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The viruses of influenza
PUBLIC HEALTH where overcrowding exists such diseases attack, on the average, at an earlier age, with the consequently greater risks of complications and death. It is not unreasonable, too, to make directly attributable to poor housing the observation that the incidence of some digestive diseases was higher in households without inside flush toilets not shared by other households than in those which enjoyed such facilities, since the digestive diseases not thought to be associated with sanitation show no such trend. Despite the impossibility of assessing the precise effect of housing conditions, there is no difficulty m accepting the authors' observation that an excess illness rate certainly occurs in the low-income, poorlyhoused populations, or, in other words, in those least able to meet the burden of disease.
In view of proposed developments in the organisation of fracture treatment and of the recent extension of the classes of fracture cases admitted under the Emergency Hospital Scheme, the Minister of Health has had under review the need for increasing the number of trained occupational therapists whose services can be made available for patients treated under the Scheme. The new arrangements for training are set out in Circular 2889. The Dorset House School of Occupational Therapy, evacuated from Bristol, has arranged to provide special shortened courses of six months' training at Barnsley Hall Emergency Hospital, Bromsgrove, Worcestershire. These courses are designed for candidates who are qualified masseuses and, if successfully completed, will entitle the student to a special War Emergency Diploma of the Association of Occupational Therapists. The masseuses accepted for the course will be transferred for the six months to Barnsley Hall, where they will be accommodated and boarded free of charge and will not be expected to pay any fees or other charges in connection with the training course or the taking of the Diploma. They will, in addition, receive a personal allowance of £25 for the six months' course. They will be required to undertake to serve in hospitals in the Emergency Hospital Scheme on the completion of training. The first course began on July 1st, 1941, and will continue until December 80th. The Minister is anxious that hospitals in the Scheme which are employing masseuses should bring these facilities to their early notice.
British Drug Houses, Ltd., have put on the market vitamin C in tablets containing 5, 25 and 50 rag. of ascorbic acid respectively, and also in a sterile solution for injection. Tablets for infants (5 mg.) dissolve readily in warm milk or in the infant's feed. It is pointed out that in solution vitamin C is not a stable substance. For this reason the tablets should not be dissolved in very hot liquids nor should they be added a long time before the feed is given. 206
AUGUST THE VIRUSES OF INFLUENZA By RALPH M. F. PICKEN, M.B., CH.B., B.SC., D.P.H.,
Mansel Talbat Pro[essor o[ Preventive Medicine, The University o[ Wales When medical interest in influenza was sharply awakened by the epidemics of 1918-19, the evolution of the disease in individual eases, the pathological findings in those patients who died, and the contrast between the summer outbreak of 1918 and the subsequent winter and spring phases, all pointed to a basic infection by an unknown pathogen of relatively slight lethal power, paving the way for secondary invasion by several known micro-organisms which might lead to death by setting up pneumonia dr some other grave complication. The nature of the basic infection became clear later, when a virus was isolated from patients suffering from the disease (Smith et al., 1933). Its identification made possible a study of the clinical symptoms in successive waves of influenza-like disease, in order to ascertain whether these symptoms differed sufficiently in cases harbouring and not harbouring the virus to justify the differentiation between true influenza and its mimics by clinical means alone. Stuart-Harris and his colleagues (1938) thought that they had partly succeeded in achieving this distinction after studying closely the behaviour of a number of outbreaks in 1936-37. They contrasted true influenza--a disease of sudden onset, severe cor~stitutional symptoms, dry pharyngitis, and bronchiolitis--with "febrile catarrh"--more gradual in onset, with less constitutional disturbance, pronounced exudative catarrh, and bronchitis. In the former, isolation of the virus and serological reaction to it were to be expected, but not so in the latter. When, however, similar enquiries were pursued by the same workers in 1939 (Stuart Harris et al., 1940), there was far less success in isolating the virus from cases seeming to present the true clinical picture, and the clinical distinction between positive and negative cases could no longer be sustained. All along they had emphasised the difficulties which might be anticipated from the accumulating evidence that viruses varied in their response to laboratory tests, although overlapping antigenically, and several of those isolated in 1939 were anomalous in their unready adaptability to mice. The definite identification by Francis (1940) of a second strain, serologically quite unrelated to those already known, therefore came as no surprise, and now the slightly varying virus originally isolated has been styled Influenza virus A, while that recently identified by Francis is known as Influenza virus B. Possibly strains of this virus may come to be as numerous as those of Streptococcus pyogenes or the types of Streptococcus pneumoniae.
