308 EXPLANATIONS OF THE TUBERCULIN REACTION 



without invoking the aid of the complements. But the whole 

 subject is theoretical to a degree, and needs, moreover, independent 

 experimental verification. 



Bail's researches on the aggressins have been referred to already. 

 The application of his theory to Koch's phenomenon is obvious. 

 According to him the endotoxins are only set at liberty when 

 bacteriolysis occurs, not after phagocytosis. This is in all prob- 

 ability correct in most cases, though perhaps not in all. When, 

 therefore, tubercle bacilli are injected into the peritoneal cavity of 

 a normal guinea-pig and extensive phagocytosis occurs, there is 

 little or no febrile reaction ; but in the tuberculous animal the 

 bacilli produce aggressins, which paralyze the phagocytes, and, 

 when a second injection is made, the bacteria undergo rapid 

 bacteriolysis, endotoxin is set free, and rapid death follows. Bail 

 compares the results of the solution of large quantities of cholera 

 bacilli in an immunized animal with what is seen after the injec- 

 tion of tubercle bacilli along with a small amount of the peritoneal 

 exudate from a tuberculous animal. In each case there is extra- 

 cellular bacteriolysis, and death in a few hours, obviously from the 

 toxin set free. 



This might account in a satisfactory way for Koch's phenomena 

 when caused by the injection of cultures, but seems to fail utterly 

 when applied to the tuberculin reaction ; for tuberculin is neither 

 an "aggressin" in Bail's sense, nor an endotoxin of the tubercle 

 bacillus, and it cannot undergo bacteriolysis. The theory resembles 

 that of Marmorek. 



Von Pirquet's explanation of the early reaction after Jennerian 

 vaccination calls for some notice, though it is not immediately 

 applicable to Koch's phenomenon. It introduces some new and 

 interesting conceptions. According to this author, the result of 

 an infection is to alter the way in which an animal reacts subse- 

 quently to a second infection w T ith the same organism. This he 

 calls alleygia. In some cases this may lead to hypersensitiveness, 

 but in the majority it leads to a temporary immunity, followed by 

 a condition in which the animal is no longer immune, but possesses 

 the power of forming antibodies in the region of inoculation more 

 quickly and easily than a normal one can do. When a second 

 inoculation is made, the bacteriolysins present in the blood may be 

 sufficient to destroy the bacteria introduced, setting free their 

 toxins, which act locally and cause the early reaction. Or this 

 may be delayed until local antibodies are formed. This occurs 



