172 ANAPHYLAXIS IN ITS RELATION TO DISEASE 



If now we pass on to a consideration of an infection with an organ- 

 ism which is a pure toxin producer the interpretation of the clinical 

 picture will be different. In diphtheria, for example, we have coin- 

 cidently with the multiplication of the invading organisms a pro- 

 duction of toxin. This in itself is, of course, quite sufficient to account 

 for practically all the clinical symptoms that we observe. These 

 set in early, since comparatively few organisms are capable of pro- 

 ducing toxin in sufficient amount to call forth clinical evidence of 

 disease. There is hence not the usual incubation period of eight days, 

 and the initial symptoms in any event are not due to any antigen- 

 antibody reaction, but to the toxin itself. When the antibodies 

 then appear we may, of course, rightfully assume that precipitins 

 are formed, as well as lysins and antitoxins, and theoretically we 

 might expect a clinical reaction due to anaphylatoxins. Clinically, 

 however, we have no clear evidence of this, which is probably owing 

 to the fact that the toxin effect by itself controls the entire picture. 

 In scarlatina, v. Pirquet concedes that the primary malady, i. e., 

 the eruptive fever per se, is similarly a pure toxic effect, but that 

 the sequelae and notably the nephritis, are the expression of the 

 action of anaphylatoxins, which are formed, if at a time, when the 

 corresponding antibodies are present, an autoreinfection (from 

 a broken-down lymph gland for example) occurs. A toxic effect, 

 of the primary type, is then not produced, since antitoxins are at 

 the time present in sufficient quantity to counteract their effect 

 (Fig. 10). 



It would, of course, lead too far to continue the analysis of the 

 different infectious diseases along these lines, but I believe, I have 

 shown that the anaphylactic principle serves to explain many points 

 in clinical symptomatology for which an adequate explanation has 

 heretofore been lacking. If we consider that the absorption of alien 

 proteins (and hence of bacterial proteins) probably always gives 

 rise to the production of corresponding antibodies of the anaphyl- 

 actin type, we can also understand that there is probably not a 

 single infectious disease in which they are not formed, and in which 

 they cannot, theoretically at least, play an active part. Besides 

 the diseases already discussed this would certainly seem most likely 

 in syphilis, in typhoid fever, measles, glanders, and pneumonia, and 

 future studies of these diseases from this standpoint will no doubt 

 lead to interesting results. All along the line a start has indeed only 



