The diarrlimal disorders of childhood occurring, in conjunction with elevated summer temperature appear first as functional (chemical) disturbances and subsequently as profound organic lesions of the intestinal wall. For the develop ment of these conditions the ordinary saprophytic bacteria of the intestinal contents, and not specific bacteria, must be held responsible. The active organ isms cause injury to the intestinal walls through the putrefactive processes of toxic character or through products usu ally non-toxic in character (ammonia and its derivatives), inasmuch as they aet as inflammatory irritants; or they cause degeneration of the vegetative and the most important excretory organs (liver, kidneys, etc.) through the blood-stream and the lymph-stream. As a result of the interference with nutrition and the diminution in the resistance of the tis sues thus brought a.bout, the organism is exposed to the invasion of pathogenic bacteria of all kinds (staphylococci, streptococci, pneumococci, °Whim albi cans, etc.). There also results a predis position to disease, as manifested by numerous complications. Baginsky (Berl. klin. Woeh., jan. 11, '97).
Study of thirteen cases leading to the following conclusions:— 1. The bacterium coil appears to be the pathogenic agent of the greater number of summer infantile diarrhceas.
2. This organism is the more often associated with the streptococcus pyog enes.
3. The virulence, more considerable than in the intestine of a healthy child, is almost always in direct relation to the condition of the child at the time the culture is taken, and does not appear to be proportional to the ulterior gravity of the ease.
4. The mobility of the bacterium coli is, in general, proportional to its viru lence. The jumping movement, never theless, does not correspond to an ex alted virulence in coniparison with the eases in which the mobility was very considerable without presenting these jumping movements.
5. The virulence of the bacterium coli found in the blood and other organs is identical to that of the bacterium coli taken from the intestine of the same in dividual. C. G. Cumston (Inter. Med. .lour., Mar., '97).
The toxic symptoms of gastro-intes tinal infection depend upon the intro duction into the alimentary canal of poisonous substances which are con tained in the food: tyrotoxicon, for in stance, which originates in mill:, and is poisonous for man and animals. Bac teria may be introduced from without; or the ordinary saprophytic bacteria which inha.bit the intestinal canal may take on a special virulence. But the most severe disturbances are caused by the metabolism of bacteria; these micro-organisms by their activity either produce acids or cause decomposition of albuminoid substances; the products act as powerful irritants to the intes tines, and by injuring the intestinal wall gain access to the blood and lymphatics, in this way producing the local and con stitutional symptoms. A. ..-1/2.bt (Medi
cine, Feb., 1900).
Pathology. — There are very few changes found after death either in the intestinal canal or in any of the organs. The only lesion present may often be a desquamative catarrh of the gastro-in testinal tract. In those cases which de velop hydrencephalic symptoms, the ap pearances found after death bear no proper relation to the gravity of the symptoms. The kidneys are generally found paler than usual, with a moderate cloudy swelling of the cortex, but not to a greater extent than may be present in other febrile disorders of infancy (Holt). The earlier symptoms may, therefore. reasonably be ascribed to the influence of some toxin upon the heart, nerve-centres, and vasomotor nerves of the intestines, while many of the later symptoms must be referred to the great abstraction of serous fluid from the body.
in cholera infantum a bacillus found which was colored after the method of Gram. Cultivated in gelatin or bouillon, an alkaline product is obtained, having a distinctive odor, which it retains many months. It is more resistant to external agents than the common bacillus, and more tenacious of life. Isolated, it is capable of producing experimental chol era, like several other microbes. It prob ably plays an important part in the pro duction of cholera infantum, as proved by the following reasons: 1. It exists only in cases of cholera infantum, fre quently in large numbers. 2. It produces experimental cholera. 3. It produces a substance apparently identical with that produced by the comma bacillus. In doses of 4 to 5 milligrammes (3/0 to 7/20 grain) it is toxic, and causes the death of the animal. 4. It produces choleraic intestinal lesions. Lesage (1,a Sem. MM., Apr. 9, 90).
In spite of the most careful researches, no constant micro-organism has been found, the comma bacillus not being present. At times, when cholera infan t= is prevalent the temperature of the child is often considerably above normal, especially toward the end of the day. it suppos.ed that the high temperature indirectly induces some changes favor able to tbe rapid growth of saprophytic germs already present. Alfred H. Carter (Provincial Med. Jour., July, '93).