Age.Variations in Hungary Some observations made in Hungary (Taylor et al., 1941) suggest that there may be an epidemiological means of differentiating between outbreaks of disease of an influenzal type although the symptoms and signs are clinically indistinguishable. "Complicated influenza" is a notifiable disease in Hungary, the term no doubt covering cases the majority of which would correspond with our influenzal pneumonia. When the
1941
PUBLIC HEALTH
age-grouping of such cases is studied from year to year in Hungary a material difference is observed in socalled epidemic years, when the virus can be isolated from cases, and in non-epidemic years, presenting few such cases. In the latter, ages under 5, and to a less extent under 10, bear the brunt of the incidence. ILl epidemic years, on the other hand, the incidence is far less concentrated upon these ages. If it be assumed that epidemic influenza in certain years--when widespread infection with the virus can be technically established-is something superimposed on the annual recurrence of influenza-like disease, and the average incidence at each age during a series of non-epidemic years is subtracted from the average of epidemic years, it is shown that the excess mortality in the latter varies comparatively little from age to age and affects old people to an unusual extent. It is in fact nearly as heavy at ages over 55 as it is under 5. A sudden change of age in persons notified as suffering from complicated influenza (or presumably from influenzal pneumonia) might therefore be a useful indication that an epidemic of true influenza had begun.
perhaps safer to leave this year out of calculation. The years 1931 and 1932 had an intermediate position as regards mortality and may also be disregarded in the search for contrasts. If there is any contrast it should be shown by the epidemic and non-epidemic years as defined above. The average mortality from influenza at certain ages for these two groups of years is shown in. Table L It is quite obvious that the form of distribution is the same whether we consider epidemic years, or nonepidemic years, or the excess mortality in epidemic years over expectation based on non-epidemic years. If anything, this excess falls more heavily at the extremes of life than the usual mortality in nonepidemic years; but the difference is negligible. There is no cbnfirmation whatever that influenza of the modern type in England and Wales differs from year to year in its power to kill at different periods of life, in the way in which the incidence of "complicated" influenza varies in Hungary. The comparison, of course, between notification-rates and death-rates is not a good one, but as most cases of influenza die of complications there should be a fairly close association, Age Variations in England and Wales changes in the age of incidence of complicated inThe age-distribution of notified cases of influenzal fluenza, if they occurred, being reflected in some pneumonia for England and Wales is not given in any change in the ages at death. official returns. The Annual Report of the Department of Health for Scotland has included such a dis- The Influenza of 1918-19 tribution of infectious diseases for a number of years, It is generally recognised that the pandemic of but influenzal pneumonia has been distinguished from 1918-19 presented unique features apart from its grave acute primary pneumonias only since 1937. The annual reports of the medical officers of health of large fatality. It came in three waves, first in the summer of towns also usually do not distinguish between different 1918, disorganising works and schools by its sudden forms of pneumonia as regards age-distribution. Pneu- and widespread occurrence, and yet the death returns monia is such a mixed group of infections that its showed comparatively little sign of its presence; the study in mass would not be informative. Tile matter, succeeding waves in early winter and early spring were therefore, can be examined only from death returns. characterised by a high mortality from respirator3" and When the death-rate from influenza at several ages in other complications, especially the earlier of these two England and Wales is studied for each year from 1929 exacerbations. The age-distribution of the death-rate The exceptionally high mortality in (when influenza was highly prevalent) to 1938 it is was unusual. adolescents and young adults is well exhibited in a apparent that the age.distribution is very constant. The "epidemic" years, as judged by the mortality at table compiled by the Registrar-General to compare all ages, were 1929, 1933, and 1937. Those in which 1918 with earlier and subsequent years (Registrarthe disease, by the same criterion, may be said to have General's Review, 1929), and the whole subiect of agebeen non-epidemic were 1930, 1934, 1935, and 1936. incidence and mortality is exhaustively dealt with in a This was almost certainly true also of 1938, but as Special Report on the pandemic (Ministry of Health, sulphonamides had come widely into use in the treat- 1920). Not so widely known are the epidemiologieat ment of pneumonia, and as it is conceivable that the investigations in America of the 1918-19 epidemic by efficacy of these drugs varies from age to age, it is Britten (1932) and of the 1928-29 epidemic by Collins (1934). T h e s e were carried out TABLE I.--ENC, I.AND AND VCALES by means of Average Death-Rate from Influenza per Million :::: special surveys Age by canvassers, a 4555method wh ich All Ages 0515~ °535has become highly organised (1) Epidemic years . . . . . . . . . 584 448 57 1t7 177 359 617 °112 in the U.S.A. (2) Non-epidemic years ...... 119 109 20 3.5 51 93 165 511 Excess of ( l ) over (2) ...... 435 339 37 82 126 266 452 1601 From these reports Table II Death Rate at Each Age compared with Death-Rate at All Ages, taken as 100 has been prepared, Non-epidemic years ...... 100 73 13 23 34 62 111 343 The a c t u a l Excess of (1) over (2) ...... 100 78 8 19 29 61 104 368 rates are not .
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:,
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2:',
",. . . . . . . . .
,
.....
207
PUBLIC HEALTH
AUGUST TABLE II.--U.S.A. SURVEYEDCITIES
comparable with those given for England and Wales in Table
Death Rate from Influenza and Pneumonia per 1,000
Age
I, since t h e y re-
fer to town populations only and
All ages
0-
5-
10-
15- 20-
25-
0.98 100 5.0 100
2.52 257 7.9 158
0.17 17 2.-2 44
0.13 13 2.1 42
0.25 0.35 25 36 3.4 6.2 9.9 68 124 198
0.55 56 7.9 6.3 158 126
90 134
102 116
~-w- •
i n c l u d e all d e a t h s
1928-29 ...
from pneumonia whether due to
1918-19 ...
a n d a g a i n at t h e beginning of the
1928-29 . . . . . . 1918-19 . . . . . .
30-
35-
~
40-
45-
50-
60-
1-17 119 2.6 52
4.3 86
70-
~---v-----~ 4,0 80
0.82 84 2.9 58
4.20 429 5.1 102
influenza or not. The comparison between the American experience of 1928-29, which is also improbable that lowered resistance would might be called a normal influenza epidemic have accounted for the sudden changes in ageperiod, and the exceptional epidemic of 1918-19 is incidence and age-fatality which charaeterised thia not so vitiated, and the difference in age-distribution outbreak, even :though it may be admitted that an is very striking. Whereas in 1928-29 the extremes of important part of the gradual changes in the agelife were chiefly affected, in 1918-19 an exceptional mortality during and after the war from a chronic mortality was suffered in adolescence and young adult infectious disease, tuberculosis, was attributable to this life. The American data enable the age-specific in- cause. On the whole, it is most likely that the 1918-19 cidence rates for influenza and pneumonia in the sur- epidemic was due to the dissemination of an infection veyed cities to be compared, as in Table III. of exceptional virulence. This may have been an If the age-distribution of the incidence for 1928-29 unusual influenza virus or one or other of the microbe taken as representing the usual experience, that for organisms which give rise to the grave complications 1918-19 was obviously abnormal. Ages from 10 to 24, and most of the deaths. The secondary infections were which are usually least affected, were specially hit in due to several bacteria, of which H. influenzae and 1918-19, and the relative incidence over 40 was excep- S. tryogenes were predominant (Ministry of Health, tionally low. This is a different picture from that 1920). If the cause of the exceptional nature of the presented by the contrast between recent epidemic and epidemics of 1918-19 was an unfamiliar micronon-epidemic years in Hungary. Moreover, the 1918-19 organism, it is, on the whole, more likely to have been age-incidence does not entirely account for the age- the virus than one or more of the secondary invaders, distribution of the mortality in that epidemic, which and this is in consonance with the large and seasonally showed a marked excess at somewhat later ages-- unusual, but comparatively non-fatal, first wave in the namely from 20 to 39. This was mainly due, as shown summer of 1918. In this connection it is interesting by the American reports, to heavy complication with to note that Shope (1936) concluded from serological pneumonia at these ages, which was absent in 1928-29. tests on human beings that a strain of virus which he Although the British figures are not presented in quite isolated from cases of swine influenza, a disease appearthe same way, their general form suggests that the ing in America contemporaneously with the 1918-19 behaviour of the epidemic here resembled generally epidemic, and which has persisted since then, was that in America (Ministry of Health, 1929). possibly the survivor of the virus peculiar to that The contrast in age-distribution of the 1918-19 epi- human epidemic. demic with ordinary recurrent outbreaks, together with Burnet (1940) has given reasons in support of the its extreme virulence throughout the world, has pro- view, which has occurred to many others, that a new moted speculation as to its cause. Coming as it did at antigenic strain of virus cropped up during the Four the end of an exhausting world war, its virulence has Years War, its dissemination pandemically being naturally been attributed to the lowered resistance favoured by the crowding in Europe of men induced by that prolonged ordeal. It is unlikely, from many parts of the world. Its exuberant however, that people in the U.S.A., or in neutral lands, multiplication may have been accompanied by where deprivation and exhaustion were far less experi- mutations in. such a way that those dominant in enced than here, were rendered susceptible in this way. the earlier of the three waves left no immunity to those It is conceivable that the same circumstances which responsible for the later, and, like other new infections, light up in war-time that other air-borne infection, it caused no specially selective mortality among cerebrospinal fever, might have had the same effect on children, but rather in young adults. It has always influenza, but in that case the TABLE III.--U.S.A. SURVEYEDCITIES epidemics would Incidence-Rate of Influenza and Pneumonia have been ex(Rate for All Ages taken as 100) pected at the beginning, not at Age the end, of the Four Years War All Ages 0- 5- 10- 15- 20- 25- 80- 35- 40- 45- 50- 60- 70present one. 208
It
100 100
118 104
122 142
78 118
87 108
113 111
111 102
105 80
93 70
90 55
94 42
106 31
1941
PUBLIC HEALTH
seemed to me that this theory leaves unexplained the absence of as great an increase of mortality in the elderly as among young adults. Otherwise it fits the picture well. The question has been discussed at some length because influenza is among the war diseases against which we are being warned to be on our guard. It is right that we should be, but it would also be unwise to assume that because the Four Years War was followed by such a devastating pandemic the one was the cause of the other, and that deprivation and fatigue were the factors underlying it.
