The problem of infantile diarrhoea is in great part the same as the problem of rickets. The peculiar summer disease of town-bred infants is especially apt to assail the rickety: probably a very large number of the infants under one who are cut off by it would have become obviously rickety if they had lived a few months longer. But even if there were not this well-known correspondence between the subjects of infantile diarrhoea and of rickets, we should find analogies in the pathology of each. Rickets is an exquisitely congenital disease, or a disease acquired by the child in the womb from the kind of intra-uterine nutrition that it receives. In recent times it has been usual to restrict the term congenital in rickets to the very few cases that have rickets developed at birth. This is a typical instance of the peculiar narrowness of view in modern pathology. All rickets is congenital, although it is rare to find the symptoms made manifest until the infant is nearly a year old. Cullen’s reasoning on this point a century ago has never been answered nor superseded. The theories of that day to explain rickets by injudicious feeding or regimen after birth seemed to him beside the mark: “Upon the whole I am of opinion that hired nurses seldom occasion this disease unless when a predisposition to it has proceeded from the parents.... I am very much persuaded that the circumstances in the rearing of children have less effect in producing rickets than has been imagined.... I doubt if any of the former [dietetic errors and the like] would produce it where there was no predisposition in the child’s original constitution.... So far as I can refer the disease of the children to the state of the parents, it has appeared to me most commonly to arise from some weakness, and pretty frequently from a scrofulous habit, in the mother,” (Cullen, First Lines, Part III. Bk. II. chapter 4). The chief exponent of the diathetic views on rickets in our time has been Sir William Jenner (Med. Times and Gaz., 1860, I. 466); but I remember at the Pathological Society on 7 Dec., 1880, how unacceptable, or perhaps unintelligible, that part of his exposition was to a younger generation who appeared to have forgotten the meaning of mala stamina vitae.
The congenital nature of rickets is not only an empirical fact, based upon experience, but it is a doctrine of rational pathology. The latter aspect of it rests upon the correct physiology of intra-uterine nutrition, for which I refer to my investigations on the structure and function of the placenta (Journal of Anatomy and Physiology, July, 1878, and January, 1879). The detailed application of the physiological facts to rickets I have attempted deductively in section 5 of the article “Pathology” in the Encyclopaedia Britannica, vol. XVIII., 1884. The building up of the placenta by the mother, and the due performance of function by that great and wonderful extemporised organ, require certain favouring conditions, which have been never unperceived by the common sense of mankind. Those conditions are certainly not to be found in factory labour. A woman who has to be thinking of the time-keeper at the gate and the foreman in the mill, who has ever in her ears the din of belts and wheels and mill-stones, who has dust in her lungs and weariness in her back, can hardly do justice to the child in her womb. The rearing of the child after it is born is of small consequence beside the rearing of it before it is born. The opportunity comes once (heredity apart) of giving it good stamina or bad; and in the circumstances of factory labour the wonder is that breeding women provide so well as they do for their unborn offspring. It is undoubted that they often tax themselves beyond measure to do so, in tacit obedience to the great law of maternity.
While the connexion of rickets in the child with the laborious or anxious preoccupations of the mother during gestation can be followed out in physiological or pathological detail, the connexion with the same of a disposition to summer diarrhoea remains empirical, except in so far as it is a part of the rickety constitution itself. Some congenital weakness, we may suppose, attends the functions of digestion and assimilation, and, under the relaxing influence of continued high temperature, leads to vomiting and purging, to which many infants succumb through the eventual implication of the cerebral functions.
Ballard gives a table to show that of 332 infants (in a total of 340) who died of diarrhoea at Leicester in 1881 and 1882, 141, or 42·5 per cent. were “healthy,” and 191, or 57·5 per cent. were “weakly,” and other tables to show that “our experience of these Leicester epidemics by no means supports an opinion commonly held that a summer diarrhoeal epidemic makes its first fatal swoop upon the weakliest children[1407].” If “weakly” and “healthy” were as determinate as bushels of wheat or barley, there would be some fitness in this resort to numerical precision. But, in the circumstances, common experience will come as near the truth as the statistical method can, and will assign poor stamina to a much larger proportion of the infants that die. The poor stamina may be more a matter of inference than of direct observation. Thus, the last case of a death from infantile summer diarrhoea that came under my notice was in a big-boned and well-grown infant in the country. But it was the twelfth child of an equally large-built country woman, then big with her thirteenth, whose husband, a farm labourer, earned on an average not more than ten shillings a week. The rate of fecundity has, of course, a direct influence upon the stamina of the children. Its bearing upon the death-rate from infantile diarrhoea is shown in one of the columns of the table at p. 762.
Cholera Nostras.
Thus far I have considered diarrhoea as the “disease of the season” for the age of infancy or early childhood; and undoubtedly the large totals of deaths from it in the London bills, whether under the name of “griping in the guts” or afterwards under the generic name of “convulsions” were nearly all infantile deaths, both in earlier and later times. If we had regard only to the statistics of mortality and the effects upon population, we might now pass from the subject of epidemic diarrhoea, having said all that has to be said of it in those respects. But the deaths from epidemic diarrhoea, mostly of the summer and autumn, are far from being a correct measure of its prevalence, whether in our own time or in earlier times. Adults suffered from it in a fair proportion of the numbers living at the higher ages, although few of them died of it, except among the elderly and aged. It is only for modern times that we have any figures of the number of persons attacked at the respective periods of life; and these I shall take first in order, as illustrating the probabilities or generalities that may be collected from earlier writers such as Willis and Sydenham.
The following Table of the ages attacked at Leicester during a recent series of years shows a smaller proportion of attacks in infancy than some other modern tables do; but it is not misleading for general experience, and it will serve emphatically to correct the illusion that infants, because they contribute the bulk of the deaths, are most obnoxious to the attacks[1408]:
44,678 cases of Summer Diarrhoea at Leicester in seven epidemic seasons, 1881-87.
| Age | Cases | Per cent. | ||
| Under one year | 2,284 | 5·2 | ||
| One year and under five | 8,956 | 20·0 | ||
| Five years and upwards | 33,438 | 74·8 | ||
| 44,678 | 100·0 | |||
On the other hand, the fatalities from diarrhoea in all England during the same seven years had the following very different incidence upon the periods of life: