MECHANISM IN INFECTIONS WITH SEMIPARASITES 81 



a primary destruction of the organisms, comparable to what occurs 

 in the peritoneal cavity is not seen; on the contrary, there is active 

 multiplication from the start. The explanation of this difference is 

 no doubt to be sought in the greater difficulties which would present 

 themselves to a prompt collection of cells and serum at the point of 

 attack. 



In either event the infection, when once it has started, progresses 

 without resistance and ultimately leads to the death of the animal. 

 How this is brought about is unknown. So much, however, seems 

 to be certain that unlike the infections with the so-called necropara- 

 sites (tetanus, diphtheria, botulismus) toxins do not play a role in 

 anthrax, and we can accordingly only say that the fatal end in infec- 

 tions of this order must result in an indirect way. Significant in 

 this connection is the fact that anthrax infection in animals that 

 are naturally somewhat resistant, or in others in which a certain 

 degree of resistance has been artificially produced, is followed by 

 symptoms of actual disease and a gradual decline until death 

 ultimately occurs. 



Offensive-defensive Mechanism in Infections with Semiparasites. 

 If now we turn our attention to the offensive-defensive mechanism 

 which is thrown into operation in infections with the so-called semi- 

 parasites, of which the typhoid bacillus and the cholera vibrio are 

 typical examples, we meet with still a different picture, which is 

 fairly well defined also, although it has not been worked out in its 

 details so thoroughly as we have seen it in anthrax. A great deal 

 again depends upon the quantitative relations at the point of infection. 

 If the infecting dose (of the cholera vibrio, for example, given intra- 

 peritoneally) is large, e. g. y several multiples of the quantity which will 

 just produce infection, there is virtually no evidence of a defensive 

 reaction. The organisms multiply from the start, or at least do not 

 diminish in number even during the first few hours; there is no evi- 

 dence of phagocytosis or of extracellular degeneration. Leukocytes 

 indeed are relatively scant, while the abdominal cavity is filled with 

 a serous exudate, in which the bacteria multiply as in an ordinary 

 culture medium. The animal at the same time shows evident 

 signs of being ill; the abdomen is tense and exceedingly tender, the 

 hair is ruffled, the temperature drops, and death soon results. 



From such a picture one would be led to conclude that the animal 

 was devoid of all defensive means against the organism in question. 



