These epidemics of a
disease clinically resembling influenza have frequently occurred among
horses at the same time with true epidemics of influenza in man.
Nevertheless there has been no clear cut evidence to prove that the
disease is the same.
Leichtenstern discusses the incidence of respiratory disease among
animals, particularly household pets during epidemics of influenza. He
comes to the conclusion that human influenza is a disease limited
entirely to the human race and having no connection with animal disease.
This is particularly true with regard to diseases reported among cats,
dogs, canaries and other captive birds. He also believes that the
epizootics among horses which have been reported from time to time as
occurring with influenza epidemics have nothing to do with the disease
in man. The symptoms are frequently very similar, but epizootics have
frequently occurred at times when there was no epidemic of disease among
humans.
Abbott concluded that during the great horse epidemic of 1872 which bore
a strong resemblance to influenza the disease was not unusually
prevalent among men except in a few limited localities; while other
infectious diseases, such as measles, small pox, scarlet fever and
cholera infantum were unusually prevalent in that year.
Soper writes that, “Economically, influenza is the most important
disease of horses in temperate climates. The mortality among remounts
has been many times greater from influenza than from all other diseases
put together. It is estimated that over 25,000 horses purchased by the
British Government in America and Canada, during two years of the war,
died in those countries while awaiting shipment to Europe. In a circular
issued January 12, 1918, by the Surgeon General of the United States
Army to the veterinarians of remount depots, it was stated that the
losses from influenza among American army horses amounted to over
$100,000 a week. The disease spoken of as influenza in the horse has
many other names. It is commonly called pink-eye, shipping fever, stable
pneumonia and bronchitis. By some influenza is not believed to be a
single disease, but a group of diseases. By others it is considered to
be a definite entity, varying in its symptom complex at different times
and with various horses. Infectious laryngitis and infectious
pharyngitis seem to be independent diseases. Two forms of influenza are
generally distinguished: catarrhal and pectoral.”
Even after the last pandemic of influenza the question has again arisen
as to the identity of the disease among animals. Orticoni and his
co-workers observe that there was an extensive epizootic among horses at
the time of the 1918 epidemic in the area which they had under
observation. There have been other similar reports. The popular press,
during the height of the 1918 spread, reported that there was a highly
fatal influenza infesting the monkeys of South Africa and that the
baboons were dying in scores, their dead bodies being found on the
roadsides and in the vicinity of homesteads. Another report tells of the
influenza decimating the big game in Canada, and yet another tells of
the havoc wrought among the buffalos and other animals in the United
States National Parks. These reports have not been corroborated by
scientific observations.
Soper has analyzed the subject of so-called influenza among horses. He
finds that the disease is quite generally distributed, that it has many
points of close similarity to the influenza of man, but that it is a
distinct and separate disease. The two diseases are not identical and
neither can be transmuted into the other.
“Briefly, the symptoms, as stated in a recent publication of the United
States Department of Agriculture, are sudden onset; fever in some cases
preceded by chill; great physical prostration and depression of nervous
force; sometimes injected mucous membranes, especially those of the eye,
and loss of appetite. In uncomplicated cases the fever abates after
about a week and there is a general restoration to health. Pneumonia is
one of the frequent complications and is always serious. The death rate
varies between two and seven per cent. The most usual form is the
catarrhal type. The attack may last only two or three days; in other
cases the course may extend to two weeks, in which event it takes the
animal a long time to get well. Horses which have passed through this
form of disease may be considered to have recovered two weeks after the
disappearance of the fever.
“The diagnosis of influenza depends as much upon its epidemiological
aspects as upon the symptoms. Law bases it on the suddenness of the
attack, its epizootic character, the numbers attacked in rapid
succession and over a large area as compared with ordinary contagious
pneumonia, the sudden and extreme prostration, the mildness of the
average case, the congestion of the upper air passages, the watering and
discoloration of the eyes, and the history of the case. Points of
interest in the history are the arrival of the infected horses within a
few days from an infected place, or coming through such a place, or the
attacking of new arrivals in a previously infected stable, or the known
advance of the disease toward the place where the patients are located.”
Soper found that the progress of the epidemic of 1872–73 among the
horses in this country was as generalized, but much slower than the
progress of the recent pandemic among human beings, the rapidity of
progress corresponding with the rapidity of the transport of the horses
at that time. Just as we have found in the case of influenza so also at
that time the spread only followed lines of communication and actual
contact between horses.
It is highly interesting that attempts to transfer the disease from
horse to horse experimentally met with the same degree of failure that
was experienced in similar attempts to transfer influenza experimentally
from man to man. In fact Lieut. Col. Watkins Pitchford of the British
Army Veterinary Corps in a report in July, 1917, stated that it was
impossible to produce infection experimentally. Nose bags were kept upon
horses with profuse nasal discharges and high temperature, and these
nose bags were then used to contain the food of other horses without
infection taking place.
There are several other points of resemblance between horse influenza
and human influenza. The mortality from influenza among horses is under
ordinary circumstances between two and seven per cent., and is highest
in horses worn out by fatigue after a long railroad journey, among fat
horses out of condition, and among horses which have been driven after
they were sick. The death rate in the simple catarrhal form of influenza
rarely exceeds one-half of one per cent., while in the pectoral form it
is never less than four or five per cent., and may reach 16 per cent.
The only measure of prevention which has been found wholly satisfactory
is strict isolation. Usually influenza occurs in horses who have newly
arrived in a stable from elsewhere. Practically all the newly arrived
horses and country horses are almost alone susceptible. Soper, who has
studied the records, such as they are, in the army veterinary corps, and
also the records from the Bureau of Animal Industry, concludes that they
show nothing to indicate that any general epizootic of influenza
occurred among horses during the year 1918 corresponding to, or
connectable with the pandemic of influenza among human beings. There was
influenza among the horses, but he does not think it was extensive
enough to be allied with influenza among human beings. He concludes that
there are two types of influenza among horses, first a mild form which
nearly all horses get when transferred to a contaminated stable, after
which there develops immunity, and the second type, a true epizootic
which may sweep the entire country, attacking practically every horse. A
most suggestive result of his study lies in the fact that predisposing
influences play a most important part in the production of serious
influenza among horses.
Aside from noting a certain similarity between the epizootic of
so-called influenza in horses and influenza as we know it in man, we
cannot acquire much additional information concerning influenza itself
from a consideration of this subject. The important conclusion is that
in several of the most important epidemiologic features the two diseases
are similar and that the study of human influenza may be furthered by
critical studies of influenza in horses. We shall attempt to demonstrate
that influenza in a similar manner is not unlike other epidemic
diseases.
_Asiatic cholera._—There are those who claim that the disease should be
compared with Asiatic cholera which remains constantly endemic on the
banks of the Ganges and at intervals spreads from there throughout
Indo-China, and formerly at times throughout the civilized world. Those
who compare influenza with this disease believe that this is additional
evidence in favor of a single focus of endemicity of influenza.
_Epidemic meningitis._—On the contrary the disease may well be compared
with epidemic meningitis. The germ of this disease, distributed
throughout the world, is usually in an avirulent form and produces no
epidemic of meningitis. Only an occasional case arises. There are
certain localities in which the disease is particularly prevalent at all
times. We may speak of these as endemic foci, but must remember that at
the same time the virus is distributed elsewhere. Thus South Carolina,
Missouri and Kansas have been shown to be localities in which meningitis
has been more or less widely distributed for some years.
We can carry the analogy still farther. During the concentration of
forces early in the war, camps were established at Columbia, S. C. and
at Fort Riley, Kansas. In these camps, Jackson and Funston, there very
rapidly developed quite extensive epidemics of cerebrospinal meningitis.
Here and in Camp Beauregard, the incidence of the disease was out of all
proportion to that in the other camps. Just as the exaltation of
virulence of the influenza virus has been favored by gross changes in
the environment, the occupation, the density of, and the disease
incidence in the host as a community, so also do these appear to have
been factors in the development of a meningitis prevalence in the army.
It was more prevalent in those camps situated in the territories where
the disease was particularly endemic, but was also present in all camps.
Had the meningococcus been able to assume the high degree of virulence
and invasiveness possessed by the influenza virus it is reasonable to
assume that a pandemic spread would have begun in one of the two or
three camps where the disease was especially prevalent. It would have
spread thence and have attacked those camps in which a mildly virulent
meningococcus had already been causing disease. Just as in influenza the
pandemic spread would have been due not to the universally distributed
virus, but to the one or few which finally acquired the greatest
exaltation of virulence.
