The extension to Scotland in 1866 was late in the season and insignificant compared with former epidemics. It was heard of about the end of summer in Fraserburgh and one or two other ports or fishing places on the East Coast, but it was not until October and November that it attracted notice in the eight principal towns, the whole mortality from it in Glasgow being 53, in Edinburgh 154, in Dundee 105, in Aberdeen 62, in Paisley 2, in Greenock 14, in Leith 95, and in Perth 15. Besides these deaths there were 435 more in smaller towns or villages. The year was a very healthy one, the death-rates of Glasgow, Greenock and Perth having been below the mean of the previous ten years.
In Ireland the cholera of 1866 was even slighter than in Scotland, the only considerable epidemic having been at Belfast.
Cholera has never obtained a footing in London since the epidemic of 1866. In 1873, while the disease was unusually active in some parts of Europe, a few cases occurred in Wapping among Scandinavian emigrants on their way to America, who had been landed for a few days. But the infection did not spread. In 1884, when cholera came from Cochin China to Toulon and Marseilles, two or three cases occurred on board steamships arriving at Cardiff and Liverpool. In 1893, when the disease raged in Hamburg, a number of choleraic cases occurred at Grimsby in August, which were considered certainly Asiatic owing to their high degree of fatality. In August-October, the deaths from cholera, whether cholera nostras or the Asiatic type, or both together, were about thirty in Grimsby, eighteen in Hull, and about fifty more in various other places, chiefly in the south of Yorkshire. The autumn of that year was favourable to bowel-complaints and to enteric fever.
The Antecedents of Epidemic Cholera in India.
The antecedents and circumstances that made the year 1817 so critical for cholera in India, and for its diffusiveness far beyond India, constitute one of the greatest problems in epidemiology. A full and minute examination of them cannot be attempted here; but the chapter would be incomplete without some statement on the subject, which, if summary, need not be dogmatic. Cholera with the same symptoms and a similar degree of fatality was certainly not new to India about the year 1817; it can be traced from the earliest records of the Portuguese and other Europeans in India, if not also in other countries in ancient times[1578]. The mortalities among troops during the military operations in the Northern Circars in 1781 and 1790, and the deaths of some 20,000 pilgrims in eight days during the Hurdwar festival of 1783, were undoubtedly from the same epidemic infective cholera that was seen fifty years after in Europe. But these were occasional great explosions, which arose suddenly and ceased abruptly; whereas from about 1817 onwards the infection became, as it were, a seasonal product of the soil of Lower Bengal year after year, and at the same time began to range widely beyond its “endemic area” to other provinces of India, beyond the North-Western frontier to Central Asia and to Europe, and across the ocean to America. It was not by any sudden change in the year 1817, we may be sure, that cholera began to be endemic at various places far apart in the valley of the Ganges. Things must have been tending towards that manifestation for some time before, and those things must have been of the same kind that made the great explosion at Hurdwar in 1783 and have made many other great explosions at the Indian religious festivals in later times. Briefly the opinion may be hazarded, that it was the permeation with excremental matters of the soil at large in and around Bengali villages that gave rise to the endemic miasmatic infection of cholera. The odor stercoreus of those innumerable village communities is, or used to be, a familiar fact, just as it is well known to be the custom there to dispense with latrines or other systematic provision for the disposal of faecal matters. But it may seem improbable that personal habits of the peasantry, not unknown in other countries, and immemorial in Lower Bengal itself, should have led to a definite disease-effect in a certain year of the 19th century and perennially thereafter. As to the special risk of engendering such a soil-poison in the valley of the Ganges, it has to be said that the region is peculiar in its alternations from extreme saturation to extreme dryness, within a stratum of alluvial or other porous soil which has a bed of impervious blue clay beneath it at a depth seldom more than 10 feet. It is just where such extreme fluctuations of the ground-water within a limited range occur from season to season, that organic matters in the soil are most apt to develop a miasmatic infective property. But why should the year 1817 have been, by the general consent of Anglo-Indian observers, the beginning of a new era in the history of cholera? The guiding principle in all such cases is, that things must have been moving that way before, and that in the particular season there had been reached at length such a degree of aggravation as to make a specific result manifest or the cumulative causes effective. Two things may be indicated as relevant to this assumed aggravation, or integration of accumulating causes. One was a certain gradual change in the beds of rivers, especially in the province of Behar, which entirely altered the relative amount of water flowing above ground and under ground, and must have made a difference in kind and in degree to the decomposition-processes in the soil. (In Burdwan these changes in the ground-water have caused much miasmatic fever since about thirty years ago.) The other thing was the increase of the number of cultivators per square mile under British rule. The latter cannot be stated with even approximate exactness for periods before the census of 1872; but there can be no reasonable doubt that the increase was great and progressive from the end of last century, owing to the cessation of intertribal wars, and of famines which were chiefly caused by the overflow of rivers now no longer subject to floods, and of wilful and barbarous checks to population. Among the cholera localities of 1817 were some that have now the greatest pressure of inhabitants on the soil, not in cities, but in uniformly dispersed rural communities—such as the division of Patna with 637 inhabitants per square mile, the district of Jessore with 693, and of Dacca with 756. This is of course a very general account of the matter, which a minute study of localities and seasons might show to be highly inadequate; but in seeking for some circumstances of aggravation at the particular juncture, the two things that have been mentioned, both of them coincident historical matters of fact, will appear to be not irrelevant according to the received teaching on the favouring conditions of cholera.
Note on Cerebro-spinal Fever.
