Abstract

Prior to the discovery of the etiology of “San Joaquin fever” (1) the comparison of coccidioidal infection and tuberculosis was restricted to the clinical and pathological mimicry of coccidioidal granuloma and tuberculosis of the reinfection type. The outstanding difference lay in the fact that there was but one recognized manifestation of coccidioidal infection, coccidioidal granuloma, which was, and still is, highly fatal. In contrast, reinfection type tuberculosis constitutes only a fraction of tuberculous infections. We now realize that this divergence was only apparent; it has given place to the most striking parallelism, since in both diseases mild and even subclinical infections are the rule and serious disease is the exception. It is the current status of this comparison that will be reviewed here. In presenting this comparison, the etiologic agents constitute a logical starting point. In the rest of this paper I must be on the defensive and point out how my protege resembles tuberculosis, but here, with great satisfaction, I can reverse the roles. For the tubercle bacillus is funguslike, else why the Myco of Mycobacterium? There is no suggestion that this relationship is close. The tubercle bacillus may have been accused of having a filtrable stage, but never has it masqueraded as an animal parasite. It never undergoes a spectacular metamorphosis such as Coccidioides immitis displays when its chlamydospores enter living animal tissue. The studies of Lack (2) and Baker and Mrak (3) suggest that spherule formation, the so-called “parasitic phase,” is the response of Coccidioides to a less favorable environment. The tubercle bacillus, with much more consistency, just wraps its waxy coat around it and hangs on. There are, nevertheless, additional points to consider. While mammals, birds, and reptiles have their own tubercle bacilli, and mammalian tubercle bacilli may be subdivided into bovine and human types, we have no evidence of such a situation with Coccidioides. Coccidioides immitis and the human type of M. tuberculosis are alike in that no evidence exists associating differences in severity of the clinical infection in man with strain differences of the organisms. Various investigators have remarked on apparent differences in strain virulence in laboratory animals, but admitted that no correlation exists with clinical pictures of the human illnesses from which the strains were isolated. We have never been able to demonstrate by animal inoculations, by cultural character istics, or even by making and testing with specific coccidioidins, that the fungus of a coccidioidal granuloma patient differed from that of a patient with the erythema nodosum of “San Joaquin fever,” or from that of another patient with transient respiratory symptoms.

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