TYPHOID FEVER. 598 TYPHOID FEVER. follicles, swelling of spleen and mesenteric glands, and parenchymatous changes in many organs. Tyi)hoid fever is due to the presence in the body and to the etl'eets upon the body-tissues of a specific micro-organism known as the typhoid bacillus, or l)acillus typhosus. This is a small bacillus with rounded ends about two micro- millimeters in length and about one-third as broad. It is motile and grows at room tempera- ture on the ordinary culture media, preferably in the presence of air or oxygen, but capable of life without. (See Plate of Disease Germs.) Whether growing in the body or on artifi- cial culture media, the bacillus produces a poisonous substance know-n as typhotoxin, be- longing to the same general class as the toxins of diphtheria, tetanus, etc. During typhoid fever the bacillus is found regularly in the intestinal and mesenteric lymph nodes and as a rule in the spleen. In the early stage of the disease, when the nodes are simply enlarged, few or no bacilli are present in the bowel evacuations. Later, when ulceration of the nodules has occurred, the bacilli are usually found in the stools. In urine and bile it is quite connnon to find the typhoid bacillus, and in these secretions they may per- sist long after the passage of the fever, thus furnishing possible sources of infection long after the danger is supposed to have passed. Typhoid bacilli have also been reported in the blood, lungs, pleura, liver, kidney, uterus, and in other organs in which typhoid lesions occur; also in ty- phoid serous exudates and in the heart in tj'- phoid endometritis. Contraction of typhoid fever is believed to be always caused by the taking of the bacilli into the mouth and thence into the intestine. Food and drink are usually the vehicles which serve for the entrance of the bacillus, water and milk being probably the most frequent sources c' in- fection. The latter is especially dangerous from the fact that the typhoid bacillus not only lives but multiplies in it. Water and milk, however, are only dangerous when they actually contain the tyjVhoid bacilli which have entered into them from the excretions of typhoid patients. The initial seat of activity of the typhoid bacillus is undoubtedly in the intestines. Here the bacillus first sets up a catarrhal iniJamma- tion of the mucous membrane. This is followed by the most characteristic lesion of typhoid, namely, inflammation of the intestinal lymph- nodes. Both solitary nodules and Peyer's patches are affected, although it is in the latter that the changes are usually most marked. There is first congestion of the nodule and of the surrounding tissues, then increase in the size of the nodule. This increase in size of the nodule appears to be due to a proliferation of its cellular elements. Thus there is more or less extensive increase in number of the lymphoid cells and of the endothe- lial cells which" line the lymph-sinuses. When the inflammation is severe it may extend not only peripherally to the tissues laterally adjacent, but also into the deeper tissues of the intestinal walls involving the muscular and serous coats. These changes are apparently due to the pres- ence in and effects upon the nodules of the ty- phoid bacillus. Such inflamed nodules may un- dergo resolution. The results of the inflamma- tion may be absorbed or cast off, or both, and the nodules return to their normal condition. On the other hand, in the more severe grades of the infection, the nodules, instead of undergoing such early repair, go on to necrosis and to the formation of the so-called typhoid ulcers. These ulcers are formed in Peyer's patches, gradually increase in size, and discharge into the intestines. (See Peyer's Glakd. ) Xot infrequently they open up blood vessels of considerable size and thus cause one of the gravest accidents of typhoid fever, namely intestinal hemorrhage. Or an ulcer may eat its way through the muscular and serous coats and, opening into the peritoneum, produce what is known as a 'perforation.' This, probably the gravest accident of typlioid, allows bacteria and intestinal contents to soil the peri- toneum and leads frequently to the setting up of a general and rapidly fatal peritonitis. Changes in the liver and spleen are of common occurrence in typhoid fever. Of the two the spleen is most frequently affected. This might be expected on account of the character of the spleen as a lymphatic organ. The changes con- sist of congestion with proliferation of the cell- ular elements of the spleen and consequent in- crease in the size of the organ. Of the conditions which may be present in the liver, the most com- mon is a simple acute degeneration, such as oc- curs in other infectious diseases. Lesions not distinctly a part of, but more properly the result of, the typhoid lesions also occur. Thus, in addition to the inflammation o[ the intestinal lymph nodes already described, there may be extensive involvement of the in- 1 estinal mucous membrane. This may lead to gangrene of considerable areas or to the forma- tion of false membranes. Extension of the in- flammation through the muscular coat may cause infection of the serous coat and, setting up a localized peritonitis, result in the formation of adhesions. Involvement of lymph glands in other parts of ;,he body may be secondary to the ty- phoid lesions in the intestinal glands. Cases of typhoid infection resembling septi- cemia, presenting no characteristic lesions and recognizable only by the finding of the bacillus ty- phosus, have been reported. Typhoid fever is widely distributed through- out the world, but is especially prevalent in the temperate zones. From its prevalence during the autumn it has been called autumnal fever. Young adults are usually attacked, the affection being comparatively rare among children and old per- sons. ■ Hot and dry weather are favorable for its development. The incubation period of enteric fever lasts from 8 to 14 days, or, exceptionally, longer. The onset is gradual, feelings of lassitude and malaise being followed by nausea, loss of appetite, head- ache, pains in the back and extremities, nose- bleed, and perhaps a distinct chill. For a few days the patient may go about his work, but at the end of that time is compelled to go to bed. This may be reckoned the definite onset of the disease. The fever is very characteristic. During the first week the temperature rises steadily by a degree or a degree and a half a day until 103° to 105° F. is reached; during the second week the fever remains high : during the third week, in eases of moderate severity, it gradually declines, and in the fourth week convalescence begins. The pulse is rapid, full and soft, and the respirations increased in number. About the 7th to the 10th