British experience, or the records of it, afford so little material for the history of epidemic cerebro-spinal fever (very abundant for France, Germany and the United States of America, see Hirsch, III. 547) that it has not seemed desirable to interpolate the subject in the chapter on Typhus and other Continued Fevers. Although our experience of it has fallen perhaps wholly within the period of exact statistics of the causes of death (saving some doubtful identifications in the 18th century), yet the registration tables contain so few deaths from it that it hardly seems as if a new and remarkable type of fever of the typhus kind had really been in our midst. There are, however, two periods when a good many papers were written upon it in Ireland and England, the years 1865-67 and the year 1876. When the first cases were seen in London in 1865 Murchison pronounced the new fever to be closely allied to typhus (Lancet, 1865, p. 1417). At the same time in Ireland it was sometimes called “the black death,” from the dark or livid vibices of the skin, or purpura maligna, or purpuric fever (J. T. Banks, Dubl. Quart. Journ. Med. Sc. XLIII. 98; E. W. Collins, ibid. XLVI. 170; Cogan, ibid. XLIV. 172; Gordon, ibid. XLIV. 408; H. Wilson, ibid. XLIII.; Haverty, ibid.; T. W. Belcher, Med. Press, N. S. III. 167; J. H. Benson, ibid. III. 387; editor, ibid. 506. For England, S. Wilks, Lancet, 1865, I. 388, Brit. Med. Journ. 1868, I. 427; F. J. Brown, Trans. Epid. Soc. II. (1865), 391; J. N. Radcliffe in Reynolds’ System of Medicine, 1st ed. II. 676; H. Day, Lancet, 1867, I. 731). In the second period, 1876, there were many cases in England, especially in the Midlands, but it is said that they were usually diagnosed as typhoid fever (Sir Walter Foster, Brit. Med. Journ. 1892, II. 278, and Lancet, 1876, I. 849; Neville Hart (for Birmingham), St Barth. Hosp. Rep. XII. (1876), 105; H. Thompson, Lancet, 1876, I. 849. The Irish papers in the second period are by T. W. Grimshaw, Dub. Journ. Med. Sc. LXI. 520, and LVII. 375; E. H. Bennett, ibid. LIX.; Brabazon, Brit. Med. Journ. 1876, I. 509). An epidemic of cerebro-spinal fever, resembling typhoid, was described for a Shropshire village in May, 1891 (Monk, Brit. Med. Journ. 1892, II. 278). A case which came under my notice on 19 March, 1894, in an eastern parish of London, has led me to doubt whether the half-dozen or so of deaths annually certified in London as from cerebro-spinal fever (contrasting with as many hundreds in New York), are of the slightest statistical value.
A young woman, aged 16, an artificial flower maker, became ill with pains in the limbs and was taken as an out-patient to a hospital. Thereafter she became light-headed. A private practitioner (M.R.C.S.) was called in, who found her with a temperature of 103°, excited, and inclined to clutch spasmodically at his arms; her coarse black hair was full of pediculi and nits. She died next day, having had sent her by the practitioner a draught of chlorodyne on account of her extreme restlessness. An inquest was appointed, and the practitioner ordered to make a post-mortem examination. He attended the inquest and gave evidence that death was due to “congestion of the brain.” The jury were dissatisfied, and the coroner adjourned the inquest for a second examination by a skilled pathologist. After spending two hours looking for the cause of death (there was no congestion of the brain), I discovered that the base of the brain had been left in the skull intact, the hemispheres having been sliced off by a horizontal section in the plane of the saw-draught round the cranium. On raising the frontal lobes I saw green flaky lymph lying on the orbital plates and on the corresponding surfaces of the arachnoid; the same was found on the optic commissure, the surface of the pons, the medulla and over a small area of the under convexities of the lateral lobes of the cerebellum, where it amounted to little more than whitish opacity. The lymph was purely basal, solely on the arachnoid, not in the fissures or sulci. The examination having already lasted over two hours, it was found impracticable to expose the spinal cord. The facts previously found were: an extensive blood-shot state of the left conjunctiva with oedema of the upper lid (there was no obvious intra-orbital disease); round dusky-red spots on the outer sides of the thighs and on the shoulders; both lungs in a state of solid purple congestion at the bases, crepitant at the apices, the costal pleura dark red or livid; the tongue large and flabby, congested around the broad papillae; the stomach at the cardiac end, exactly corresponding to the pressure of a mass of hard undigested food, dotted with numerous small round ecchymoses under the serosa; six inches of the lower end of the jejunum, corresponding to a mass of hard impacted faeces, dotted with the same subserous ecchymoses; a narrow belt of deep congestion round the broad ends of the kidney pyramids; the mucosa of the fundus uteri haemorrhagic. There was no herpetic eruption. At the adjourned inquest the cause of death was found to be cerebro-spinal fever, and was so certified by the coroner to the Registrar-General. The practitioner who attended the deceased was unable to say whether the most distinctive of all the symptoms, the violent retraction of the occiput upon the shoulders, was present or absent. It is improbable that this was a solitary case of epidemic cerebro-spinal meningitis in the East End of London in the spring of 1894, (the early spring being the distinctive season of the infection). Even if it were the only case, it narrowly missed being returned as a death from “congestion of the brain,” and that, too, after post-mortem inquisition. The practitioner’s statutory fees were three guineas. There has lately been collected much evidence upon certificates of death, and upon diagnosis under the Notification Act, which makes it doubtful whether our mortality statistics are as correct in substance as they are methodical and exhaustive in form.