52 BACTERIAL POISONS 



masses of anthrax bacilli, or, as in some of the severest types of 

 tropical malaria, with masses of plasmodia, was directly responsible 

 for the fatal issue. This purely mechanical element cannot, of course, 

 be ignored, but in the light of our present knowledge of the physio- 

 logical pathology of the infectious diseases, we are warranted in the 

 belief that the future will bring a more satisfactory explanation. 



Infection with Animal Parasite. While the foregoing considerations 

 apply more particularly to bacterial infections, similar conditions no 

 doubt exist in infections with animal parasites. Primary infection 

 is here often facilitated by the intervention of special infection car- 

 riers. We thus know that malaria is transmitted through the bite 

 of infected mosquitoes (Anopheles maculipennis), trypanosomiasis 

 through biting flies (Glossina fusca and tachinoides), African relapsing 

 fever and Texas cattle fever through certain ticks (Ornithodorus 

 moubata and Boophilus bovis respectively). 



With other organisms, such as the Trepoiiema pallidum (Spirochete) 

 we may assume the existence of tiny breaks in the continuity of the 

 epithelial covering, as in the majority of the bacterial infections, 

 while with still others, like the ameba coli, we may imagine that the 

 epithelial lining is first destroyed by the parasite itself. What, then, 

 happens, after actual invasion of the deeper structures has taken 

 place, we can only surmise, but it would appear that the aggressivity 

 of the animal parasites is upon the whole even greater than that of 

 the bacteria. A more or less extensive infection apparently occurs 

 in all cases, in which the microorganism has once gained a foothold, 

 some of the organisms in question multiplying in the blood stream 

 (malaria, trypanosomiasis, relapsing fever), others in the tissues 

 (syphilis, amebiasis), only too often without much show of active 

 resistance on the part of the host. What are the aggressive forces 

 which the animal parasite has at its disposal we do not know. In 

 the case of the malarial parasite these are manifestly directed with a 

 remarkable degree of specificity against the red corpuscles. Having 

 once gained an entrance they are evidently perfectly secure; appar- 

 ently they are open to attack only while they exist free in the plasma. 



Of the formation of toxic products on the part of the animal para- 

 sites nothing definite is known. The clinical history, however, would 

 suggest this. In malaria the occurrence of the chill and fever and 

 the lack of relation, which exists between the degree of anemia and 



