﻿358 MARSHALL. 



complements, "and usually bactericidal complement not only for chol- 

 era and typhoid, but also for anthrax." This is a tacit confession that 

 different complements are needed in these different reactions. 



He does not agree with Citron in attributing to natural aggressin the 

 power of complement absorption, but he gives examples showing how 

 natural aggressins may lead to the blocking of haemolysis. 



Bail considers that the leucocytes are the chief source of complement. 

 He thinks that extracts of bacilli hold back leucocytes more than natural 

 aggressins do. He believes that inoculation of extracts acts just as does 

 the inoculation of larger amounts of bacteria, to promote the growth of 

 the inoculated bacteria so that these, by means of their newly acquired 

 aggressivity, restrain the growth of leucocytes. This is rather a com- 

 plicated mode of procedure. Aggressin alone has no power to bind 

 leucocytes, but only acts in the presence of bacteria. This he can not 

 explain, but he found qualitative differences. The addition of cholera 

 aggressin causes death by intoxication with no leucocytosis in a guinea 

 pig previously inoculated with cholera and anti-cholera serum, the action 

 being unlike that following the addition of cholera extracts or of sterile 

 bouillon. This he brings forward as an additional proof of the difference 

 between artificial and natural aggressins. 



Turning to the question of immunity against infections, Bail holds 

 that anti-bacterial immunity is not a true immunity, and that this can 

 be given only by creating "anti-aggressin." These anti-aggressins are 

 distinctly different from anti-bacterial substances, for the anti-aggressin 

 immunity is certainly not bactericidal immunity in the cases of anthrax, 

 chicken cholera, swine plague, and plague, dysentery, eapsulated bacillus, 

 and typhoid : while in the case of cholera he has never succeeded in 

 obtaining an anti-aggressin immunity which did not also exhibit a 

 bacteriolytic immunity. The determinations in these cases were made 

 both by test-tube experiments and by Pfeiffer tests. The anti-aggressin 

 immunity is a phagocytic immunity, at least in the case of typhoid. 



However, even with strong anti-aggressive immunity, the infecting 

 bacteria may survive and multiply in the host, but they cause no symp- 

 toms. Citron could also verify this, finding virulent hog cholera bacilli 

 in an immunized animal after five and one-half months. He contends 

 not only that bactericidal immunity is not a true immunity, but that this 

 bactericidal power can not be deduced from the power of the serum to 

 block haemolysis; and, further, he claims that Wassermann and Citon 

 are wrong in regarding the presence of amboceptors in an inoculated 

 animal as an index that the reaction of immunity has occurred in those 

 eases in which the cholera germ is still capable of living somewhere in 

 the body of the immunized individual. 



Bail gives the occurrence of strong phagocytosis in spite of severe 

 infection as a characteristic of anti-aggressin immunity. 



There is a negative stage after the inoculation of aggressin during 



