CHAPTER X 

 ANAPHYLAXIS 



IT has long been recognized that while certain infections, such 

 as smallpox, scarlatina, measles, whooping cough, typhoid fever, 

 cholera, typhus fever, etc., lead to immunity, others not only bring 

 about no increased, but actually a decreased resistance to subsequent 

 infection with the same organism. This is notably true of pneumonia, 

 erysipelas, influenza, diphtheria, bacillary dysentery, certain staphy- 

 lococcus infections, such as tonsillitis, acne, etc. In the past we 

 have been totally unable to explain these peculiar differences, and 

 even now our knowledge of the mechanism underlying the production 

 of hypersusceptibility to certain deleterious influences is very meager. 

 Within recent years, however, such a wealth of experimental facts 

 has been accumulated which have a direct bearing upon the problem 

 under consideration, that the day no longer seems far distant when 

 we shall be able to offer an adequate explanation for these peculiar 

 differences. Some of these observations and the resulting deduc- 

 tions will be considered in the present chapter. 



In the foregoing pages we have explained the manner in which 

 immunity to toxins may be artificially brought about, and have 

 shown that this depends essentially upon the liberation of corre- 

 sponding receptors on the part of some of the body cells. If these 

 are produced and thrown off in sufficiently large number, they fur- 

 nish a protection for the body against the toxins in question which 

 may be of a very high order. In the commercial preparation of 

 antitoxins it is, of course, desirable to obtain sera that shall be as 

 potent as possible, and it is hence customary to force the process 

 of immunization in the experimental animals to the highest limit. 

 The question now arises what happens if this be exceeded. Two 

 events may then occur. On the one hand the animal may cease to 

 produce antitoxin altogether, but simultaneously loses all suscepti- 

 bility to the corresponding toxin, and is thus absolutely immune. 



This result, as we have already shown, is explained on the basis of 

 an acquired receptoric atrophy, and we can readily conceive that this 