We see then that the followers of both theories—that of the single focus
and that of an extensive distribution—can quote other infectious
diseases in support of their theory, but the evidence in favor of
similarity to Asiatic cholera is not complete. The disease is not
similar. The mode of transmission is entirely different. The infection
is chiefly of the gastro-intestinal tract, while that in influenza is
chiefly respiratory. Since 1816 there have been five pandemics of
Asiatic cholera, the last occurring in 1883 and all of them traceable to
a primary focus in India. Frequently it was carried from India by the
faithful, to Mecca and from there was readily distributed throughout
Europe. In the last pandemic the disease spread throughout the old world
and reached New York harbor, but was refused admission.
_Plague._—The similarity in clinical symptomatology, in gross pathology
and the apparent similarity in manner of spread and epidemic features
between influenza and the pneumonic form of plague has suggested to some
that the best comparison should be made with the latter disease. Here
again is a disease which is endemic in Asia and spreads elsewhere only
at intervals. If we go back into the history of the plague we will
discover that formerly it was distributed more or less throughout the
civilized world. The plague is supposed to have been known to the
children of Israel at the time of the exodus from Egypt. The Egypt of
the Pharaohs was a country of great salubrity. Hygienic measures were
excellent. The inhabitants built aqueducts, disposed of their dead
hygienically, reared temples, maintained law and order, developed the
elements of literature and science and devised and employed simple
machinery. But as early as the exodus, Egypt had lost its salubrity.
This is indicated by many passages in the Bible. The plague was present
in that country during this period. Sticker believes that the pest among
the Philistines spoken of in the First Book of Samuel, when the captured
army was returned with five golden emerods and five golden mice, was the
bubonic plague.
Thucydides describes a plague in Athens occurring before Christ. This is
generally believed to have been “the plague.” The time of the earliest
appearance of the disease in Italy is not known but it was well
established there in the first century of our era. The plague was
endemic in Italy at that time and it developed in epidemic form with
each increase in susceptible material. At about 68 A.D. the disease
spread over the whole of Asia, Northern Africa and Europe. Exacerbations
of the disease are described in the years 80, 88 and 92 A.D. In Rome
they occurred in 102, 107 and 117 A.D. The disease was present in Wales
in 114 A.D. In 167 an unusually severe outbreak of the plague occurred
in Rome. There were other outbreaks in the Roman army in 173, 175 and
178. Had we the space to record here the history of the plague we would
find that the disease was widely distributed throughout Europe for
several hundreds of years, that it was particularly prevalent in certain
areas and that at intervals it spread from one or a few foci, throughout
the continent.
We can compare the epidemic features of influenza with these other
contagious diseases, but we will always find some points of difference
from one or another. Let us consider again for a moment epidemic
meningitis. There is no combination of predisposing causes,
environmental, meteorologic or bacteriologic which will produce
epidemics of cerebrospinal meningitis in the absence of the
meningococcus itself. The organism causing the disease must be present
before the disease will occur. The specificity of the invading organism
in the different diseases will always produce some variation among the
epidemiologic features. Other things being equal, that locality in which
this germ is most extensively distributed will be the locality in which
epidemics, when they do break out, will be most extensive.
In the case of our army camps, those individuals carrying the disease
virus from the endemic foci to the camps were not the ones who fell ill.
Generally it was those, coming from other areas in which meningitis was
not extensively distributed and who had, therefore, not acquired an
increased resistance to the disease, who fell ill. But after the disease
had acquired increased virulence at Camp Jackson, not only did it occur
in the troops at that camp, but it also became quite extensive
throughout the civilian population, presumably among those who had
previously been exposed to it in its endemic form.
In our comparison of influenza with other infectious diseases we wish to
show particularly that the disease is not in a class by itself, but that
its epidemiologic features are not unlike those of other respiratory
infections, that the manner of spread and the mode of infection are
similar to those of the other diseases. Nothing unusual or unknown need
be called into use in explaining any differences. Those differences that
very palpably exist can be explained by facts which we already know.
Leichtenstern, thirty years ago, believed that the disease was similar
in its manner of spread to other infectious diseases. He observed this
particularly in the earliest and the latest phases of epidemic spreads
where cases were scattered. He saw that in households the disease
attacked some and spared others even of those intimately connected with
the sick, just as was the case in diphtheria or meningitis. He writes:
“Comparing these later periods the disease evidences the same contagious
characteristics as the other endemic contagious diseases, such as
scarlet fever, measles, diphtheria, epidemic cerebrospinal meningitis,
etc.”
Parkes made very similar observations even before the 1889 epidemic.
_Measles._—A comparison of influenza and measles will offer some
explanation of the differences between the epidemic constitution of the
former and that of the other respiratory diseases.
We are accustomed to think of measles as a disease which, like
meningitis, is disseminated throughout the civilized world, and which
although constantly with us causes only sporadic cases. True epidemics
of measles do occur, even when there is no gross change in the
constitution of the population. We have discussed examples of this
particularly in London. Flare-ups of measles prevalence are in fact so
much the rule that in certain localities health officers anticipate a
measles epidemic about once in two years. Furthermore measles has been
known more than once to occur in extensive epidemic form, attacking
large proportions of the population invaded. We know that there is an
immunity to measles which is nearly absolute in those who have once
acquired the disease. The epidemics have, therefore, occurred
exclusively in those localities where the proportion of immune
individuals was relatively small. According to Noah Webster in 1772
measles appeared in all parts of America and was accompanied by an
unusually high mortality. In Charleston 800 or 900 children died of the
disease. The following year measles “finished its course and was
followed by a disorder of the throat.”
In 1781 measles disappeared from the Faroe Islands, and for the
following sixty-five years there was not a case of this disease anywhere
on any of the seventeen islands constituting the inhabited parts of this
group. When the disease was finally re-introduced into these islands, it
spread throughout the population, attacking practically every individual
in a relatively short interval of time, showing a much higher attack
rate than did influenza in 1918. There was this difference, that the
only individuals who did not acquire measles on its re-introduction into
the islands were those who had had it sixty-five years before. Panum did
not find an authentic case of recurrence in the same individual. There
was not a single instance of second attack of measles, although the
shortest possible interval between the previous attack and the
subsequent exposure was sixty-five years.
In 1875 measles first reached the inhabitants of the Fiji Islands. The
disease was introduced by the King of the Fiji Islanders and his escort,
upon their return from New South Wales. The entire population of the
islands was estimated at 150,000 and it is officially stated that there
were 40,000 deaths from measles in the ensuing period. In certain
islands and villages where more exact information was secured, it was
found that from twenty-seven to twenty-eight per cent. of the people
died. Panic, insanitary conditions and ignorance of how to care for the
sick resulted in this high mortality. V. C. Vaughan has remarked that
when measles is introduced into a population with a susceptibility of
100 per cent. “it strikes down so many at practically the same time that
adequate care for the sick is impossible.” The rapidity with which the
population is invaded is practically as great as it is during influenza
epidemics.
It is the opinion of the author that the phenomenon which contributes
chiefly to the occurrence of influenza in epidemics and pandemics, and
which causes the characteristic curves of a primary influenza wave, is
the absence of any permanent immunity. We have shown in our discussion
that no immunity is proven to exist after a year and a half or two years
at the most. Measles occurring in a non-immune population spreads
through that population with the same high rate as does the influenza.
In Charts XXVIII and XXIX we find the curves of incidence of measles in
certain of the United States Army camps in the fall and winter of
1917–18. The simplest curve is that for Camp Wheeler. Here the type is
similar to that found in the primary wave of influenza. There is a
quasi-symmetrical evolution and the concentration is closely grouped
around the maximum. The total duration of the epidemic is short, not
being much over eight weeks. The troops at this camp were predominantly
rural. The disease starting in this group of relatively non-immunes
spread rapidly until presumably all susceptible material was exhausted.
Compare Camp Wheeler with those camps where the population was chiefly
urban. Here the wave is of longer duration, is not as high, the increase
is slower, the decrease is more gradual and the concentration is not
grouped so closely about the maximum. In the case of the other camps
with chiefly rural population, the curve is not as simple as is the case
with Camp Wheeler, and there are at times secondary curves as in the
case of Camp Bowie, but the essential similarity to the curve at Camp
Wheeler and the difference from the curves at Devens, Dix, Custer and
Grant is striking. It may be that the double waves are explained by
acquisition of new bodies of troops, by the introduction of new
susceptible material. On this question we have no exact information.
CHART XXVIII.
[Illustration: Respiratory Disease at Army Camps]
CHART XXIX.
[Illustration: Respiratory Disease at Army Camps]
This experience was equally true during the Civil war. Although there
are no exact reports, it appears that measles prevailed in the
Confederate army and was much more highly fatal than in the Union army.
