ESMOND R. LONG 103 1 



SPONTANEOUS INTERNAL TUBERCULIN REACTIONS AS A CAUSE OF 

 PATHOLOGICAL CHANGES IN TUBERCULOSIS 



SPECIFIC TUBERCULOUS LESIONS 



Reference has just been made to the focal reactions occurring in distant tubercles 

 on flaring up, and, presumably, release of tuberculin, in another tuberculous region. 

 Local spread of tubercle bacilli is likewise accompanied by what may properly be con- 

 sidered a tuberculin reaction. In the chronic bronchiolo-pneumonic reaction or alve- 

 olar exudation occurring in the neighborhood of an ulcerating pulmonary lesion, sen- 

 sitization of the tissue probably plays a part, but the effect of tissue sensitization is 

 much more evident in the acute reactions which follow sudden release of large numbers 

 of tubercle bacilli. 



It is known from animal experimentation that in tuberculous animals superin- 

 fections in the skin, lung, liver, pleura, peritoneum, meninges, kidney, and testis are 

 acutely inflammatory at the start, instead of more slowly progressive as in the case 

 of the lesion of first infection. 



In human pathology analogous phenomena may be observed. It is believed that 

 tuberculous pneumonia, pleuritis, meningitis, arthritis, etc., partake of the nature of 

 tuberculin reactions. They represent the response of sensitized tissue to the specific 

 protein of the tubercle bacillus, followed by the development of anatomical tubercle, 

 in answer to the presence of the multiplying tubercle bacillus. 



NON-TUBERCULOUS LESIONS 



If, however, the bacilli which stimulate the acute reaction happen to be dead, as 

 not infrequently must be the case, the acute manifestations, dependent upon the pres- 

 ence of the specific protein in the bacilli may occur, and not be followed by the de- 

 velopment of progressive anatomical tuberculosis. 



Evidence pointing in this direction is available from animal experiment, and 

 much that appears analogous is seen in human pathology. Figure 6, obviously 

 a late tuberculin reaction in the testis of the type well seen in Figure i, is taken from 

 a tuberculous guinea pig, presumably highly sensitive to tuberculin protein. The at- 

 rophy of the tubules characteristic of the tuberculin reaction is in this case not the 

 result of deliberate injection of tuberculin, however, as in Figure i, but of spontaneous 

 lodgment of tubercle bacilli in the testis, as shown by the presence of the small tuber- 

 cle in the center of the field. Hematogenous tuberculosis of the testis is rare in the 

 guinea pig, and in this case the other testis was entirely normal. Dead tubercle ba- 

 cilH, even disintegrated, as shown by direct experiment, would have been just as 

 effective in causing the atrophy in this sensitized animal. It seems to me not unlikely 

 that some of the testicular atrophies occasionally observed in man, for which no other 

 cause can be assigned, may be explained on this allergic basis, the allergy not being 

 necessarily tuberculous. 



I have obtained experimental evidence that even a lesion so far removed ana- 

 tomically from true tuberculosis as subacute glomerulo-nephritis may be produced by 

 the action of tuberculin protein on the kidney of the tuberculous, and therefore sen- 

 sitized, animal. If the kidneys of normal anesthetized swine are perfused through 

 the renal artery with tuberculin protein in fine suspension in salt-citrate solution and 



