MECHANISM IN INFECTIONS WITH SEMIPARASITES 87 



ance against phagocytosis, the corresponding changes which take 

 place in the cholera vibrio and the typhoid bacillus and which 

 are represented by an hypertrophy of the ectoderm, do not lead 

 to the same degree of protection. 



Evidently, then, there is a marked difference in the character of 

 the strife between the defensive forces of the guinea-pig and the 

 two types of organisms. On the one hand, the anthrax bacillus 

 gains the upper hand through its successful resistance to phagocy- 

 tosis and the inhibitory effect of its aggressins upon the production 

 of leukins, even though the appearance of the leukocytes at the 

 point of infection is not seriously impeded. In infections with the 

 semiparasites, on the other hand, the organisms conquer essen- 

 tially through the negatively chemotactic effect of their aggressions 

 upon the cells, which are thus kept at a distance and through the 

 resistance of the animalized individuals to the ordinary bacterio- 

 lytic influences of the serum. 



Between the two extremes which have been represented above, 

 i. e., the effect following the injection of large and of subinfectious 

 doses of the cholera vibrio every possible gradation is possible and 

 can actually be reproduced in the animal experiment. If thus the 

 minimal infecting dose is injected there will usually be a primary 

 bacteriolysis of considerable extent, which then gives way to a 

 gradually developing increase in the number of the organisms. At 

 first, as the leukocytes begin to appear, this proceeds slowly, but 

 after a little while the organisms definitely secure the upper hand 

 and coincidently the further influx of cells is more or less completely 

 arrested and the disease pursues its course to a fatal termination. 



That the leukocytic insufficiency is really the deciding factor in 

 the victory of the bacteria in such a case can be very well shown 

 by previously injecting the animal with the leukocytes of a second 

 one and then introducing the minimal dose of bacteria which in 

 the untreated animal would invariably produce a fatal result. It 

 will now be seen that the animal does not succumb, and if a series 

 of corresponding experiments be carried out it can be demonstrated 

 that a number of multiples of the originally just infecting dose 

 must be injected in order to kill. Weil has shown very satisfactorily 

 that this result is purely referable to the action of the leukocytes 

 and not to any bacteriolysins that may be present, by previously 

 rendering the latter inactive with so-called complement-binding 