A recurrent influenza epidemic usually takes the form of a secondary
wave, particularly so if it follows the primary wave within a short
period of time. The difference in the character of the wave is due to
the fact that there is still a comparatively large concentration of
immune individuals, immunized by having had the disease during the
primary spread. The secondary type of the influenza wave corresponds
with the measles curves for the urban camps. There are all gradations in
influenza from the typical primary wave down to a very much flattened
wave of relatively long duration, and even on to the stage of
endemicity, with no discernible wave. In 1920 the recurrent epidemic
partook more of the form of a primary wave, because in most individuals
the period of immunity had been completed by January and February, 1920.
If we could, by some means, induce an immunity which would last for long
periods of time, pandemic influenza would disappear from the earth and
the disease would be relegated to the comparatively minor position now
occupied by measles. The disease would be constantly endemic, frequently
breaking out in small epidemics, but never becoming pandemic. This is
one object that should be held in view by the immunologists and
bacteriologists. But it is not so simple. Even were a successful vaccine
discovered, it is doubtful whether any considerable group of the
population could be persuaded to take it as often as would be necessary.
Universal vaccination against small pox has never been carried out. The
same would be true at the present time with regard to influenza.
There is another similarity between measles and influenza. Measles is as
infectious as is influenza. It is as readily transmitted and the mode of
transmission is probably the same or very similar. In both diseases we
are made poignantly aware of the great contagiousness of the disease,
and yet in neither disease has there ever been conclusive evidence of
experimental transmission from man to man. Several have reported
attempts to transfer measles, but in each case the evidence of infection
has been incomplete. The work of Hektoen has been quoted in particular,
but Sellards, after carefully reviewing his work, concludes that the
evidence of infection is insufficient. Moreover Hektoen’s patients were
not exposed subsequently to measles infection in the natural way.
SECTION VIII.
THE PREVENTION AND CONTROL OF INFLUENZA.
Dr. Hamer has visualized the present state of our knowledge of epidemic
influenza in a manner which can scarcely be improved upon. We,
therefore, quote him at length: “It seems to me that, during the last
thirty years or more, we have been making fairly steady uphill progress
along the road which constitutes the boundary between the county of
epidemiology and the county of bacteriology, and that we have at length
reached, at a height considerably above sea level, the foot of the
mountain, on the very top of which lies hidden the secret of an
‘epidemic constitution,’ and now we are face to face with a parting of
ways. Straight ahead is the frowning height, its summit in cloud. On the
right hand stretches away a fine road skirting the base of the mountain.
Along this road we have recently seen Dr. Brownlee whirled away in his
new car ‘periodogram.’ We are all hoping to hear more from him, but as
he is still insisting upon the primary, if not the exclusive, importance
of continuous variation in the virulence of the germ, we have to realize
that for the time Dr. Brownlee’s road is going down-hill. On the other
hand, on the left, there swerves away, through the territory of the old
epidemiology, another fine road, which has been explored more
particularly by believers in ‘skiey influences.’ So far as it has been
traced this road is as flat as flat can be, but of course there is
always the possibility that after a while it will begin to rise, as it
skirts round the mountain, and leads to a good vantage point from which
to start climbing. At the risk, however, of being laughed at, I venture
to bring under notice the very rough and at first sight unpromising
ground directly in front of us. Along this can be seen two obscurely
marked sheep tracks proceeding at any rate onwards and upwards. One
diverges slightly towards the left hand and it has been followed at
various times by De Schweinitz and others, naturalists bent on
collecting ‘ultravisible viruses;’ the second track, directed rather
more to the right, has been explored by Reiner, Müller, Massini,
Penfold, and others, workers at the problem of discontinuous variation
by ‘mutation.’ As a matter of fact I have reason to believe that two
travellers, each of whom follows one of these tracks, will keep in sight
of and after a while will find that they are approaching one another,
and will ultimately meet at a small and retired upland farm; then after
passing some dogs and following the track until clear of all stone
walls, they will come right out in open ground on the face of the
mountain and can start straight up the steep. But it must here be
pointed out that there remains to be considered a fourth method of
approach to the mountain, the most direct of all; but that is by
aeroplane and is of course only open to those trained in metaphysics and
statistical methods. Investigators thus equipped are able to rise in the
air, to survey with careful scrutiny the whole of the ground beneath
them and to make the best use of details of information obtained by
scouting parties below. It is to be hoped that at no very distant date a
survey of the top of the mountain will thus become an accomplished fact.
Meantime, those who cannot fly may find useful employment in examining
the track beyond the farm. There is the chance there of picking up facts
relating to such questions as the ‘parasites associated with a
parasite,’ symbiosis, and the like; take, for example, a suggestion made
fourteen or fifteen years ago that the influenza organism may at one
time live in association with Pfeiffer’s bacillus, at another with the
Micrococcus catarrhalis, and so on; or the throat distemper organism may
be yoked now with the diphtheria bacillus and now with the Streptococcus
conglomeratus. (Is that, I wonder, now to be regarded as a concept or as
an occurrence or happening?)”
At best our knowledge of the cause and manner of spread of influenza is
fragmentary and insufficient. Attempts to outline a system of control
and prevention based upon present concepts are met with many
discouragements. The next pandemic will not be prevented. The disease
will surely return. If the interval be sufficiently long it may find us
quite as unprepared as we were in 1918. Discouraging as the outlook is
there are many bright points upon which we must base our hopes for
future results.
The difficulties are many: First the _diagnosis_ of influenza is
difficult either in the individual case or in the form of a mild
epidemic. Even in 1918 the identification was often not definitely made
until after weeks had elapsed. Second, we know little concerning the
_mode of transmission_ of the disease. We speak of “respiratory
infection.” We believe that the transmission is by a mechanism similar
to that for measles, but we have never experimentally transmitted either
disease. The _short incubation period_ places us at a great
disadvantage. Were the interval between the occurrence of the first case
and the development of additional cases as long as it is in measles, the
problem of isolation and quarantine would be simplified. As in measles
the disease is probably _very early infectious_, presumably before acute
symptoms develop. The majority of cases of influenza are _ambulatory_.
Many individuals do not take to their beds, but continue about their
work, spreading the disease wherever they go.
Again, we are ignorant of the _period of infectiousness_. Dr. Meredith
Davies has made observations indicating that a patient becomes
non-infectious within one week after the temperature has become normal.
How many influenza patients remain isolated throughout this period?
A _carrier state_ probably exists and plays a most significant part in
the spread.
Yet another drawback is the _apparent wide susceptibility_ to the
disease. Were individuals definitely immunized by one attack the
proportion of susceptibles would be lessened, their concentration in a
population would be decreased, and the probability of their being
exposed would be proportionately diminished.
An additional difficulty is that after an epidemic has once become
prevalent, we must combat not only the virus causing the disease but
also the _secondary invaders_.
Epidemiologic work has shown that _crowd gatherings_ are instrumental in
the spread of influenza. The density of population has not been as
definitely proven to be a factor. Crowding, however, does play a part.
Close crowding in communities must facilitate the spread, but pandemics
of influenza were known before the great metropoleis existed. _Hygienic
conditions_ play their part in the etiology. Finally, in the presence of
every serious epidemic we must also combat the _tendency to panic_ in
the population.
_Anticipatory or preventive measures._—It is erroneous today to speak of
measures for the prevention of influenza in a community. We cannot
prevent the disease. At most, we can anticipate the occurrence of an
epidemic and take precautionary measures by which the spread and the
severity of the disease may be minimized.
First and foremost comes _education_. Education of the public, of the
medical profession and of health authorities. “Scare headlines” in the
newspapers during epidemics should be discouraged. Health cartoons are
of value, but when they express only partial truths they cannot but do
some harm. General education in hygienic methods and in a knowledge of
the spread of contagious diseases has already been most productive. Many
methods by which the public intelligence could be reached are as yet
untried. A daily paper in Boston devotes two columns a week to a
discussion of public health problems, under the title of “The Clinic.”
The statements appearing in these columns are nearly always the truth
and are not exaggerations. There are discussions of recent scientific
work of interest to the reading public. As has been emphasized by
Carnwath, a page devoted to methods of maintaining the health of the
community would probably be of more immediate value than are the many
pages devoted to financial statements, “such as the price of Mexican
Eagles or of Peruvian Corporation Preference.”
The _organization of health services_ to combat unexpected epidemics
would be of great assistance. In times of peace, prepare for war. In all
but the largest cities the health authorities are generally so free from
contact with epidemics and are so pressed with routine that they do not
organize in readiness for an epidemic which may not come. There should
be a closer co-operative organization between health officials and
practising physicians, so that the latter may aid to a greater extent in
the public health work. The physician co-operates in furnishing
information required by the health officer, but too frequently takes
little interest in what further is done with this information. The
medical profession should be made to understand the importance of public
health work, should have a general comprehension of the methods used in
its execution and should particularly develop a sympathetic and
co-operative mental attitude.
