Causes of the high death-rates from Infantile Diarrhoea.
Sydenham said that the diarrhoea or bilious colic of London in the month of August differed toto coelo from that of other seasons of the year; and Harris, writing in the year of Sydenham’s death (1689), said that more infants, affected with the epidemic gripes, died in one month of the hot season, from mid-July to mid-September, than in other three that are gentle. If this were taken to mean that the infantile mortality from all causes was trebled by the prevalence of diarrhoea during the eight warmest weeks of the year, it would be nearly borne out by the weekly bills of mortality, according to the examples given of them from the more fatal years. So far from the deaths of infants in London by summer diarrhoea having increased in the present century, they would appear to have diminished greatly. The two worst weeks of an unhealthy summer or autumn raised the London deaths in former times relatively as much as the whole diarrhoeal season would do now. If this great change for the better be admitted as correct, it may throw some light upon the causes of excessive infantile diarrhoeal mortality in London in former times, and in some other English towns at the present time.
The London populace in the 17th and 18th centuries were not only the single great urban community in the kingdom, but they were far more “urban” than now, in Milton’s sense of being
“long in populous city pent,
Where houses thick and sewers annoy the air.”
The houses stood closer together, many of them back to back in courts and alleys. The streets were narrower. The inhabited area had few or no open spaces besides the bed of the Thames. Not only the City and Liberties, but also the out-parishes were compact, as if within a ring fence, joining on to the open country abruptly, and not as now in straggling suburbs. It was hardly possible to take children out for an airing, except in the west end. When Lettsom about 1770 applied the fresh-air treatment to convalescent cases of typhus, he had to send the patients to loiter on the bridges spanning the Thames. As Cobbett said, London was a “great wen,” in the correct sense of a shut sac which grew by distension. The soil was full of organic impurities, including the decompositions of many generations of the dead. A hot summer in former times raised effluvia from the ground such as the modern residents have no experience of. The life indoors was equally adverse to infants. Fustiness was favoured by the window-tax; a tenement-house was apt to be pervaded by the excremental effluvia from the “vault” at the bottom of the stair. The worst time of all in London was the great drunken period from about 1720 onwards. Doubtless drink was then used, as it is sometimes now, to drug the fretful infants into torpor; but it told also upon them indirectly, inasmuch as dissolute parents would have bred children with mala stamina vitae[1404]. In all these respects there has been so great an improvement in London that, although its population now exceeds four millions, its death-rate from infantile diarrhoea, a distinctively urban disease, exceeds only by a little the mean of all England and Wales.
While the mortality from infantile diarrhoea in London has undoubtedly decreased since the 17th and 18th centuries per head of the population, it is equally certain that there has been within the present century a great relative increase of the deaths from that cause in the country generally. The reason is that there has been an enormous increase of population and that the increase has been almost wholly urban. The rise of new manufacturing towns, with the great extension of the borders of old towns, as in Lancashire and Yorkshire, has inevitably brought to the front this distinctive fatality of town-bred infants. If the additional millions had been dispersed in village communities over the face of the country, as in Bengal, the mere density of population per square mile would have had its effect on the public health, but not the same effect. There are now two or three provincial cities comparable in size to 18th century London, and there are some twenty more large enough to be in the same group. In most of these the mortality from infantile diarrhoea has held its ground, for all the improvements in sanitation and in well-being whereby the death-rate from all causes has been considerably reduced. It is mainly owing to that disease, and to whooping-cough, that the death-rate in the first year of life, although it has ranged widely from year to year, has fallen but little in the successive decennial periods. The bad eminence of some towns in the list already given is probably due to a composition of causes, among which the situation, soil, depth of ground-water, and the like, would count. It is remarkable, however, that there are only a few of them, such as Liverpool and Hull, that have been the chosen seats of great epidemics of Asiatic cholera. On the other hand, Leicester and Birmingham never had an epidemic of that disease, while Preston and the cotton-weaving towns of Lancashire generally have had but slight outbreaks of it. Again, the deaths from diarrhoea have been more purely infantile in the group of towns which have had little or no Asiatic cholera[1405].
That which distinguishes the Lancashire and West Riding towns with highest proportions of diarrhoeal death-rates in their infantile death-rates generally, as well as such towns as Leicester, Worcester, Northampton, Coventry and Norwich, Birmingham, Nottingham and Stoke-on-Trent, is the extensive employment of women in factory work and other labour of the factory kind. The Census returns do not adequately show this for married women, who may be returned simply as of the married rank whether they be wage-earners or not; but it is well known that the female labour of industrial towns is to a large extent the labour of child-bearing women. Among the towns that stand highest for infantile diarrhoea, Preston, in the Census of 1881, had 32 per cent. of its adult female population occupied in the cotton mills; Leicester had 20 per cent. of all its women occupied in various industries, of which the chief are the hosiery and boot-making; Northampton only 13 per cent., all at boot-making; Worcester, a percentage, unknown for the city, occupied mostly at glove-making; Norwich about 10 per cent. of its women returned as employed at boot-making, silk manufacture, and various smaller industries.
One obvious result of married women engaging in factory labour, or piece labour of the same kind at home, is that they do not suckle their infants; and it has long been known that infants brought up with milk from a feeding-bottle are much more liable to diarrhoea than infants brought up at the breast. But the feeding-bottle is now too universal an appurtenance of infancy among all classes and in all places to be a sufficient explanation without something else, although there is no doubt that feeding-bottles which are not kept very carefully clean are a real danger in the particular way. Again, young children above the age for suckling or feeding by the bottle are attacked by summer diarrhoea in about the same proportions (e.g. at Leicester) as infants under one year, although they do not contribute an equal quota to the death-roll.
In the discussions upon this question it has been commonly assumed that the fault lies with the mother after the birth of her child, and all the remedial measures, such as crèches for the infants of workwomen, have that assumption underlying them[1406]. I believe that this is a very inadequate account of the cause of this great modern evil, and that the remedies proposed are mere palliatives which are destined to fail. The importance of the matter may justify me for once in making an excursus into physiology and pathology.
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.