To make the significance of these epidemic figures clear, it
should be added that in the intervening period 1861–1889 the
average annual death-rate from influenza was only fifteen, and
in the ten years immediately preceding the 1890 outbreak it
was only three. Moreover, in epidemic influenza, the mortality
directly attributed to that disease is only a fraction of that actually
caused by it. For instance, in January 1890 the deaths from
influenza in London were 304, while the excess of deaths from
respiratory diseases was 1454 and from all causes 1958 above
the average.
We have seen above that the mortality was far greater in the second epidemic year than in the first, and this applies to all parts of England, and to rural as well as to urban communities, as the following table shows:—
Deaths from Influenza.
1890. | 1891. | |
London | 624 | 2302 |
24 Great Towns over 80,000 population | 439 | 2417 |
35 Towns between 20,000 and 80,000 | 186 | 765 |
21 Towns between 10,000 and 20,000 | 46 | 196 |
60 Towns under 10,000 | 62 | 196 |
85 Rural Sanitary Districts | 317 | 841 |
In spite of these figures, it appears that the 1890 attack, which was in general much more sudden in its onset than that of 1891, also caused a great deal more sickness. More people were “down with influenza,” though fewer died. For Instance, the number of persons treated at the Middlesex Hospital in the two months’ winter epidemic of 1890 was 1279; in the far more fatal three months’ spring epidemic of 1891 it was only 726. One explanation of this discrepancy between the incidence of sickness and mortality is that in the second attack, which was more protracted and more insidious, the stress of the disease fell more upon the lungs. Another is that its comparative mildness, combined with the time of year, in itself proved dangerous, because it tempted people to disregard the illness, whereas in the first epidemic they were too ill to resist. On the whole, rural districts showed a higher death-rate than towns, and small towns a higher one than large ones in both years. This is explained by the age distribution in such localities; influenza being particularly fatal to aged people, though no age is exempt. Certain counties were much more severely affected than others. The eastern counties, namely, Essex, Suffolk and Norfolk, together with Hampshire and one or two others, escaped lightly in both years; the western counties, namely, North and South Wales, with the adjoining counties of Monmouth, Hereford and Shropshire, suffered heavily in both years.
It will be convenient to discuss seriatim the various points of interest on which light has been thrown by the experience described above.
The bacteriology of influenza is discussed in the article on Parasitic Diseases. The disease is often called “Russian” influenza, and its origin in 1889 suggests that the name may have some foundation in fact. A writer, who saw the epidemic break out in Bokhara, is quoted by him to the following effect:—“The summer of 1888 was exceptionally hot and dry, and was followed by a bitterly cold winter and a rainy spring. The dried-up earth was full of cracks and holes from drought and subsequent frost, so that the spring rains formed ponds in these holes, inundated the new railway cuttings, and turned the country into a perfect marsh. When the hot weather set in the water gave off poisonous exhalations, rendering malaria general.” On account of the severe winter, the people were enfeebled from lack of nourishment, and when influenza broke out suddenly they died in large numbers. Europeans were very severely affected. Russians, hurrying home, carried the disease westwards, and caravans passing eastwards took it into Siberia. There is a striking similarity in the conditions described to those observed in connexion with outbreaks of other diseases, particularly typhoid fever and diphtheria, which have occurred on the supervention of heavy rain after a dry period, causing cracks and fissures in the earth. Assuming the existence of a living poison in the ground, we can easily understand that under certain conditions, such as an exceptionally dry season, it may develop exceptional properties and then be driven out by the subsequent rains, causing a violent outbreak of illness. Some such explanation is required to account for the periodical occurrence of epidemic and pandemic diffusions starting from an endemic centre. We may suppose that a micro-organism of peculiar robustness and virulence is bred and brought into activity by a combination of favourable conditions, and is then disseminated more or less widely according to its “staying power,” by human agency. Whether central Asia is an endemic centre for influenza or not there is no evidence, but the disease seems to be more often prevalent in the Russian Empire than elsewhere. Extensive outbreaks occurred there in 1886 and 1887, and it is certain that the 1889 wave was active in Siberia at an earlier date than in Europe, and that it moved eastwards. The hypothesis that it originated in China is unsupported by evidence. But whatever may be the truth with regard to origin, the dissemination of influenza by human agency must be held to be proved. This is the most important addition to our knowledge of the subject contributed by recent research. The upshot of the inquiry by Dr Parsons was to negative all theories of atmospheric influence, and to establish the conclusion that the disease was “propagated mainly, perhaps entirely, by human intercourse.”
He found that it prevailed independently of climate, season and weather; that it moved in a contrary direction to the prevailing winds; that it travelled along the lines of human intercourse, and not faster than human beings can travel; that in 1889 it travelled much faster than in previous epidemics, when the means of locomotion were very inferior; that it appeared first in capital towns, seaports and frontier towns, and only affected country districts later; that it never commenced suddenly with a large number of cases in a place previously free from disease, but that epidemic manifestations were generally preceded for some days or weeks by scattered cases; that conveyance of infection by individuals and its introduction into fresh places had been observed in many instances; that persons brought much into contact with others were generally the first to suffer; that persons brought together in large numbers in enclosed spaces suffered more in proportion than others, and that the rapidity and extent of the outbreak in institutions corresponded with the massing together of the inmates.
These conclusions, based upon the 1889–1890 epidemic, have been confirmed by subsequent experience, especially in regard to the complete independence of season and weather shown by influenza. It has appeared and disappeared at all seasons and in all weathers and only popular ignorance continues to ascribe its behaviour to atmospheric conditions. In Europe, however, it has prevailed more often in winter than in summer, which may be due to the greater susceptibility of persons in winter, or, more probably, to the fact that they congregate more in buildings and are less in the open air during that part of the year. No doubt is any longer entertained of its infectious character, though the degree of infectivity appears to vary considerably. Many cases have been recorded of individuals introducing it into houses, and of all or most of the other inmates then taking it from the first case. Difficulties in preventing the spread of infection are due to (1) the shortness of the period of incubation, (2) the disease being infectious in the earliest stages before the nature of the illness is recognized, (3) the milder varieties being equally infectious with the severe attacks, and the patient going to work and spreading the infection, (4) the diagnosis often being difficult, influenza being possibly confused with ordinary catarrhal attacks, typhoid fever and other diseases. Domestic animals seem to be free from any suspicion of being liable to human influenza. Sanitary conditions, other than overcrowding, do not appear to exercise any influence on the spread of influenza.
Influenza has been shown to be an acute specific fever having nothing whatever to do with a “bad cold.” There may be some inflammation of the respiratory passages, and then symptoms of catarrh are present, but that is not necessarily the case, and in some epidemics such symptoms are quite exceptional. This had been recognized by various writers