The medical societies of the country should be so organized that at a
moment’s notice their membership can be mobilized for the defense of the
community. There is much that the practising physician does not know
about influenza. One of the leading internists in one of our largest
cities, during the 1920 epidemic, refused to call his cases influenza
and treated them as mild “grip.” It is stated that he lost an unusually
large number of his patients. There are still many who believe that the
two diseases are not identical. Not only is this detrimental to the
patient, but as it results in failure to isolate the sick, it is
detrimental to the community.
Nursing groups should be organized to aid at a moment’s notice.
Much work has been done and great experience gained by both the
physicians and the nursing organizations during the last epidemic. Now
is the time to prepare for the next epidemic or pandemic. With the
remembrance of 1918 fresh in our minds we can establish a working
system, while if we delay until the expected arrival of another epidemic
much of our painfully acquired knowledge will have been forgotten.
Opinion differs as to whether influenza should be made a _reportable
disease_. The added expense would be not insignificant. This particular
malady presents the additional complication of being difficult of
diagnosis. The records would at best be inaccurate. The author believes
that certain experiments in reporting the disease even in interepidemic
times should be carried out. This should be done by competent
epidemiologists who could later formulate plans for the permanent
reporting of the disease. We will discuss this further under the
heading, “Constructive Research.”
The use of _vaccines_ has been tried. In 1918 it was almost universally
begun too late—after the epidemic had become prevalent. Prophylactic
vaccination should be inaugurated before the disease actually becomes
epidemic. Vaccination, particularly against the secondary invaders, is
entirely rational. It may not prevent influenza, but it may protect
against the serious complications in individuals and may prevent to an
extent the spread of secondary invaders in the community.
Greenwood aptly remarks that, “In estimating the total effects produced
upon morbidity and mortality by disease, the non-specific secondary
invaders are as important as the specific causes. The camp followers of
an army may do more damage than the regular soldiers, and the same camp
followers may ravage in the wake of different armies.”
At a conference held at the London War Office, October 14, 1918, the
subject of vaccination for influenza was discussed. It was decided that
only three organisms should be employed in each case in the preparation
of the vaccine; that these races should be recently isolated from cases
of the disease developing during the course of the epidemic and that the
microorganisms should be submitted to a rigorous study as to race and
type. The first dose should include 30,000,000 of Bacillus influenzae,
100,000,000 pneumococcus, 40,000,000 streptococcus; the second dose
60,000,000 Bacillus influenzae, 200,000,000 pneumonococcus, 50,000,000
streptococcus. The vaccine should be sterilized at 55° C. and one-half
per cent. phenol should be added. The administration should be at ten
days’ intervals.
In the United States the vaccines employed have often contained a
greater variety of organisms. It is unnecessary to enumerate the results
obtained by various investigators. Some have been mildly enthusiastic,
while others have obtained no demonstrable benefit. It will suffice to
say that there has been no clear evidence that vaccination has been
beneficial, but that the procedure has not been given a thorough trial.
If the causative organism of the disease is eventually determined,
vaccination will probably be attempted with it as antigen. For the
success of vaccination it is important that practically entire
communities be inoculated, and that they be so inoculated before the
development of epidemic prevalence.
_Palliative measures in the presence of an epidemic._—An epidemic, once
having obtained a start will run its course. Our attempts will be to
lessen its extent and diminish its explosiveness. Or, more probably, we
will best succeed by _extending_ the duration and making the invasion
less explosive. We must know of its earliest appearance. _Notification_
must be made by physicians to the health authorities in order that the
earliest increase may be detected. This again renders the reporting of
the disease at all times an essential feature. The _administrative
control_ and the _publicity_ to be given have already been discussed.
What general measures should be taken against the disease? Should the
_public schools_ be closed? Winslow and Rogers found that the orthodox
methods of combating epidemics applied in Connecticut exerted no
appreciable influence on the spread of influenza. Bridgeport, Hartford
and New Haven _did not close_ their schools and suffered from death
rates near the average for the State, lower than the rates which
prevailed in cities like New London and Waterbury, which closed their
schools. No deductions can be drawn from this fact, however, because the
closing of the schools in most cases was forced because of the severity
of the outbreak.
The data obtained by Jordan indicate that schools were not important
distributing centers for the infection. No explosive outbreak occurred
in any one grade, and the four days of the Thanksgiving holiday
evidently afforded more favorable opportunities for infection than did
the days of regular school attendance.
Carnwath believes that in view mainly of the marked prevalence of the
disease amongst school children, the balance of opinion is in favor of
closure, even in densely populated urban districts. In the author’s
investigation there was a slightly higher incidence of the disease among
children attending school than among those younger children who were not
at school. The spread is probably not facilitated so much in the class
room as it is on the play ground. In the school room the children are
constrained to remain at a certain distance from each other. Probably
they would come into as close contact with cases if they were not at
school. Certainly it has not been demonstrated that the school room is a
factor of great importance in the spread of influenza. It would,
perhaps, be better not to close the schools in the presence of an
epidemic, but to discontinue any congregation on the play grounds, and
to discourage the grouping of children in play on the streets.
With children and with all individuals, large or small, a great factor
in exposure and probably in the transmission of the disease is the
necessary _crowding on street cars and in public buildings_. Here is a
potent source which requires deep study and new treatment. Some cities
have with partial success attempted lessening the congestion in public
conveyances at the beginning and closing of business hours by arranging
with the various offices, stores, etc., that the opening and closing
times occur at different hours. In order that this procedure may work it
is important that the employees of a factory or store which closes early
must ride to their destination at the time of closing and not remain in
the congested business districts. Here again it is a problem of
educating the public to a point where they will co-operate
intelligently.
It has been amply demonstrated that _crowd gatherings_ markedly
facilitate the spread of the disease. Mass meetings should be prohibited
and gatherings in and out of doors should be discouraged. The public
should be taught that the safest place is at home.
What _instructions_ can we give _to the individual_ for his own
protection? There are at least six precautions based on scientific
knowledge. They are:
First: Avoid crowds.
Second: Avoid crowding in the family.
Third: Sleep alone.
Fourth: Pay particular attention to personal hygiene.
Fifth: Boil all dishes, etc., after meals.
Sixth: Do not eat in insanitary restaurants. Eat at home.
Should cases be _isolated_? Should they be quarantined until no longer
infective? The experience of the last epidemic has rendered us
pessimistic. We have found that isolation and quarantine does little or
no good. Institutions which were held under rigid quarantine for the
first months of the epidemic were later invaded when discipline became
lax. The disease thereafter spread often as extensively as it would
have, had there been no delay. But, on the other hand, there is record
of some institutions in which the quarantine lasted throughout the
epidemic and in which the inmates never became ill. All of our past
experience with infectious diseases leads us to believe that isolation
of cases should be enforced. The experience of 1918 should not cause us
to change from this point of view. Up until now the procedure has been
without results. It has been nearly impossible to enforce it. Further
study must be made before any definite conclusion can be reached.
The same in general may be said regarding _disinfection_ after recovery
of a case of influenza. Today most people believe that disinfection is
unnecessary. The work of Lynch and Cumming, if correct, would indicate
the contrary. The possibility of transmission through inanimate objects
has not as yet been completely eliminated.
The _efficacy of face masks_ is still open to question. Certainly the
face mask as extensively used during the 1918 epidemic was of little
benefit and in many cases was, without doubt, a decided detriment. The
same mask was worn until it was filthy. It was not worn in such a way as
to be a protection. Even had the nose and mouth been efficiently
protected, the conjunctivae remained unprotected. The work of Maxcy and
of Vincent and others has demonstrated the importance of the
naso-lachrymal duct as a possible portal of entry into the respiratory
tract proper. After cultures of Bacillus prodigiosus were sprayed upon
the ocular conjunctivae these organisms have been recovered from the
nose within five minutes, from the nasopharynx within fifteen minutes
and from the feces within twenty-four hours. One difficulty in the use
of the face mask is the failure of co-operation on the part of the
public. When, in pneumonia and influenza wards, it has been nearly
impossible to force the orderlies or even some of the physicians and
nurses to wear their masks as prescribed, it is difficult to see how a
general measure of this nature could be enforced in the community at
large. If masks are to be used they should be employed in the same
manner as for protection against the plague. They should be made to
cover the entire head. This procedure has been recommended particularly
by Vincent and by Thorne.
It is safe to say that the face mask as used was a failure.
_Problems for the future._ _Constructive research._—While pure
epidemiologic study of influenza will not demonstrate the causative
agent, it is the chief procedure upon which we can at present rely for
improvement in our methods of combat. Many important laboratory
contributions have been made during the last two years. The majority
have been without immediate value to the health officer. The author
suggests in the following paragraphs a plan of study, based upon past
epidemics and the experiences of the last pandemic, as epitomized in the
preceding chapters. During the exposition of this subject we have drawn
certain conclusions and have developed some theories. We believe that
they explain the facts correctly, but should the hypotheses prove not
entirely correct the value of the following outline for study will be in
no way impaired.
