160 ANAPHYLAXIS IN ITS RELATION TO DISEASE 



tuberculosis follows an attack of measles, in a subject having a latent 

 (inactive) tubercular infection. 



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

 organism which is a pure toxin producer the interpretation of the 

 clinical picture will be different. In diphtheria, for example, we 

 have coincidently with the multiplication of the invading organ- 

 isms a production 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 producing toxin in sufficient amount to call forth clinical evi- 

 dence 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 theo- 

 retically 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 pri- 

 mary malady, i. e., the eruptive fever per se, is similarly a pure toxin 

 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 auto- 

 reinfection (from a broken-down lymph gland for example) occurs. 

 A toxin effect, of the primary type, is then not produced, since anti- 

 toxins 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 to 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 