Summary' (1) The viruses of influenza have been shown by laboratory workers to vary. (2) In Hungary it has been suggested that this variation is accompanied by changes in the age-incidence of the disease in recent years. (3) No statistical confirmation of this can be found in England and Wales. (4) On the other hand the age-incidence of the disease in 1918-19, and of the complications which caused death, was most unusual. (5) This and other evidence points to a special strain of virus, not now persisting, as the cause of that epidemic, rather than special susceptibility of the population due to war conditions. REFERENCES BRITTEN, R. H.
(1932). Publ. Hlth. Rep. Wash., 47, 303.
BUaNET, F. M. (1940). Biological Aspects of Infectious Disease, p. 250. COLLINS, S. D. (1934). Publ. Hlth. Rep. Wash., 49, 1. Ft~ANcIs, T. (1940). Science, 92, 405. MXr-~ISTRVOF HEALTH. (1920). Rep. Pub. Hlth. med. Subj., No. 4. REGISTRAR-GENERAL'S REPORT FOR ENGLAND AND WALES.
(1020). Ann. Stat. Rev., Text, 41. SHOPE, R.E. (1936). y. Exp. Med., 63, 669. SMITH, W., ANDamVES,C. H., AND LAIDLAW,P. P. (1933). Lancet, 2, 66. STUART-HARRIS, C. H., ANDREWI~, C. H., AND SMITH, W. (1938). M. R. C., Spec. Rep, Ser., No. 228.
TAYLOR, R. M., P~'ramLA, A., ^ND DaEOUSS, M. (1941). y. inf. Dis., 68, 90.
AN OUTBREAK OF ACUTE POLIOMYELITIS IN HARROGATE DURING 1 9 4 0 By D. D. PAYNE, M.D., D.P.H., Medical Officer o[ Health and School Medical Officer, Harragate. Epidemics of acute poliomyelitis have fortunately been uncommon in this country, and those which have eccurred in England and Wales have usually been in the nature of small localised outbreaks. The year 1926 stands out prominently in the history of poliomyelitis in this country, no fewer than 1,397 cases being notified, with 176 deaths; the chief outbreaks were in the County Borough of Leicester (81 cases), Grays in Essex (58 cases), and Broadstairs in Kent (74 cases). A full description and discussion of the epidemiology of these outbreaks is given in the Annual Report of the Chief Medical Officer of the Ministry of Health for 1926 (pp. 84-108); in the same report there is also a summary of the chief epidemics of poliomyelitis in
England and Wales between the years 1897 and 1926. The U.S.A., Australia, and Scandinavia have been the centres of major epidemics. In 1937, in Victoria, Australia, there was a total of 38,250 cases, and irt 1916 in New York State alone there were 13,164 cases with 3,331 deaths. Fortunately we have had nothing comparable in this country. Acute poliomyelitis as a clearly differentiated epidemic disease has a short history. With its accompanying disabilities it appears to have been recognised clinically towards the end of the eighteenth century. The first epidemic to be carefully studied was that occurring in Sweden in t887, and described by Medin (1890) of Stockholm. Sir Walter Scott, born in 1771, was undoubtedly a victim of the disease at the age of 18 months. He ,states, " I n the morning I was discovered to be affected with the fever which often accompanies the cutting of large teeth. It held me three days. On the fourth, when they went to bathe me as usual, they discovered that I had lost the power of my right leg; " and later he goes on to state that "the limb affected was much shrunk and contracted" (Lockhart, 1837). Acute poliomyelitis was made notifiable in 1912, and polio-encephalitis was made separately notifiable in 1919.
