Endogenous Activation in Blastomycosis

Recent work established the fact that the portal of entry in blastomycosis is the lung. After the initial exposure to the fungus, a pneumonic process develops that may heal spontaneously or progress locally or at distant sites, or both. Frequently, however, patients present with disseminated disease, whose chest roentgenograms do not show any lesions We have recently seen three patients with disseminated blastomycosis with negative chest roentgenograms at the time of diagnosis. Past history showed a pneumonic illness 33, 32, and 4 months before diagnosis. Chest roentgenograms from the time of the original illness showed a pneumonic process compatible with blastomycosis in all three. Examination of postbronchoscopy sputa showed the characteristic yeasts of Blastomyces dermatitidis. These three patients document for the first time apparent endogenous activation in blastomycosis. A possible explanation for this apparent endogenous activation may reside in the histopathologic similarity between blastomycosis and other chronic granulomatous diseases, especially tuberculosis. BLASTOMYCOSIS, an infection caused by the dimorphic fungus, Blastomyces dermatitidis, presents with a clinical spectrum ranging from isolated pulmonary involvement to disseminated multisystem disease (1-3). Initially con-sidered to be a primary dermatologic infection, blastomy-cosis was subsequently proved to be a systemic infection with a respiratory portal of entry (4). Previous papers have adequately described the various clinical forms of the disease, including the acute (5) and the disseminated (2, 3) forms. Whereas the acute and disseminated forms were relatively easy to define, chronic blastomycosis has proved to be more troublesome. Fre-quently, patients were seen after a variable period of low-grade illness without a definable acute onset. We have recently seen three patients, with either osse-ous or cutaneous blastomycosis at the time of diagnosis, in whom careful history and review of histopathologic and roentgenologic material strongly suggested the oc-currence of endogenous reinfection. In all three patients the initial pulmonary infection resolved spontaneously to be followed from 4 to 33 months later by appearance of disseminated disease to extrapulmonary sites