in which we used to speak of "scrofula." Of course, nothing could be more misleading, for the very use of the term withdraws attention from the chief cause of the trouble, viz., infected food. To say a child has " marasmus," is only to say that it has wasted and is exhausted, and though it may be difficult sometimes to discover the reason of this mal-nutrition, yet in the summer time, and when a child has diarrhoea, it ought not to be hard to understand the cause of the atrophy. I think that there are, of course, many exceedingly delicate children whom it is difficult to rear artificially, but I would certainly sign a death certificate of such a case after the manner of a certificate lately given by a medical 'man, at present in suburban practise-First, want of breast milk; second, exhaustion. I think nothing could be better than that or truer. So strongly convinced are many leading pædiatrists of the truth of the opinion which I have expressed concerning the cause of summer diarrhoea, that in the two most recent leading text-books upon diseases of children, one author calls summer diarrhoea, acute mycotic diarrhoea, and another describes it as acute or subacute milk infection.

In discussing the etiology, I have said nothing about the bacteriology of the disease, for nothing very definite can be said. To quote Vaughan on this subject.-"These diarrhoeas are due to toxicogenic bacteria. There is not a specific micro-organism, but any one or more of a large class of germs, the individual members of which differ from one another sufficiently morphologically to be regarded as distinct species, may be present and may produce the symptoms. These germs grow and multiply in milk and fluid food, both before and after they have been taken into the alimentary canal, and elaborate chemical poisons which induce the diarrhoea and other untoward symptoms."

I will now pass on to the consideration of the pathological anatomy associated with the disease. During the last two years I have had some opportunities of making post-mortem examinations of infants who have died in the summer, and who have suffered from diarrhoea. I wish to point out at once that it is of no practical advantage to make the clinical classification of diarrhoeal diseases correspond exactly to the classification of the anatomical lesions found in those complaints, because similar symptoms are known to be caused during life by diverse pathological changes, discovered after death. It is probable that all the post-mortem changes may result from similar poisons in different degrees of

concentration, or acting through varying periods of time; still, the thorough recognition of the morbid anatomy of the disease is of the utmost importance, because from the locality of the inflammatory changes we gather hints for treatment. For instance, it is now recognised that the chief incidence of this intestinal inflammation is on the mucous membrane of the colon, and this fact justifies the plan of treatment by thorough irrigation of the lower bowel. Again, many medical men are still under the impression that the intestinal changes are not sufficient to account for death, and are forced then to find the cause of death in some supposed change in other organs-the brain is said to be " congested," or death is said to be caused by "effusion on the brain." Under these circumstances, and apparently on rational grounds, sedative treatment is directed to the brain, and nothing could be more unwise. If it is generally recognised where and what are the intestinal changes in fatal cases, and that these changes are due to direct irritation by the products of toxicogenic bacteria, and that in consequence a kind of septic poisoning goes on simultaneously with an exhausting discharge, and that such a condition is incompatible in many instances with the life of a child, a good step forward will be taken in the treatment of these The pathological classification cannot be quite so simple as the clinical division of these cases into acute and subacute milk infection. In many acute cases the changes found post-mortem are disappointingly slight. For instance, in many genuine cases of cholera infantum, no very obvious changes are to be seen. Such cases are pathologically classed as "acute desquamative catarrh of the intestine," and microscopically there is found to be a loss of the superficial epithelium. Macroscopically, the mucous membrane of the intestinal tract is either somewhat injected, sometimes of an intense rosy red, or it may be pale in consequence of post-mortem changes, but always, and this is most important, the ileum and large intestines contain no fæcal matter, or only an offensive fluid. I have seen in cases of cholera infantum, in addition to the catarrhal condition, marked swelling of the lymph follicles and of the mesenteric glands. Even if the changes are not all obvious, we must recognise the fact that the intestinal trouble, associated with septic poisoning, is a sufficient cause of death. Remember that in true Asiatic cholera no great changes are observed. In only very rare instances, in which the post-mortem examination has been made within six hours or earlier after death, would it be safe to

cases.

judge even of the microscopic appearances, for very rapidly does desquamation of the epithelium and maceration of the mucous membrane take place post-mortem.

The majority of cases of diarrhoeal diseases may be definitely classed under four heads :-(1) Catarrhal enteritis, generally associated with number (2). (2) Follicular or nodular enteritis. (3) Follicular ulceration of the intestines. (4) Membranous enteritis. By far the greater number of cases come under the first and second heading, and generally the intestines show both catarrhal and follicular inflammation. It is important to recognise the purely post-mortem changes. It has been pointed out, that the inflamed injected mucous membrane of the intestines rapidly becomes pale and bloodless after death, and so appears as though there had been no inflammation during life; in fact, it is often recorded that the intestines were bloodless, although clinically there had been abundant evidence of enteritis during life. On the other hand, it is necessary to realise that the whole mucous membrane becomes softened post-mortem and macerated, and that swollen follicles become softened and partly burst out, leaving little pits which look like minute ulcers.

I have found, as a rule, and this also is the experience of all observers, that the colon throughout its entire length, and the ileum in its lowest part only, are most affected. In cases of some standing, this is very obvious. Vaughan says in reference to this point, "the contents of the small intestines accumulate before passing through the ileo-cæcal valve, while inflammatory changes in the large intestine are invariably present in protracted cases, and more marked here than elsewhere; this is due to the fact that the intestinal contents become more irritating the longer they are subjected to the fermentative action of the bacteria; the inflammation is most marked generally just above the sigmoid flexure, in consequence there, again, of some delay in the passage of the irritating substance." It is now unnecessary to point out the great value of proper irrigation of the lower bowel in all stages of diarrhoeal disease. In the more acute cases, the small intestines seem to be affected as much as the rest of the intestinal tract.

The examination of the stomach has always been disappointing. It is only rarely that it is possible to find any changes which are certainly other than purely post-mortem, though in a few cases I have observed signs of a catarrhal inflammation. Many observers have pointed out that the stomach remains free from any lesion,