To become thoroughly acquainted with epidemic influenza in all its
manifestations would require a life time of study. Knowledge of the
disease would be greatly furthered if competent epidemiologists should
see fit to devote their entire time to a study of the disease in its
various ramifications. The author suggests a research organization of
individuals whose function it would be to become completely acquainted
with influenza. The organization should be under the direction of a
competent board of epidemiologists. Under them would work several groups
composed of epidemiologists, bacteriologists and others. There should be
sufficient groups so that they might be distributed to diverse regions
of the earth. They should be equipped for travel, with mobile
bacteriologic laboratories and all the necessary equipment for
epidemiologic surveys, so that at a moment’s notice they could proceed
to wherever an epidemic of any disease simulating influenza is reported
to be prevalent. The working groups would be under the administrative
control of the central directors and would make their reports to them.
All groups should be so distributed geographically as to have easy and
rapid access to any community in which an epidemic might occur. They
would keep themselves informed concerning the disease prevalence in all
communities under their jurisdiction. This would be done through the
co-operation of the civil health authorities and through the utilization
of all other available sources of information. The central board should
be constantly in touch with the groups, so that the infectious disease
prevalence in all parts of the world would be known at all times.
Had such an organization been in existence during the last thirty years,
every one of the so-called influenza epidemics reported in one place or
another would have been investigated. Detailed epidemiologic,
statistical, demographic and bacteriologic reports would have been made.
It matters little how small or insignificant the outbreak appears to be.
Even the smallest have their characteristic features and are worthy of
study. If we study epidemic influenza but once in thirty years, we will
never become well acquainted with the disease. We must see it repeatedly
and frequently. If it does not exist during the intervals we must study
the diseases simulating it. It is surprising how much of the knowledge
acquired in 1889 was forgotten by 1918. Even some of the more important
features had passed from memory. Thus we find statements in 1918 that
the age morbidity was quite different from that in all preceding
epidemics. Research into the literature of the past does not corroborate
this impression.
If influenza is scattered throughout the earth in mild form, it would
avail us but little to send a commission to Bokhara to study the endemic
focus supposed by some to exist in Turkestan. Even though the disease
were endemic in that country, one would not expect to discover epidemics
there. The general immunity of the population in the endemic area is
probably increased. Nevertheless one unit might well be stationed in
Turkestan, there to study the existing conditions regarding infectious
diseases.
There would be ample work for all groups at all times. The study would
not be limited to a consideration of infectious diseases. Sociologic
conditions may be of importance. We have recorded instances of this.
Wherever there is an unusual concentration of large masses of
individuals the investigators should study the results of such
concentration.
An advantage of this organization would be that the groups through their
central bureau would establish an information bureau of infectious
disease prevalence analogous to the popular weather bureau of today.
They would report the presence of a cloud before it had appeared on the
local horizon.
In the absence of any epidemics resembling influenza, there would be
abundant opportunity for correlated work. We have mentioned the
epidemiologic resemblances between influenza and certain other
infectious diseases. Comparative study of any or all of them is of
importance. The bacteriologist and the immunologist would find plenty of
material in the study of measles prevalences. The two diseases are so
similar in their manner of spread, in the probable mode of transmission,
in their clinical characteristics and in the results of laboratory
attempts at transmission, that one must assume that the causative
viruses are not dissimilar. Any new facts that we may gain concerning
measles will be of value in the study of influenza.
Many years could be well devoted merely to a study of immunity in
influenza.
The results obtained by this proposed organization for the investigation
of influenza would be slow in achievement. The study is not of a type
calculated to appeal to the popular imagination. Communities in which
the dread of an imminent pestilence is not present would subscribe with
some hesitation to appeals for pecuniary assistance. Fortunately,
however, there are in existence several organizations already well
developed along these lines, organizations chiefly interested in certain
other diseases. There can be no doubt but that at the present time the
financing of such a broad project could be arranged, and that the groups
could be efficiently organized on the basis of experience already gained
in similar projects.
Crookshank well remarks that our present epidemiologic intelligence
service is hardly superior to that of a Meteorologic Office which only
gives warning of rain when unfurled umbrellas pass along the street.
Influenza will surely return. There will be mild epidemics within the
next few years. In time another pandemic will arrive, and after it will
come pandemic after pandemic. In 1918 as in 1889 we were caught
unprepared. Let us do our utmost to prevent the recurrence of this
tragedy. To delay is to loose the valuable information gained during the
last two years. The future is not without well grounded hope, but
success will not be achieved until we have attained a much deeper
understanding of the epidemiology of influenza.
BIBLIOGRAPHY.
ABBOTT, SAMUEL W.
1890. The influenza epidemic of 1889–90. 21st Annual Report of
State Board of Health of Mass. Pub. Doc. No. 34, 307–384.
1892. Twenty-third Annual Report of the State Board of Health of
Mass., 745.
1893. Twenty-fourth Annual Report of the State Board of Health of
Mass., 33.
1894. Twenty-fifth Annual Report of the State Board of Health of
Mass., 41.
ABRAHAMS, HALLOWS, EYRE AND FRENCH.
1917. Purulent bronchitis; its influenzal and pneumococcal
bacteriology. Lancet, II, 377.
ABT, ISAAC, A.
1919. Influenza in a newly born infant. Jour. Am. Med. Ass.,
LXXII, 980.
ACHARD, C., LEBLANC, A. AND LAVEDAN.
1919. Influenza in infants. Reviewed in Jour. Am. Med. Ass.,
LXXIII, 370.
AMBERSON, J. B., JR. AND PETERS, A., JR.
1919. Epidemic influenza among tuberculous patients at the Loomis
Sanatorium. Am. Rev. Tuberculosis, III, 359.
1920. Influenza and tuberculosis. Ibid., IV, 71.
AMELUNG, W.
1919. Influenza in relation to pulmonary tuberculosis. Münch. Med.
Woch., LXVI, 1321.
AMERICAN PUBLIC HEALTH ASSOCIATION.
1919. Section on vital statistics; committee on statistical study
of the influenza epidemic. Boston Med. and Surg. Jour.,
CLXXX, 22.
ARMSTRONG, D. B.
1919. Influenza: Is it a hazard to be healthy? Certain tentative
considerations. Ibid., 65.
1919. Influenza observations in Framingham, Mass. Am. Jour. Pub.
Health, IX, 960.
APERT AND FLIPO.
1920. Influence du sex aux différents ages sur la gravité de la
grippe. Bull. et Mém. Soc. Méd. des Hôp. de Paris, 321.
ATILES, F. DEL VALLE.
1919. Influenza in Porto Rico. Abstr. in Jour. Am. Med. Ass.,
LXXII, 688.
BARTHÉLEMY.
1920. La pandemie grippale de 1918–1919 à Bizerte. Rev. d’Hygiène
et de Police Sanit., XLII, 41.
BENJAFIELD, J. D.
1919. Notes on the influenza epidemic in the Egyptian
Expeditionary Force. Brit. Med. Jour., II, 167.
BERGHOFF, R. S.
1919. Influenza as a factor in reactivation of quiescent and
healed pulmonary tuberculosis. Am. Rev. Tuberculosis, III,
370.
BLASCO, A. N.
1919. Influence of the influenza epidemic on pulmonary
tuberculosis. Abstr. in Jour. Am. Med. Ass., LXXII, 79.
BREWER, I. W.
1918. Report of epidemic of “Spanish Influenza” which occurred at
Camp A. A. Humphreys, Va., during September and October,
1918. Jour. Lab. and Clin. Med., IV, 87.
BROWNLEE, JOHN.
1919. The next epidemic of influenza. Lancet, II, 856.
1920. Public Health Administration in epidemics of measles. Brit.
Med. Jour., I, 534.
CADBURY, W. W.
1920. Influenza pandemic as it affected Canton, China. Med. Rec.,
XCVII, 391 and China Med. Jour., XXXIV, 1.
CADHAM, F. T.
1919. The use of a vaccine in the recent epidemic of influenza.
Lancet, I, 885.
CARNWATH, T.
1918–1919. Influenza—Extracts from the Annual Report of the Medical
Department of the Local Government Board, 1918–19.
1918. Lessons of the Influenza Epidemic of 1918. Jour. State Med.,
XXVII, 142.
CHAUFFARD.
1920. L’immunité acquise au cours des épidémies recentes de
grippe. Bull. Acad. de Med., LXXXIII, 394.
CHICAGO DEPT. OF HEALTH.
1919. A report on the epidemic of influenza in Chicago occurring
during the fall of 1918. Reprinted from the octennial report
1911–1918. Dept. of Health, CL, 80, Chicago.
