MECHANISM IN INFECTIONS WITH TRUE PARASITES 83 



spite of the fact that leukocytes are present in abundance. Phago- 

 cytosis then no longer occurs and signs of extracellular degeneration 

 are altogether wanting. Simultaneously bacilli have appeared in the 

 circulating blood and multiply here also without hindrance. 



It might be argued that this change in conditions was brought 

 about through a gradual loss of those defensive substances in the 

 peritoneal fluid of the guinea-pig, to which the primary successful 

 resistance was due; but this is disproven by the fact that if a new lot 

 of "culture" bacilli, like those used to bring about the infection in the 

 beginning, be now injected, these will be destroyed as readily and in 

 the same manner as the first. Evidently, then, the same defensive 

 factors of the host are still available. 



The conclusion, hence, suggests itself that some change may have 

 taken place in the bacteria, and microscopic examination shows, as 

 a matter of fact, that the newly developed brood really differs from 

 the stock culture in having become encapsulated. Further experi- 

 ments, however, show that the capsule formation in itself does not 

 explain the result, for if some of these capsulated bacilli are injected 

 into the peritoneal cavity of another guinea-pig, they do not imme- 

 diately multiply without hindrance; but, as in the beginning of the 

 first experiment, they undergo extensive extracellular degeneration, 

 and here, as there, the peritoneal cavity may be temporarily freed of 

 bacteria, although phagocytic destruction apparently does not take 

 place. 



This shows clearly that while the phagocytic forces are no longer 

 operative in combating the capsulated organisms, some of the normal 

 extracellularly active lytic forces are still available. But, if so, why 

 do they remain inactive in the body of the first animal? It can 

 easily be shown that guinea-pig serum in itself has little or no bacteri- 

 cidal power, so far as the anthrax bacillus is concerned. If, then, the 

 peritoneal exudate has this to a marked extent the thought naturally 

 suggests itself that the destruction of the bacilli may be the out- 

 come of the combined serum-leukocyte effect possibly in the sense 

 of Schneider's leukins or Peterson's leukocytic endolysins. 



If Schneider's experiments permit the inference that these sub- 

 stances are formed through the secretory activity of the living cells, 

 then the possibility also suggests itself that this activity may be 

 impaired or paralyzed as a consequence of bacterial action, and this 

 is what Bail actually claims for his aggressins. He has shown, 