Baeteriology and Transmission of Infection The infective agent is a neurotropic virus and can be identified on.ly by injecting and reproducing the disease in monkeys. Owing to war-time conditions it was not deemed possible to attempt any such identification or experimental work in the Harrogate outbreak. A brief survey of the recent work on the poliomyelitic group of viruses was given in the Lancet of November 16th, 1940. A mouse virus has been isolated from the brains of mice that had developed a flaccid paralysis of the hind legs. In America the same virus has now been found in the intestines of a high percentage of normal mice, although few develop symptoms. There is no serological relationship between the mouse virus and the human poliomyelitic virus. Two human strains, the Lansing and SK strain of virus, have, however, been isolated, and are pathogenic for cotton-rats and mice. Most mouse poliomyelitic viruses are pathogenic only for mice, but one strain is pathogenic also for cotton-rats. The Lancet makes the following comment: " The crucial question is the exact status of the Lansing and SK strains of poliomyelitic viruses. Are they human viruses that have become pathogenic for mice, or mouse viruses that have become pathogenic for man?" The virus of poliomyelitis has been isolated from the stools of human cases on numerous occasions, even as long as 123 days after a mild abortive attack (Lrpine, Srdallian, and Sauter, 1939), also from the stools of healthy human contacts who remained well during the period of exposure (Trask, Paul, and Vignec, 1940). In two out of three urban epidemics of poliomyelitis in 1939 the virus was isolated from samples of sewage, and could not be isolated when the epidemics were over. From the results obtained, the following conclusions were drawn: (1) Poliomyelitis virus can be isolated occasionally from urban sewage during the course of an epidemic. (2) It can~not be 209
In view of proposed developments in the organisation of fracture treatment and of the recent extension of the classes of fracture cases admitted under the Emergency Hospital Scheme, the Minister of Health has had under review the need for increasing the number of trained occupational therapists whose services can be made available for patients treated under the Scheme. The new arrangements for training are set out in Circular 2889. The Dorset House School of Occupational Therapy, evacuated from Bristol, has arranged to provide special shortened courses of six months' training at Barnsley Hall Emergency Hospital, Bromsgrove, Worcestershire. These courses are designed for candidates who are qualified masseuses and, if successfully completed, will entitle the student to a special War Emergency Diploma of the Association of Occupational Therapists. The masseuses accepted for the course will be transferred for the six months to Barnsley Hall, where they will be accommodated and boarded free of charge and will not be expected to pay any fees or other charges in connection with the training course or the taking of the Diploma. They will, in addition, receive a personal allowance of £25 for the six months' course. They will be required to undertake to serve in hospitals in the Emergency Hospital Scheme on the completion of training. The first course began on July 1st, 1941, and will continue until December 80th. The Minister is anxious that hospitals in the Scheme which are employing masseuses should bring these facilities to their early notice.
British Drug Houses, Ltd., have put on the market vitamin C in tablets containing 5, 25 and 50 rag. of ascorbic acid respectively, and also in a sterile solution for injection. Tablets for infants (5 mg.) dissolve readily in warm milk or in the infant's feed. It is pointed out that in solution vitamin C is not a stable substance. For this reason the tablets should not be dissolved in very hot liquids nor should they be added a long time before the feed is given. 206
AUGUST THE VIRUSES OF INFLUENZA By RALPH M. F. PICKEN, M.B., CH.B., B.SC., D.P.H.,
Mansel Talbat Pro[essor o[ Preventive Medicine, The University o[ Wales When medical interest in influenza was sharply awakened by the epidemics of 1918-19, the evolution of the disease in individual eases, the pathological findings in those patients who died, and the contrast between the summer outbreak of 1918 and the subsequent winter and spring phases, all pointed to a basic infection by an unknown pathogen of relatively slight lethal power, paving the way for secondary invasion by several known micro-organisms which might lead to death by setting up pneumonia dr some other grave complication. The nature of the basic infection became clear later, when a virus was isolated from patients suffering from the disease (Smith et al., 1933). Its identification made possible a study of the clinical symptoms in successive waves of influenza-like disease, in order to ascertain whether these symptoms differed sufficiently in cases harbouring and not harbouring the virus to justify the differentiation between true influenza and its mimics by clinical means alone. Stuart-Harris and his colleagues (1938) thought that they had partly succeeded in achieving this distinction after studying closely the behaviour of a number of outbreaks in 1936-37. They contrasted true influenza--a disease of sudden onset, severe cor~stitutional symptoms, dry pharyngitis, and bronchiolitis--with "febrile catarrh"--more gradual in onset, with less constitutional disturbance, pronounced exudative catarrh, and bronchitis. In the former, isolation of the virus and serological reaction to it were to be expected, but not so in the latter. When, however, similar enquiries were pursued by the same workers in 1939 (Stuart Harris et al., 1940), there was far less success in isolating the virus from cases seeming to present the true clinical picture, and the clinical distinction between positive and negative cases could no longer be sustained. All along they had emphasised the difficulties which might be anticipated from the accumulating evidence that viruses varied in their response to laboratory tests, although overlapping antigenically, and several of those isolated in 1939 were anomalous in their unready adaptability to mice. The definite identification by Francis (1940) of a second strain, serologically quite unrelated to those already known, therefore came as no surprise, and now the slightly varying virus originally isolated has been styled Influenza virus A, while that recently identified by Francis is known as Influenza virus B. Possibly strains of this virus may come to be as numerous as those of Streptococcus pyogenes or the types of Streptococcus pneumoniae.
Age.Variations in Hungary Some observations made in Hungary (Taylor et al., 1941) suggest that there may be an epidemiological means of differentiating between outbreaks of disease of an influenzal type although the symptoms and signs are clinically indistinguishable. "Complicated influenza" is a notifiable disease in Hungary, the term no doubt covering cases the majority of which would correspond with our influenzal pneumonia. When the
1941
PUBLIC HEALTH
age-grouping of such cases is studied from year to year in Hungary a material difference is observed in socalled epidemic years, when the virus can be isolated from cases, and in non-epidemic years, presenting few such cases. In the latter, ages under 5, and to a less extent under 10, bear the brunt of the incidence. ILl epidemic years, on the other hand, the incidence is far less concentrated upon these ages. If it be assumed that epidemic influenza in certain years--when widespread infection with the virus can be technically established-is something superimposed on the annual recurrence of influenza-like disease, and the average incidence at each age during a series of non-epidemic years is subtracted from the average of epidemic years, it is shown that the excess mortality in the latter varies comparatively little from age to age and affects old people to an unusual extent. It is in fact nearly as heavy at ages over 55 as it is under 5. A sudden change of age in persons notified as suffering from complicated influenza (or presumably from influenzal pneumonia) might therefore be a useful indication that an epidemic of true influenza had begun.
