606 ANAPHYLAXIS IN RELATION TO INFECTION AND IMMUNITY 



antibody appears. The colony is attacked, its contents are digested, 

 a toxic substance is formed that diffuses into the neighboring tissues, 

 and the intense local inflammation which we call the areola appears. 

 In addition the toxin enters the general circulation and fever sets in. 

 Simultaneously the microorganisms are destroyed, and we may no 

 longer be able to vaccinate with the contents of the now yellow pustule. 

 After two or three days the real struggle is ended, although the local 

 lesion may be aggravated by secondary infection, and the body contains 

 the new antibody for a long time. 



If we now revaccinate, the antibody present will at once attack and 

 digest the microorganisms introduced into the scarification, and, as 

 these do not have time to multiply, only an extremely small amount of 

 toxin is formed, which gives the " immediate or early reaction" in 

 vaccinia. If a number of years have elapsed between the first and the 

 second vaccination, antibodies may be absent or present in only small 

 amount, but the body-cells have 'been " keyed up" by the first vac- 

 cination, and hence react more quickly to the second. The antibodies 

 are produced in from three to five days, and attack the microorganisms 

 before they have had time to multiply in sufficient numbers; the rel- 

 atively small amount of digestion product produces a comparatively 

 mild local inflammation and practically no general symptoms. This is 

 sometimes known as the "immunity reaction," or vaccinoid, and is 

 illustrated in Fig. 135. 



It would, of course, lead us too far were we to analyze all the different 

 infectious diseases along these lines; suffice it to say that the anaphy- 

 lactic principle serves to explain many points in the clinical sympto- 

 matology of disease that were not explained heretofore, or were ascribed 

 to the effects of the bacteria and the bacterial products. I am not 

 among those who, with Vaughan, would ascribe all symptoms to the 

 protein poison alone; nor do I regard the part played by the microorgan- 

 ism as simply dependent upon whether or not it can grow in the body and 

 produce the ferment antibody. In the acute toxemias, for instance, such 

 as tetanus and diphtheria, where the amount and toxicity of the toxin 

 are out of all proportion to the number of bacteria, and where the 

 symptoms develop after a very brief incubation period, tissue changes 

 and symptoms are in all probability not primarily due to any antigen- 

 antibody reaction, with liberation of the protein poison, but are rather 

 to be attributed to a direct action of the toxin upon the body-cells, 

 especially upon those for which the toxin possesses a special affinity. 



