Parkes, writing in Reynolds’ System of M_Influenza（#72239）

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.

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