perhaps safer to leave this year out of calculation. The years 1931 and 1932 had an intermediate position as regards mortality and may also be disregarded in the search for contrasts. If there is any contrast it should be shown by the epidemic and non-epidemic years as defined above. The average mortality from influenza at certain ages for these two groups of years is shown in. Table L It is quite obvious that the form of distribution is the same whether we consider epidemic years, or nonepidemic years, or the excess mortality in epidemic years over expectation based on non-epidemic years. If anything, this excess falls more heavily at the extremes of life than the usual mortality in nonepidemic years; but the difference is negligible. There is no cbnfirmation whatever that influenza of the modern type in England and Wales differs from year to year in its power to kill at different periods of life, in the way in which the incidence of "complicated" influenza varies in Hungary. The comparison, of course, between notification-rates and death-rates is not a good one, but as most cases of influenza die of complications there should be a fairly close association, Age Variations in England and Wales changes in the age of incidence of complicated inThe age-distribution of notified cases of influenzal fluenza, if they occurred, being reflected in some pneumonia for England and Wales is not given in any change in the ages at death. official returns. The Annual Report of the Department of Health for Scotland has included such a dis- The Influenza of 1918-19 tribution of infectious diseases for a number of years, It is generally recognised that the pandemic of but influenzal pneumonia has been distinguished from 1918-19 presented unique features apart from its grave acute primary pneumonias only since 1937. The annual reports of the medical officers of health of large fatality. It came in three waves, first in the summer of towns also usually do not distinguish between different 1918, disorganising works and schools by its sudden forms of pneumonia as regards age-distribution. Pneu- and widespread occurrence, and yet the death returns monia is such a mixed group of infections that its showed comparatively little sign of its presence; the study in mass would not be informative. Tile matter, succeeding waves in early winter and early spring were therefore, can be examined only from death returns. characterised by a high mortality from respirator3" and When the death-rate from influenza at several ages in other complications, especially the earlier of these two England and Wales is studied for each year from 1929 exacerbations. The age-distribution of the death-rate The exceptionally high mortality in (when influenza was highly prevalent) to 1938 it is was unusual. adolescents and young adults is well exhibited in a apparent that the age.distribution is very constant. The "epidemic" years, as judged by the mortality at table compiled by the Registrar-General to compare all ages, were 1929, 1933, and 1937. Those in which 1918 with earlier and subsequent years (Registrarthe disease, by the same criterion, may be said to have General's Review, 1929), and the whole subiect of agebeen non-epidemic were 1930, 1934, 1935, and 1936. incidence and mortality is exhaustively dealt with in a This was almost certainly true also of 1938, but as Special Report on the pandemic (Ministry of Health, sulphonamides had come widely into use in the treat- 1920). Not so widely known are the epidemiologieat ment of pneumonia, and as it is conceivable that the investigations in America of the 1918-19 epidemic by efficacy of these drugs varies from age to age, it is Britten (1932) and of the 1928-29 epidemic by Collins (1934). T h e s e were carried out TABLE I.--ENC, I.AND AND VCALES by means of Average Death-Rate from Influenza per Million :::: special surveys Age by canvassers, a 4555method wh ich All Ages 0515~ °535has become highly organised (1) Epidemic years . . . . . . . . . 584 448 57 1t7 177 359 617 °112 in the U.S.A. (2) Non-epidemic years ...... 119 109 20 3.5 51 93 165 511 Excess of ( l ) over (2) ...... 435 339 37 82 126 266 452 1601 From these reports Table II Death Rate at Each Age compared with Death-Rate at All Ages, taken as 100 has been prepared, Non-epidemic years ...... 100 73 13 23 34 62 111 343 The a c t u a l Excess of (1) over (2) ...... 100 78 8 19 29 61 104 368 rates are not .
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
.
:,
'
2:',
",. . . . . . . . .
,
.....
207
PUBLIC HEALTH
AUGUST TABLE II.--U.S.A. SURVEYEDCITIES
comparable with those given for England and Wales in Table
Death Rate from Influenza and Pneumonia per 1,000
Age
I, since t h e y re-
fer to town populations only and
All ages
0-
5-
10-
15- 20-
25-
0.98 100 5.0 100
2.52 257 7.9 158
0.17 17 2.-2 44
0.13 13 2.1 42
0.25 0.35 25 36 3.4 6.2 9.9 68 124 198
0.55 56 7.9 6.3 158 126
90 134
102 116
~-w- •
i n c l u d e all d e a t h s
1928-29 ...
from pneumonia whether due to
1918-19 ...
a n d a g a i n at t h e beginning of the
1928-29 . . . . . . 1918-19 . . . . . .
