Avian Tuberculosis. 611 



spontaneously infected mice or rats may be the means of 

 spreading the disease (Rabinowitsch). 



Infection may also take place through injuries of the mouth 

 or of the skin; the possibility of an infection through the air 

 passages by means of inhaled air containing the bacilli must 

 also be admitted. 



Heredity plays only a subordinate role in the dissemination of 

 the disease. Maffucci demonstrated that the embryo of experimentally 

 infected eggs is capable of development and the possibility also exists 

 that they may become infected through tuberculous ovaries. Accord- 

 ing to Lichtenstein, who found that all the progeny of an infected 

 cock had the disease, there exists also the possibility of a germinative 

 infection through the male parent. Chicks however that have been 

 hatched from infected eggs live at most only a few months before 

 they succumb to the effects of the disease. On the other hand the 

 plague may be introduced into healthy flocks through the means of 

 infected eggs the albumen of which occasionally contains bacilli (Mohler 

 & Washburn). Rabinowitsch observed the hatching of 8 chicks from 

 32 experimentally infected eggs. Of the eggs infected with avian 

 tuberculosis the embryos died in 90%, of those infected with guinea pig 

 tuberculosis 70% and of those infected with bovine tuberculosis 40 %i 

 died. 



Pathogenesis. The bacilli, which usually gain entrance into 

 the alimentary canal with the food, usually pass through the 

 solitary and agminated lymph follicles of the large and small 

 intestines into the intestinal walls and thence, with the blood 

 of the portal vein, enter the liver or they gain access into the 

 general circulation and lodge in other organs and portions 

 of the body, thus in the spleen, lungs, joints and tendon 

 sheaths, causing the development of specific lesions. The in- 

 testinal mucous membrane may remain perfectly intact or 

 small nodules may develop in its tissue. The overlying villi 

 may present no changes in the beginning but ulceration follows 

 at a later time. These ulcers may heal with the formation of 

 granulation tissue (Schern). The nodules occurring in the 

 intestinal walls under the serosa develop from the lymph nodes 

 in the peripheral layers of the intestinal walls, or between 

 the serosa and muscularis of the cecums, or from the agminated 

 follicles in the mucous membrane wdthout causing any observa- 

 ble changes in the intestinal mucous membrane which, ho^v- 

 ever, they perforate at a later stage and then communicate 

 with the lumen of the intestine (M. Koch & Rabinowitsch). 



The symptoms of cachexia observable in diseased fowds 

 (emaciation, anemia, marasmus) are a result of the toxic ac- 

 tion of the chemical products of the bacilli. These toxins, 

 which kill guinea pigs wdth the same symptoms as those ob- 

 served in chickens, may be produced from artificial cultures, 

 particularly those grown on liquid glycerin serum (Maffucci, 

 Hericourt & Richet). The death of dogs and guinea pigs 



