Host-parasite relationship in paracoccidioidomycosis.

Abstract

Paracoccidioidomycosis (Pbmycosis) is a systemic disease confined to Latin America; its endemic areas extends from Mexico through Central and South America down to Argentina. Paracoccidioides brasiliensis (Pb), its agent, causes disease and mortality specially in rural populations being a major public health problem1). The disease was first reconized by Adolfo Lutz in 1908, in Sao Paulo. Its agent was identified by Floriano de Almeida and its clinical and pathological features described by Pupo and CunhaMota, the three of them from the, today, University of Sao Paulo Medical School1). Eighty years after the first references to this mycosis we still do not know for sure the habitat of the fungus or how man is infected. As a consequence we also do not know the early manifestations of this disease that after an insidious onset and slow course end up compromissing several organs in an umpredictable sequence. The great majority of the knowledge on host parasite relationship in Pbmycosis is based on clinical and radiological descriptions of lesions and on the study of biopsies obtained when the infection is already well stablished; a few studies have included autopsies done almost always in patients who died in the final stages of the disease. The result of these difficulties is that certain concepts about the pathogenesis of Pbmycosis have been mainly derived from animal experiments in which large number of P, brasiliensis in its yeast form have been inoculated in susceptible animals. Yeasts almost certainly are not the infecting forms of the fungus since yeasts only develop at temperatures well above the ones observed in the environment where the man-fungus interaction appears to occur. Experimental animal models are somewhat artificial but they have offered useful information and allowed a progressively better understanding of this mycosis2). Early investigators were of the opinion that the fungus invaded throught the oropharingeal mucosa but latter clinical and radiological evidences, experimentaly corroborated suggested that the lungs were the portal of entry. Nowadays the majority of the data favor the inhalatory route with early pulmonary lesions as the rule; exceptionally trauma and other routes have been reasonably well documented. Once within the tissues the parasite can either be destroyed or allowed to multiply to produce a primary inoculation lesion. The fungus is then drained to the regional lymph nodes where a satelite lymphatic lesion is stablished. As described in tuberculosis, a Pbmycotic primary complex with