30-
35-
~
40-
45-
50-
60-
1-17 119 2.6 52
4.3 86
70-
~---v-----~ 4,0 80
0.82 84 2.9 58
4.20 429 5.1 102
influenza or not. The comparison between the American experience of 1928-29, which is also improbable that lowered resistance would might be called a normal influenza epidemic have accounted for the sudden changes in ageperiod, and the exceptional epidemic of 1918-19 is incidence and age-fatality which charaeterised thia not so vitiated, and the difference in age-distribution outbreak, even :though it may be admitted that an is very striking. Whereas in 1928-29 the extremes of important part of the gradual changes in the agelife were chiefly affected, in 1918-19 an exceptional mortality during and after the war from a chronic mortality was suffered in adolescence and young adult infectious disease, tuberculosis, was attributable to this life. The American data enable the age-specific in- cause. On the whole, it is most likely that the 1918-19 cidence rates for influenza and pneumonia in the sur- epidemic was due to the dissemination of an infection veyed cities to be compared, as in Table III. of exceptional virulence. This may have been an If the age-distribution of the incidence for 1928-29 unusual influenza virus or one or other of the microbe taken as representing the usual experience, that for organisms which give rise to the grave complications 1918-19 was obviously abnormal. Ages from 10 to 24, and most of the deaths. The secondary infections were which are usually least affected, were specially hit in due to several bacteria, of which H. influenzae and 1918-19, and the relative incidence over 40 was excep- S. tryogenes were predominant (Ministry of Health, tionally low. This is a different picture from that 1920). If the cause of the exceptional nature of the presented by the contrast between recent epidemic and epidemics of 1918-19 was an unfamiliar micronon-epidemic years in Hungary. Moreover, the 1918-19 organism, it is, on the whole, more likely to have been age-incidence does not entirely account for the age- the virus than one or more of the secondary invaders, distribution of the mortality in that epidemic, which and this is in consonance with the large and seasonally showed a marked excess at somewhat later ages-- unusual, but comparatively non-fatal, first wave in the namely from 20 to 39. This was mainly due, as shown summer of 1918. In this connection it is interesting by the American reports, to heavy complication with to note that Shope (1936) concluded from serological pneumonia at these ages, which was absent in 1928-29. tests on human beings that a strain of virus which he Although the British figures are not presented in quite isolated from cases of swine influenza, a disease appearthe same way, their general form suggests that the ing in America contemporaneously with the 1918-19 behaviour of the epidemic here resembled generally epidemic, and which has persisted since then, was that in America (Ministry of Health, 1929). possibly the survivor of the virus peculiar to that The contrast in age-distribution of the 1918-19 epi- human epidemic. demic with ordinary recurrent outbreaks, together with Burnet (1940) has given reasons in support of the its extreme virulence throughout the world, has pro- view, which has occurred to many others, that a new moted speculation as to its cause. Coming as it did at antigenic strain of virus cropped up during the Four the end of an exhausting world war, its virulence has Years War, its dissemination pandemically being naturally been attributed to the lowered resistance favoured by the crowding in Europe of men induced by that prolonged ordeal. It is unlikely, from many parts of the world. Its exuberant however, that people in the U.S.A., or in neutral lands, multiplication may have been accompanied by where deprivation and exhaustion were far less experi- mutations in. such a way that those dominant in enced than here, were rendered susceptible in this way. the earlier of the three waves left no immunity to those It is conceivable that the same circumstances which responsible for the later, and, like other new infections, light up in war-time that other air-borne infection, it caused no specially selective mortality among cerebrospinal fever, might have had the same effect on children, but rather in young adults. It has always influenza, but in that case the TABLE III.--U.S.A. SURVEYEDCITIES epidemics would Incidence-Rate of Influenza and Pneumonia have been ex(Rate for All Ages taken as 100) pected at the beginning, not at Age the end, of the Four Years War All Ages 0- 5- 10- 15- 20- 25- 80- 35- 40- 45- 50- 60- 70present one. 208
It
100 100
118 104
122 142
78 118
87 108
113 111
111 102
105 80
93 70
90 55
94 42
106 31
1941
PUBLIC HEALTH
seemed to me that this theory leaves unexplained the absence of as great an increase of mortality in the elderly as among young adults. Otherwise it fits the picture well. The question has been discussed at some length because influenza is among the war diseases against which we are being warned to be on our guard. It is right that we should be, but it would also be unwise to assume that because the Four Years War was followed by such a devastating pandemic the one was the cause of the other, and that deprivation and fatigue were the factors underlying it.
