The course of this disease is very rapid, terminating in many cases in collapse and death within twenty-four or forty eight hours after its commencement. Should hydrencephaloid symptoms set in, the end may be delayed for a day or two longer. In the few cases which go on to recovery, cessation of vomiting ap pears to be one of the earliest symptoms of improvement; gradually the char acter of the stools alters, and they be come more kecal; the restlessness abates, and improvement may be noted in the pulse and general appearance of the in fant. Convalescence, however, is always tardy, and relapses are not uncommon.
character of the on set, the persistent vomiting, the profuse serous dejections, the high temperature, and the symptoms of profound collapse rapidly developing within a few hours, form a picture unlikely to be mistaken for any other condition.
The odor of the stools makes it pos sible to determine two general classes of fermentation. The fermentation of the carbohydrate foods leads to the develop ment of a_eids and gases, but under no circumstances to products with fL putrid odor. Proteids yield either odorless or putrid products. Fitch (Va.Med.:111thly., *9-1).
Etiology.—Tlie exact nature of cholera infantum has not yet been proved, but analogy points strongly to its being a toxic condition produced by the absorp tion from the intestinal tract of some special toxin originating in fermenting or decomposing food. The prolonged heat of July and August appears to be a distinctly predisposing factor. Infants living under faulty hygienic conditions, and supplied either with an injudicious dietary or with milk food in the prepara tion of which due care has not been taken, appear to be among those most prone to attack. Although the disease may develop suddenly in the compara tively healthy, yet we find that, in the majority of cases, there has been a more or less severe antecedent disorder of the gastro-intestinal tract.
From 22 obsen-ations, the following conclusions are drawn: (1) the spores present in acute dyspepsia and intro duced with the food will grow luxuri 1 antly at the body-temperature, and these are capable of withstanding the action of the acids of the stomach; (2) since severe dyspepsias, especially of the chol era-infantum type, present the phenom ena of acute intoxication, and increase in severity with the temperature of the atmosphere, their cause is to be sought in the poisons generated by the sapro phytic germs of the stomach and intes tines; (3) some of these cases have the general characteristics of acute infectious diseases in their etiology, but the ma jority are not particularly endemic or epidemic, and the special characteristics of infectious diseases (stage of incuba tion, typical course, etc.) are rare. Seif
fert (Jahrbuch f. Kinderh. u. physische Erziehung, B. 32, H. 4, '91).
1. When the heat rises above 165° F. the galactozymose, or starch-liquefying ferment, is destroyed. It is present in cows' milk only in minute quantities. 2. A portion of the lactalbumin is coagu lated. 3. The casein, after the action of prolonged heat, is less readily coagulated by rennet, and yields slowly and imper fcctly to the action of pepsin and pan creatin. 4. Fat is so affected by the heat that, after the milk has stood for some time, small lumps collect on the surface. 5. Milk-sugar is completely de stroyed by prolonged heating. Leeds and Hiesland (N. Y. Med. Jour., Nov. 7, '91).
Careful bacterial examinations of the stools in ninety-two different cases of various degrees of intensity, and in the fatal cases similar examinations of the intestinal contents and of the various internal organs, were coupled with his tological examinations with a view to determining the relation of the intestinal infections and lesions to the remoter changes in the body. Conclusion that the intestinal disorders of children arc to be attributed to no one specific form of bacteria. That in many eases the actual damage is done more by the prod ucts of the bacterial growth than by the germs themselves seems clear, since we know that these products are often strongly toxic, and since in many even fatal cases no penetration of the body tissues by the bacteria can be demon strated. In the milder forms of these disorders it is not unlikely that the acids, which Baginsky has shown are generated by the obligatory milk--fmces bacteria in moderate quantity even under normal conditions may be the irritant of the intestinal mucous membrane chiefly responsible for the symptoms; and this conception seems fully in accord with the decided acidity of the stools in these eases. In the severer cases, and particularly when pyogenic or necrotiz ing species of bacteria are present, dis tinct inflammatory changes in the intes tinal mucosa are usually present and seem often to permit the entry of the bacteria to the underlying tissues, whence they may be disseminated throughout the body and induce a gen eral pyxmic condition of which pneu monia is not an infrequent manifesta tion. Booker (Johns Hopkins Hosp. Re ports, vol. vi. 159, '96).