SENSITIZATION 125 



dead or injured tissue or its products, that they have sHght inherent 

 invasive power, and that they are able to spread only after some 

 change has occurred in the fungi themselves or in their environment. 

 If some change in the fungi has occurred the fungus, when isolated 

 from the disease at a late stage, might be expected to show an in- 

 creased primary virulence when introduced into a new host. Such 

 a change has not been demonstrated. It seems more probable that 

 the host tissues become altered. 



Increased susceptibility of the host might be explained by the 

 endotoxin theory of Pfeiffer or the allergic theory of von Pirquet. 

 According to the former, as the cells of the parasite die or are killed 

 by the host they liberate toxins which so alter the neighboring host 

 tissue that the surviving cells of the pathogen are able to grow and 

 extend the lesion. According to the second theory it is assumed 

 that the pathogen exerts little toxic action directly upon the host, 

 but that its long-continued presence in the primary lesion sensitizes 

 the neighboring cells so that they become susceptible. Actually 

 both of these mechanisms may be operative. In most of the patho- 

 gens technical difficulties prevent the demonstration of endotoxins and 

 their presence therefore is speculative. There is some circumstantial 

 evidence for the presence of toxins, however, in the case of certain 

 mycoses. In blastomycosis Martin and his associates have shown 

 that the administration of iodides in systemic blastomycosis may 

 cause a rapid extension of the disease unless the patient is first de- 

 sensitized, presumably because of substances liberated by killed 

 cells of the fungus. In the histopathology of coccidioidomycosis the 

 immature cells of the fungus may cause comparatively little response, 

 but upon reaching maturity, when the sporangium ruptures and per- 

 mits the dissemination of the endospores, it incidentally releases a 

 substance, unable to pass the previously intact wall of the fungus 

 cell, which excites an immediate tissue response. At the same time, 

 it is conceivable that this substance may promote the invasion of 

 the neighboring tissues by the newly liberated endospores. 



As with the bacteria, the pathogenic fungi have various portals 

 of entry to the body which are to some extent specific. Thus there 

 are the dermatophytes mentioned above which grow on the skin 

 and hair; others like the thrush organism are primarily parasites of 

 mucuous membranes, causing lesions of the mouth and vagina. In 

 some cases the primary lesions are in the lungs, the fungi being 

 inhaled. There are fungi which are primarily saprophytes but are 

 capable of growing superficially in the external ear causing otomyco- 