Summary' (1) The viruses of influenza have been shown by laboratory workers to vary. (2) In Hungary it has been suggested that this variation is accompanied by changes in the age-incidence of the disease in recent years. (3) No statistical confirmation of this can be found in England and Wales. (4) On the other hand the age-incidence of the disease in 1918-19, and of the complications which caused death, was most unusual. (5) This and other evidence points to a special strain of virus, not now persisting, as the cause of that epidemic, rather than special susceptibility of the population due to war conditions. REFERENCES BRITTEN, R. H.
(1932). Publ. Hlth. Rep. Wash., 47, 303.
BUaNET, F. M. (1940). Biological Aspects of Infectious Disease, p. 250. COLLINS, S. D. (1934). Publ. Hlth. Rep. Wash., 49, 1. Ft~ANcIs, T. (1940). Science, 92, 405. MXr-~ISTRVOF HEALTH. (1920). Rep. Pub. Hlth. med. Subj., No. 4. REGISTRAR-GENERAL'S REPORT FOR ENGLAND AND WALES.
(1020). Ann. Stat. Rev., Text, 41. SHOPE, R.E. (1936). y. Exp. Med., 63, 669. SMITH, W., ANDamVES,C. H., AND LAIDLAW,P. P. (1933). Lancet, 2, 66. STUART-HARRIS, C. H., ANDREWI~, C. H., AND SMITH, W. (1938). M. R. C., Spec. Rep, Ser., No. 228.
TAYLOR, R. M., P~'ramLA, A., ^ND DaEOUSS, M. (1941). y. inf. Dis., 68, 90.
AN OUTBREAK OF ACUTE POLIOMYELITIS IN HARROGATE DURING 1 9 4 0 By D. D. PAYNE, M.D., D.P.H., Medical Officer o[ Health and School Medical Officer, Harragate. Epidemics of acute poliomyelitis have fortunately been uncommon in this country, and those which have eccurred in England and Wales have usually been in the nature of small localised outbreaks. The year 1926 stands out prominently in the history of poliomyelitis in this country, no fewer than 1,397 cases being notified, with 176 deaths; the chief outbreaks were in the County Borough of Leicester (81 cases), Grays in Essex (58 cases), and Broadstairs in Kent (74 cases). A full description and discussion of the epidemiology of these outbreaks is given in the Annual Report of the Chief Medical Officer of the Ministry of Health for 1926 (pp. 84-108); in the same report there is also a summary of the chief epidemics of poliomyelitis in
England and Wales between the years 1897 and 1926. The U.S.A., Australia, and Scandinavia have been the centres of major epidemics. In 1937, in Victoria, Australia, there was a total of 38,250 cases, and irt 1916 in New York State alone there were 13,164 cases with 3,331 deaths. Fortunately we have had nothing comparable in this country. Acute poliomyelitis as a clearly differentiated epidemic disease has a short history. With its accompanying disabilities it appears to have been recognised clinically towards the end of the eighteenth century. The first epidemic to be carefully studied was that occurring in Sweden in t887, and described by Medin (1890) of Stockholm. Sir Walter Scott, born in 1771, was undoubtedly a victim of the disease at the age of 18 months. He ,states, " I n the morning I was discovered to be affected with the fever which often accompanies the cutting of large teeth. It held me three days. On the fourth, when they went to bathe me as usual, they discovered that I had lost the power of my right leg; " and later he goes on to state that "the limb affected was much shrunk and contracted" (Lockhart, 1837). Acute poliomyelitis was made notifiable in 1912, and polio-encephalitis was made separately notifiable in 1919.
Baeteriology and Transmission of Infection The infective agent is a neurotropic virus and can be identified on.ly by injecting and reproducing the disease in monkeys. Owing to war-time conditions it was not deemed possible to attempt any such identification or experimental work in the Harrogate outbreak. A brief survey of the recent work on the poliomyelitic group of viruses was given in the Lancet of November 16th, 1940. A mouse virus has been isolated from the brains of mice that had developed a flaccid paralysis of the hind legs. In America the same virus has now been found in the intestines of a high percentage of normal mice, although few develop symptoms. There is no serological relationship between the mouse virus and the human poliomyelitic virus. Two human strains, the Lansing and SK strain of virus, have, however, been isolated, and are pathogenic for cotton-rats and mice. Most mouse poliomyelitic viruses are pathogenic only for mice, but one strain is pathogenic also for cotton-rats. The Lancet makes the following comment: " The crucial question is the exact status of the Lansing and SK strains of poliomyelitic viruses. Are they human viruses that have become pathogenic for mice, or mouse viruses that have become pathogenic for man?" The virus of poliomyelitis has been isolated from the stools of human cases on numerous occasions, even as long as 123 days after a mild abortive attack (Lrpine, Srdallian, and Sauter, 1939), also from the stools of healthy human contacts who remained well during the period of exposure (Trask, Paul, and Vignec, 1940). In two out of three urban epidemics of poliomyelitis in 1939 the virus was isolated from samples of sewage, and could not be isolated when the epidemics were over. From the results obtained, the following conclusions were drawn: (1) Poliomyelitis virus can be isolated occasionally from urban sewage during the course of an epidemic. (2) It can~not be 209