PHAGOCYTOSIS 67 



in the subsequent animals, and as we have come to look upon Bail's 

 aggressins as being nothing more than endotoxins which have been 

 set free after the death of the organisms, we are forced to the con- 

 clusion that the negatively chemotactic effect must be referable to 

 such substances. In this sense a certain parallelism undoubtedly exists 

 between the virulence of an organism and the chemotactic effect 

 which it produces. 



Phagocytosis as a Defensive Factor. From the foregoing consider- 

 ations it is clear that the leukocytes can rank as defensive factors 

 only in the presence of opsonins or tropins, and providing that the 

 aggressivity of the invading organisms is not above a certain level; 

 it accordingly follows that any factor which tends to lower the normal 

 content of opsonins or prevents the prompt formation of tropins will 

 virtually be equivalent to an aggressive influence and simulate an 

 increased virulence on the part of the infecting organisms. The 

 recognition of this possibility offers an explanation of the formerly 

 more or less obscure modus operandi of some of those factors which 

 the clinician speaks of as predisposing causes of disease. 



Everyone is familiar with the serious course which pneumonia 

 is apt to take in drunkards and with the liability to staphylococcus 

 infections of diabetics. Both are types of infection in which phagocy- 

 tosis plays a prominent defensive role, and we have already sufficient 

 evidence to show that both ajgojiolism and diabetes tend to lower 

 the opsonic content of the blood. In such cases we could readily 

 understand that an increased virulence on the part of the infecting 

 organism would, in itself, not be necessary to produce the infection 

 or to favor its generalization. This, indeed, seems to be Wright's 

 attitude in reference to those infections in general, in which phago- 

 cytosis is the mainstay of defence on the part of the body, for he 

 expressed the belief that primary infection occurs in consequence 

 of a lowered opsonic content of the blood, in contradistinction to 

 the idea that the opsonic content drops because of the infection. 



On the other hand, we can now understand why hyperemia at the 

 point of infection should be of use in combating the infection, no 

 matter w r hether the hyperemia be the direct outcome of the bacterial 

 invasion or produced artificially (Bier's method; counter-irritation 

 by cautery, sinapisms, applications of iodin, turpentine, etc.). 



Variation in Opsonic Content of Blood. That the opsonic content of 

 the blood does not remain constant after infection has once begun 