COAKLEY, C. G.
1908. Throat and sinus complications of grip. N. Y. State Jour. of
Med., VIII, 192.
COLALÉ, N.
1919. Quinine in prophylaxis of influenza. Abstr. in Jour. Am.
Med. Ass., LXXII, 969.
CONSTABLE, EVELYN A.
1919. Influenza and diphtheria. Lancet, I, 563.
CROOKSHANK, F. G.
1919. Epidemic encephalo-myelitis and influenza. Lancet, I, 79.
CUMMING, J. G.
1919. A brief review of indirect contact transmission and a
preliminary report of corroborative laboratory research. Am.
Jour. Pub. Health, IX, 414.
DAVIS, W. H.
1919. The influenza epidemic as shown in the weekly health index.
Am. Jour. Pub. Health. Ibid., 50.
DEBRÉ, ROBERT AND JACQUET, PAUL.
1920. Grippe et Tuberculose. L’anergie grippale et la tuberculose
de l’adulte. Paris Medical, 24.
DENCH, EDWARD B.
1918. The aural complications of grip. N. Y. State Jour. of Med.,
VIII, 193.
DEWAR, MICHAEL.
1905. Influenza. Brit. Med. Jour., II, 131.
DICKINSON, W. H.
1919. Influenza and chronic lung disease. Lancet, I, 314.
DOPTER.
1920. Sur l’immunité acquise par une première atteinte de grippe.
Bull. Acad. de Med., LXXXIII, 415.
DÖRBECH, F.
1919. Die Influenzapandemie des Jahres 1918. Deutsche Med. Woch.,
XLV, 716–743.
DUBLIN, L. I.
1919. Jour. Am. Med. Ass., LXXIII, 89.
1920. The mortality of bituminous coal miners from
influenza-pneumonia. Oct. to Dec., 1918. Jour. Indust.
Hygiene, I, 483.
DUDLEY, S. F.
1919. The epidemic of grippe as it was observed at Scapa Flow.
Jour. Roy. Nav. Med. Service, V, 359.
DUNLOP, J. C.
1919. Notes on the influenza mortality in Scotland during the
period July, 1918, to March, 1919. Edinb. Med. Jour., XXII,
403, and XXIII, 46.
DUNN, R. A. AND GORDAN, M. H.
1905. An epidemic simulating influenza, II, 425.
EICHHORST, H.
1920. Character of present epidemic influenza. Schweiz. Med.
Woch., L, 281.
EPIDEMIC OF INFLUENZA.
1918. China Med. Jour., XXXII, 399.
ERLENDSSON, V.
1919. Influenza in Iceland. Abstr. in Jour. Am. Med. Ass., LXXII,
1880.
ESCOMEL, E.
1919. Influenza in Rio de Janeiro. Abstr. in Jour. Am. Med. Ass.,
Ibid., 903.
EVANS, W. A. AND HECHARD, M. O.
1918. The 1890 epidemic of influenza in Chicago and its influence
on mortality, 1890 to 1893, inclusive. Am. Jour. Pub.
Health, VIII, 845.
FILTZOS, T. C.
1919. “Epidemic Influenza in Greece.” Public Health Reports. Mar.
14,
FINKLER, DITMAR.
1898. “Influenza” in 20th Century Practice of Medicine, XV, 1–249.
Wm. Wood & Co.
FISHBERG, M.
1919. Influenza and tuberculosis. Am. Rev. of Tuberculosis, III,
532.
FLETCHER, WM.
1919. Meningococcus bronchopneumonia in influenza. Lancet, I, 104.
FORBES, ROY G. AND SNYDER, HELEN A.
1918. Study of the leucocytes in an epidemic of influenza. Jour.
Lab. and Clin. Med., III, 758.
FRANKEL AND DUBLIN.
1919. Influenza mortality among wage earners and their families. A
preliminary statement of results. Am. Jour. Pub. Health, IX,
731.
FREY, W.
1918. Studien zur Epidemiologie der Influenza 1918. Wien. klin.
Woch., XXXI, 1370.
FROST, W. H.
1919. The epidemiology of influenza. Jour. Am. Med. Ass., LXXIII,
313.
1919. The epidemiology of influenza. Public Health Reports, XXXIV,
1823.
1920. Statistics of influenza morbidity with special reference to
certain factors in case incidence and case fatality. Public
Health Reports, XXXV, 584.
FROST, W. H. AND SYDENSTRICKER, E.
1919. Influenza in Maryland. Preliminary statistics of certain
localities. Public Health Reports, XXXIV, 491.
1919. Epidemic influenza in foreign countries. Public Health
Reports. Ibid., 1361.
GARVIE, A.
1919. The spread of influenza in an industrial area. Brit. Med.
Jour., II, 519.
GIBBON, JOHN G.
1919. Acquired immunity in influenza. Lancet, I, 583.
GREENWOOD, M.
1918. The epidemiology of influenza. Brit. Med. Jour., II, 563.
1919. On the theory of epidemic constitutions. Brit. Med. Jour.,
Sept. 27.
GUILFOY, W. H.
1918. Statistics of the epidemic of influenza in New York City.
Bull. Dep. Health, N. Y. City, N. S. XIII, 265.
HALL, H. C.
1920. Immunity to influenza. Ugeskrift for Laeger, Copenhagen.
Abstr. in Jour. Am. Med. Ass., LXXIV, 1202.
HALL, M. W.
1920. Epidemiology of influenza. Mil. Surgeon, XLVI, 564, and Ky.
Med. Jour., XVIII, 108.
HAMILTON, J. H. AND LEONARD, A. H.
1919. Acquired immunity to influenza as indicated by a recurrent
epidemic in an institution. Jour. Am. Med. Ass., LXXII, 854.
HAMMOND, ROLLAND AND SHORE.
1917. Purulent bronchitis. Lancet, II, 41.
HAWES, J. B.
1919. Experience of Massachusetts State Sanatoria for
Tuberculosis, during the recent influenza epidemic. Bost.
Med. and Surg. Jour., CLXXX, 35.
HIRSCH, A.
1861–86 Histor.-geograph. Pathologie, Stuttgart.
HSIEH, E. T.
1918. The recent epidemic of influenza in Peking. Nat. Med. Jour.
China, Shanghai, XXII, 129.
HUNZIKER, H.
1919. Epidemiologie der Grippe. Cor. Bl. f. Schweiz. Aertze.
Basel, XLIX, 551.
HURLEY, J. R.
1919. Influenza with special reference to the pandemic of 1918.
Med. Rec., N. Y., XCVI, 651.
ILVENTO, A.
1919. Il decorso epidemiologico e clinico dell’ influenza. Ann.
d’Ig. Roma. XXIX, 132.
INDIANS.
1919. Influenza among American Indians. Public Health Reports,
XXXIV, 1008.
INFLUENZA(?) IN CHINA.
1918. China Med. Jour., XXXII, 608.
INFLUENZA IN INDIA.
1919. Public Health Reports, XXXIV, 2300.
INFLUENZA IN JAPAN.
1920. China Med. Jour., XXXIV, 217.
JEANERET, MINKINE.
1918. Remarques concernant la grippe épidémique, son étiologie et
son épidémiologie. Rev. Med. de la Suisse Rom., Genève,
XXXVIII, 634.
JOLTRAIN, E. AND BAUFLE, P.
1919. Epidemic of influenza. Abstr. in Jour. Am. Med. Ass., LXXII,
527.
JONES, C. HAMPSON.
1908. The grip in Baltimore. N. Y. State Jour. of Med., VIII, 191.
JORDAN, E. O.
1918–19. Notes on the epidemiology of influenza. Proc. Inst. Med.
(Chicago), II, 135.
JORDAN, E. O. AND SHARP, W. B.
1920. Immunity in influenza. Jour. Infect. Dis., XXVI, 463.
JORDAN, E. O., REED, D. B. AND FINK, E. B.
1919. Influenza in three Chicago groups. Public Health Reports,
XXXIV, 1528.
JUNDELL, I.
1912. Influenzal meningitis and pneumonia. Hygiea, Stockholm,
LXXIV.
KELLOGG, WILFRED H.
1919. Jour. Am. Med. Ass., LXXIII, 891.
KAHN, A.
1920. Cause, prevention and cure of influenza and allied diseases.
Med. Rec., XCVII, 481.
KOPF, E. W.
1919. A statistical study of the influenza epidemic. Jour. Am.
Med. Ass., LXXII, 593.
LAMB, FREDERICK H.
1918. Epidemic cerebrospinal meningitis at Camp Cody. Jour. Lab.
and Clin. Med., IV, 387.
LAMB, F. H. AND BRAMIN, E. B.
