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Paracoccidioides brasiliensis is the aetiological agent of paracoccidioidomycosis (PCM) that is the most important systemic mycosis in Latin America (Restrepo 1985). A wide spectrum of clinical, pathological and immunological manifestations can be observed in the infected patients. The largest group of infected people remains asymptomatic. Clinical alterations may be found in two main polar presentations: hiperergic (localized) PCM that is characterized by lung, skin and visceral involvement, and anergic (disseminated) PCM that evolutes with lymphatic, liver, spleen and bone marrow dysfunction (Franco et al. 1987). In addition, the terms acute or juvenile have been used to describe anergic patients, as chronic or adult have been employed to denote hiperergic ones. From an immunopathological perspective, the juvenile type characteristically present necrotic lesions with abundant fungal cells, impairment of cellular immunity and large amounts of circulating antibodies. Adult type patients rarely present disseminated disease, cellular immunity is preserved with low antibody titres in the serum, and it is associated with granuloma formation and reduced number of fungal cells (Cano et al. 1995). Experimental models have clarified many aspects of the pathogenesis of PCM. From observations in mice, P. brasiliensis infection begins from inhalation of mycelial fragments or conidia. In the lung, these structures transform into yeasts (McEwen et al. 1987). Splendore performed the first P. brasiliensis experimental infection in 1910, when samples obtained from diseased people were inoculated in guinea-pigs, cats, dogs and monkeys (Migaki et al. 1982). The first documented report on this topic was made by Montenegro in 1927, who inoculated human samples in the testicles of guinea-pigs resulting in orchitis. Afterwards, other experimental models were developed from fungal inoculation in mice, rat, hamster, and in the fertilized chick embrio chorioallantoic membrane. Nowadays, there are two widely accepted experimental models of PCM, based on the susceptibility of inbred mice according to their genetic background. B10.A mice are used to investigate susceptibility, and A/Sn is a prototype of resistance against P. brasiliensis infection (Goldani et al. 1991; Coelho et al. 1994; Cano et al. 1995). Data obtained from these models have been important in elucidating virulence traits of the micro-organism, and in determining the immunopathogenesis of the disease. Calomys callosus, Rengger 1830, is a rodent (Cricetidae) similar in size to mice. This animal is widely distributed throughout South America, and it is found from northern Argentina to eastern Andes, and in Bolivian and Paraguayan Chaco. In Brazil, it may be found in the middle west, north-east and in the southern regions up to the Parana State (Mello, 1984). The savannah environment in the middle eastern part of Brazil is one of its main natural habitats. Calomys callosus have been described as an alternative for the construction of experimental models of trypanosomiasis, toxoplasmosis and schistosomosis (Andrade et al. 1994; De-Oliveira et al. 1997; Favoreto-Junior et al. 1998; De-Souza et al. 1999). In view of the fact that the Brazilian savannah is both the natural habitat of C. callosus and an endemic region for PCM, we believe that it would be of interest to evaluate the behaviour of this rodent after inoculation with P. brasiliensis. Results obtained from this investigation could be useful to determine whether this animal could be employed as an alternative experimental model for the disease. With this intent, the aim of this work was to investigate the behaviour of C. callosus intraperitonially infected with the Pb18 strain of P. brasiliensis, and to compare it with the established models of resistance and susceptibility available in the literature. |
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