64 THE DEFENSIVE FORCES OF THE MACROORGANISM 



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 conclu- 

 sion that the negatively chemotactic effect must be referable to such 

 substances. In this sense a certain parallel 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 of the liability to staphylococcus infections 

 in diabetes. Both are types of infection in which phagocytosis plays 

 a prominent defensive role, and we have already sufficient evidence 

 to show that both alcoholism 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 phagocytosis is 

 the mainstay of defense 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, whether 

 the hyperemia be the direct outcome of the bacterial invasion or 

 produced artificially (Bier's method ; counterirritation 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 