1919 The epidemic respiratory infection at Camp Cody, N. M.
Jour. Am. Med. Ass., LXXII, 1057.
LANCET.
1919. Lessons of the influenza epidemic. Leading Article. Lancet,
I, 72.
1920. Influenza and encephalitis lethargica in Switzerland.
Lancet, I, 888.
1920. Influenza in Zürich. Lancet, I, 838.
1920. Influenza in Paris. Lancet, I, 1133.
LEICHTENSTERN, O.
1896. Influenza und dengue. Nothnagel’s spezielle Pathologie und
Therapie. 1896.
LEE, S. T.
1919. Some of the different aspects between influenza-pneumonia
and pneumonic plague. N. Y. Med. Jour., CX, 401.
LEWIS, D. M.
1919. Epidemiology of influenza. Bost. Med. and Surg. Jour.,
CLXXXI, 540.
LICHTY, J. A.
1908. Grip—The epidemic in Pittsburgh. N. Y. State Jour. of Med.,
VIII, 191.
LONGCOPE, W. T.
1919. Survey of the epidemic of influenza in the American
Expeditionary Forces. Jour. Am. Med. Ass., LXXIII, 189.
HOWARD, D. C. AND LOVE, A. G.
1920. Influenza in the U. S. Army. Mil. Surg., XLVI, 522.
LYNCH, CHAS., AND CUMMING, JAS. G.
1920. The epidemiology of influenza-pneumonia. Jour. Lab. and
Clin. Med., V, 364.
MCAFEE, LOY.
1919. Epidemic influenza in the medical and surgical history of
the Civil War. Jour. Am. Med. Ass., LXXII, 445.
MCCALLUM, WM. G.
1918. Pathology of the pneumonia in the United States army camps
during the winter of 1917–1918. Monograph. Rock. Inst. Med.
Res.
MCCOY, G. W.
1919. Status of prophylactic vaccination against influenza. Jour.
Am. Med. Ass., LXXIII, 401.
MCCOY, G. W., MURRAY, V. B. AND TEETER, A. L.
1918. The failure of a bacterial vaccine as a prophylactic against
influenza. Jour. Am. Med. Ass., LXXI, 1997.
MCDONALD, J. H.
1920. Influenza. Indian Med. Gaz., LV, No. 6.
MCKENDRICK, A. G. AND MORISON, J.
1919. Determination of incubation periods from maritime
statistics, with particular reference to incubation period
of influenza. Indian Jour. Med. Res., VII, 364.
MCLAUGHLIN, A. J.
1920. Epidemiology and etiology of influenza. Bost. Med. and Sur.
Jour. CLXXXII.
MCNALTY.
1920. Influenza. Nelson’s System of Medicine, 1920.
MACRAE, DUNCAN M.
1919. Influenza and chronic lung disease. Lancet, I, 281.
MACKLIN.
1920. Influenza amongst the Lapps. Brit. Med. Jour., I, 465.
MAILLARD, G. AND BRUNE.
1919. Influenza and epilepsy. Abstr. in Jour. Am. Med. Ass.,
LXXII, 1038.
MALONE, R. H. AND MCKENDRICK, A. G.
1919. Evidence regarding the immunity conferred by an attack of
influenza, with a study of three local epidemics. Indian
Jour. Med. Res., VII, 373.
MASON, A. L.
1890. Bost. Med. and Surg. Jour., Feb. 13, 1890.
MATHERS, GEO.
1917. Etiology of the epidemic acute respiratory infections
commonly called influenza. Jour. Am. Med. Ass., LXVIII, 678.
MAYER, C. P.
1913. Pulmonary influenza. Semana Medica, XX.
MEDICAL SUPPLEMENT TO THE REVIEW OF THE FOREIGN PRESS.
1918–1919. July, 1918 to April, 1919, inclusive.
MERKLEN, P.
1918. Influenza in Bretagne. Bull. Soc. Méd. des Hôp. de Paris,
Oct. 11, 1918, 924.
MINAKER, A. J. AND IRVINE, R. S.
1919. Prophylactic use of mixed vaccine against pandemic influenza
and its complications. Jour. Am. Med. Ass., LXXII, 847.
MOODY, A. M. AND CAPPS, J. A.
1916. Notes on the grip epidemic in Chicago. Jour. Am. Med. Ass.,
LXVI, 1696.
MORTALITY 1889–1918.
1919. A comparison of the mortality rate by weeks during the
influenza epidemic of 1889–90 and during the primary stage
of the influenza epidemic of 1918, in twelve cities in the
United States. Public Health Reports, XXXIV, 157.
MURPHY, T. J.
1919. Postinfluenzal tuberculosis. Boston Med. and Surg. Jour.,
CLXXXI, 266.
NETTER, A.
1918. L’épidémie d’influenza de 1918. Paris Médical, Nov. 16,
1918, 382.
NEWSHOLME, A.
1920. Influenza. A discussion. Longmans, Green & Co., CII, 80.
1907. Influenza from a public health standpoint. Practitioner,
118.
1919. Jour. Am. Med. Ass., LXXIII, 890.
1919. Influenza from a public health standpoint. Practitioner,
CII, 6.
NIEMANN AND FOTH.
1919. Deutsche Med. Woch., XLV, 471.
OFFICE INTERNATIONAL D’HYGIÈNE PUBLIQUE.
1918. X, also Jan. and Feb., 1920, XII.
OPIE, FREEMAN, BLAKE, SMALL AND RIVERS.
1919. Pneumonia at Camp Funston. Report to Surgeon General. Jour.
Am. Med. Ass., LXXII, 108.
1919. Pneumonia following influenza at Camp Pike, Ark. Ibid., 556.
ORTICONI, A., BARBIÉ AND ANGÉ.
1919. Pathogenesis of influenza. Abst. in Jour. Am. Med. Ass.,
LXXIII, 69.
OVAZZA, V. E.
1919. Prophylaxis of influenza. Abst. in Jour. Am. Med. Ass.,
LXXII, 1335.
PARKES, EDMUND A.
1876. “Influenza” in Reynolds’ System of Medicine. I, 28.
PARSONS, H. FRANKLIN.
1893. Local Government Board Reports. C–6387 (1891) and C–7051
(1893).
1893. A further report on the influenza epidemics of 1889–90, 1891
and 1891–92. Local Government edition. London, 1893.
PARSONS, H. C.
1919. Official report on the influenza epidemic 1918. Canad. Med.
Ass. Jour., Toronto, IX, 351.
PEARL, RAYMOND.
1919. On certain general statistical aspects in the 1918 epidemic
in American cities. Public Health Reports, Aug. 8, 1919.
PECK, J. H.
1920. Relation of influenza to tuberculosis. Iowa State Med. Soc.
Jour., X, 42.
PÉHU, M. AND LEDOUX, E.
1918. Revue documentaire sur l’épidémie actuelle de grippe en
France. Ann. de Med., V, 579.
PNEUMONIC PLAGUE.
1918. China Med. Jour., XXXII, 146.
POLLARD, R.
1920. Control of influenza. Brit. Med. Jour., I, 258.
PRUVOST, E.
1919. Considérations inspirées par la récente épidémie de grippe
sur la pathogénie de cette maladie et sur celle de la
tuberculose. Bull. et Mém. Soc. Méd. des Hôp. de Paris, 3
s., XLIII, 783.
RAFFELT, F.
1920. Influenza Epidemie, 1918. Wien. klin. Woch., XXXIII, April
15.
RENON, L. AND MIGNOT, R.
1920. La grippe de 1920 a l’hôpital Necker. Bull, et Mém. Soc.
Med. des Hôp. de Paris, 509.
PREVENTION BUREAU.
1918. Report of the Shansi Plague. China Med. Jour., XXXII, 559.
ROUSSY, B.
1919. Nature et modes d’action de l’agent, pathogène infectieux de
la grippe ou influenza. Rev. d’hyg., XLI, 104.
ROSE, F. G.
1919. The influenza epidemic in British Guiana. Lancet, I, 421.
ROSENAU, M. J.
1919. Experiments to determine the mode of spread of influenza.
Jour. Am. Med. Ass., LXXIII, 311.
ROSENOW, E. C.
1919. Prophylactic inoculation against respiratory infections.
Jour. Am. Med. Ass., LXXII, 31.
ROYS, CHAS. K.
1918. Report on epidemic of pneumonic plague in Tsinauflu, 1918.
China Med. Jour., XXXII, 346.
RUHRÄH, J.
1919. Some of the aspects of epidemic influenza in children. Med.
Clin. North Am., II, 1597.
RUSSELL, W.
1919. Some aspects of the influenza epidemic. Lancet, I, 690.
ROBERTSON, JNO. D., AND KOEHLER, GOTTFRIED.
1918. Preliminary report on the influenza epidemic in Chicago. Am.
Jour. Pub. Health, VIII, 849.
