INFECTIONS WITH ANIMAL PARASITES 55 



that the occlusion of extensive capillary districts with densely matted 

 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. 



Infections with Animal Parasites. While the foregoing considera- 

 tions 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 relaps- 

 ing fever and Texas cattle fever through certain ticks (Ornithodorus 

 moubata and Boophilus bo vis respectively). 



With other organisms, such as the Treponema pallidum (Spiro- 

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

 of the epithelial covering, as in the majority of the bacterial infec- 

 tions, 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 appar- 

 ently 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 the aggressive forces 

 are 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 



