INFECTION AND RESISTANCE 



a reactionary formation of specific antibody occurs. Meanwhile, 

 also, the foreign protein increases and is distributed by bacterial 

 growth. In consequence of these parallel processes changes of pro- 

 portion between the reacting substances are created and a constantly 

 greater amount of anaphylatoxin is liberated and the disease pro- 

 gresses. This may kill the patient if the proportions become such 

 that the amount of poison formed exceeds the lethal dose. At any 

 rate, the symptoms may vary and fluctuate according to the relations 

 maintained between the reacting bodies, modified somewhat by the 

 supply of alexin or complement. If recovery is to take place the 

 amount of antibody (sensitizer, amboceptor) may become so great 

 that the bacteria are subjected to rapid destruction, the chemical 

 cleavage of their bodies taking place so vigorously that practically no 

 anaphylatoxin is distributed and vigorous phagocytosis is initiated. 

 Finally the antigen is completely removed. On the other hand, an 

 excessive increase of the bacteria or a defective supply of alexin 

 might also lead to a final cessation of the formation of anaphylatoxin ; 

 in this case, however, we would expect death by the metabolic dis- 

 turbance occasioned by the life processes of the great masses of bac- 

 teria. It is not unthinkable, moreover, that the bacterial enzymes in 

 such a case might produce substances comparable to the anaphyla- 

 toxins from the destroyed tissues of the host. 



It is perfectly true, as Friedberger says, that on the basis of this 

 theory, rendered so likely by experimental fact, the assumption of 

 the existence of endotoxins to explain the various manifestations of 

 infectious disease is not necessary. The poisons, according to the 

 view just outlined, are alike and non-specific. It is the reaction 

 bodies, the sensitizers, induced by the bacterial protein which in each 

 case are these specific elements. 



While it is not necessary to assume specific endotoxins, however, 

 it is not possible on present evidence to entirely exclude the partici- 

 pation of such substances in the genesis of infectious disease. The 

 rapid toxic action of bacterial extracts obtained in various ways 

 has been taken to argue in favor of this. 



It is a difficult question to settle, and must undoubtedly remain 

 an open one until a method is found by which crucial experiments 

 can be formulated. Since Neufeld and Dold have succeeded in pro- 

 ducing anaphylatoxin from bacterial extracts, the primary toxic 

 action of every bacterial extract, however rapidly produced from the 

 bacteria, can be regarded as possibly furnishing merely an antigen 

 for anaphylatoxin production, and indeed such a supposition is ren- 

 dered more likely by the almost invariable incubation time following 

 upon the administration of endotoxic extracts, even when they are 

 introduced directly into the circulation. Pfeiifer 24 himself still 



2 *R. Pfeiffer. "tiber Bakterien Endotoxine, etc.," Weichhardt's Jahres- 

 bericht, Vol. 6, p. 29, 1910. 