RONDOPOULOS, P. J.
1919. Influenza in Greece. Abstr. in Jour. Am. Med. Ass., LXXII,
1947.
SAHLI, H.
1919. Influenza. Abstr. in Jour. Am. Med. Ass., Ibid., 687.
SANZ, E. F.
1919. Jacksonian epilepsy following influenza. Abstr. in Jour. Am.
Med. Ass., LXXIII, 73.
SCHOFIELD, F. W. AND CYNN, H. C.
1919. Pandemic influenza in Korea. Jour. Am. Med. Ass., LXXII,
981.
SCOCCIA, V.
1919. Does influenza confer immunity? Abstr. in Jour. Am. Med.
Ass. Ibid., 529.
SELTER, H.
1918. Zur Aetiologie der Influenza. Deutsch. Med. Woch, XLIV, 932.
SHERMAN, C. L.
1913. Common infections that are often erroneously diagnosed as
grip. Jour. Am. Med. Ass., LXI, 1567.
SICILIANO, L.
1919. Qualche osservazione sull’epidemiologia dell’influenza. Riv.
crit. di Clin. Med. Firenze, XX, 97.
SILVESTRI, I.
1919. Quinine, malaria and influenza. Abst. in Jour. Am. Med.
Ass., LXXIII, 304.
SMALL, W. D. D.
1920. Clinical features, etiology and treatment of influenza.
Edinb. Med. Jour., XXV, 15.
SMITH, THEOBALD.
1904. Some problems in the life history of pathogenic
microorganisms. Am. Med., 711.
SOLDAN, C. E.
1919. Influenza in Lima. Abstr. in Jour. Am. Med. Ass., LXXII,
970.
SOPER, GEORGE A.
1919. The influenza-pneumonia pandemic in the American Army camps
during September and October, 1918. Science, N. S., XLVIII,
451.
1919. The efficiency of existing measures for the prevention of
disease. Jour. Am. Med. Ass., LXXIII, 1405.
1919. What is influenza? Boston Med. and Surg. Jour., CLXXXI, 635.
1919. Influenza in horses and in man. N. Y. Med. Jour., CIX, 270.
SPEAR, B. E.
1920. The periodicity of influenza. Lancet, I, 889.
SPOONER, L. H., SCOTT, J. M. AND HEATH, E. H.
1919. A bacteriologic study of the influenza epidemic at Camp
Devens, Mass. Jour. Am. Med. Ass., LXXII, 155.
STALLYBRASS, C. O.
1920. The periodicity of influenza. Lancet, CXCVIII, 372.
STANLEY, ARTHUR.
1918. Notes on pneumonic plague in China. China Med. Jour., XXXII,
207.
STANLEY, L. L.
1919. Influenza at San Quentin Prison, California. Public Health
Reports, XXXIV, 996.
STIVELMAN, B.
1919. Effects of influenza on pulmonary tuberculosis. New York
Med. Jour., LX, 20.
STURROCK.
1905. Notes on an epidemic of influenza, occurring in the
Midlothian and Peebles Asylums. Brit. Med. Jour.
SYDENSTRICKER, EDGAR.
1920. Difficulties in computing civil death rates for 1918 with
especial reference to epidemic influenza. Public Health
Reports, XXXV, 330.
1918. Preliminary statistics of the influenza epidemic. Public
Health Reports, XXXIII, 2305.
TEISSIER, J.
1920. La grippe parallèle des deux grandes pandémies de 1889 et de
1918. Paris Méd., XXXV, 69.
TELLING, W. H. M. AND HANN, R. G.
1913. Influenza with repeated rigors. Practitioner, 764.
DE LOS TERROROS, C. S.
1919. Influenza in children. Abstr. in Jour. Am. Med Ass., LXXII,
764.
TOPLEY, W. W. C.
1919. The spread of bacterial infection. Lancet, II, 1, 45, 91.
USTVEDT, Y.
1919. Influenza in Norway. Abstr. in Jour. Am. Med. Ass., LXXII,
1115.
VAUGHAN, HENRY F.
1920. Influenza in Detroit. Weekly health reports, Commissioner of
Health, Detroit.
VAUGHAN, V. C.
1918. An explosive epidemic of influenzal disease at Fort
Oglethorpe. Jour. Lab. and Clin. Med., III, 560.
1918. The influenza in Germany, Ibid., IV, 83.
1918. Notes on influenza. Ibid., 145.
1918. Influenza and pneumonia at Brest, France. Ibid., 223.
1918. Influenza at Camp Custer. Ibid., 225.
1918. Influenza and pneumonia at Camp Grant. Ibid., 306.
1918. Notes on influenza. Ibid., 309.
1918. Encephalitis lethargica. Ibid., 381.
1919. Jour. Am. Med. Ass., LXXIII, 890.
VAUGHAN, V. C. AND PALMER, GEO. T.
1919. Communicable diseases in the United States Army during the
summer and autumn of 1918. Jour. Lab. and Clin. Med., IV,
586.
1918. Communicable diseases in the National Guard and National
Army of the United States during the six months from Sept.
29, 1917, to March 29, 1918. Jour. Lab. and Clin. Med., III,
635.
VAUGHAN, W. T. AND SCHNABEL, T. G.
1919. Pneumonia and empyema at Camp Sevier. Arch. Int. Med., XXII,
441.
VAUGHAN, W. T.
1918. Clinical manifestations of empyema. Jour. Lab. and Clin.
Med., IV, 123.
VICO, G.
1919. Quinine and influenza. Abstr. in Jour. Am. Med. Ass., LXXII,
1648.
WADSWORTH, A. B.
1919. Results of preventive vaccination with suspensions of the
influenza bacillus. Abstr. in Jour. Am. Med. Ass., LXXIII,
368.
WAHL, H. R., WHITE, B. AND LYALL, H. W.
1919. Some experiments in the transmission of influenza. Jour.
Inf. Dis., XXV, 419.
WALB.
1913. Pneumococcus influenza. Deutsch. Med. Woch., XXXIX.
WALLACE, GEO. L.
1919. Report of the influenza epidemic and experience in the use
of influenza vaccine “B” at the Wrentham State School.
Boston Med. and Surg. Jour., CLXXX, 447.
WATSON, THOMAS.
1872. Principles and Practice of Physic. II, 71.
WATSON, PERCY T.
1919. The epidemic in Shansi; pneumonic plague or influenza? China
Med. Jour., XXXIII, 169.
WEBSTER, J. O.
1871. Report of an epidemic of influenza. Boston Med. and Surg.
Jour., N. S., VII, 377.
WINSLOW, C. E. A. AND ROGERS, J. F.
1920. Statistics of the 1918 epidemic of influenza in Connecticut.
Jour. Infect. Dis., XXVI.
WOLLSTEIN, M. AND GOLDBLOOM, A.
1919. Epidemic influenza in infants. Am. Jour. Dis. of Children,
XVII, 165.
WOODWARD, WM. C.
1918. Influenza in Boston. Monthly Bull, of the Health Dept, of
the City of Boston, VII, 179–186, 205–208, and VIII, 10.
WOOLEY, PAUL G.
1918. The epidemic of influenza at Camp Devens, Mass. Jour. Lab.
and Clin. Med., IV, 330.
1919. An epidemiologic fragment. Med. Quart., Ottawa, I, 325.
ZINSSER, H., BROOKS, H., ET AL.
1920. Manifestations of influenza during the earlier periods of
its appearance in France. Med. Rec., XCVII, 459.
ZINSSER, HANS.
Influenza. Oxford Medical Papers (to be published).
A most comprehensive bibliography of the literature covering the
epidemiology of influenza up until 1896 is to be found in
Leichtenstern’s original monograph.
APPENDIX
[Illustration:
FORM A.—Household record, used in Boston influenza census. (See page
127.)
]
[Illustration:
FORM A.—(_Continued._)
]
[Illustration:
FORM B.—Individual Record obtained for each person in every family
canvassed, whether the individual gave a history of influenza (1918
or 1920) or not. (See page 127.)
]
[Illustration:
FORM B.—(_Continued._)
]
------------------------------------------------------------------------
TRANSCRIBER’S NOTES
1. Silently corrected obvious typographical errors and variations in
spelling.
2. Retained archaic, non-standard, and uncertain spellings as printed.
3. Enclosed italics font in _underscores_.
4. Denoted superscripts by a caret before a single superscript
character or a series of superscripted characters enclosed in
curly braces, e.g. M^r. or M^{ister}.
5. Denoted subscripts by an underscore before a series of subscripted
characters enclosed in curly braces, e.g. H_{2}O.
*** End of this LibraryBlog Digital Book "Influenza : An epidemiologic study" ***
Copyright 2023 LibraryBlog. All rights reserved.