RESUMO
Blastomyces dermatitidis is a dimorphic fungus causing localized or systemic infection in areas where the organism is endemic in the central and southeastern United States. In this study, 19 independent isolates of B. dermatitidis from Little Rock, Ark., were grouped into three classes based on restriction fragment length polymorphism patterns in mitochondrial DNA with a heterologous probe from Histoplasma capsulatum. One large class of 15 isolates and two smaller classes (classes 2 and 3), each consisting of two isolates, were observed in BglII digests. Strain-specific arrays of PCR-amplified DNA products were obtained with arbitrarily selected primers (18 to 29 nucleotides long; G+C contents, 33 to 56%). In the large class 1 group, 13 isolates could be differentiated by the random amplified polymorphic DNA (RAPD) method with various primers. The two remaining class 1 isolates were obtained from the same patients and produced identical RAPD arrays. Dissimilar RAPD patterns were obtained from the smaller class 2 group but not from the class 3 isolates. Significant genetic diversity in clinical isolates of B. dermatitidis was observed; this may underscore a similar environmental diversification. Further application of the typing techniques may provide significant insight into the epidemiology of blastomycosis and aid in the assessment of specific virulence phenotypes.
Assuntos
Blastomyces/genética , Blastomyces/isolamento & purificação , DNA Fúngico/genética , Variação Genética , Reação em Cadeia da Polimerase/métodos , Sequência de Bases , Blastomyces/classificação , Primers do DNA/genética , Estudos de Avaliação como Assunto , Humanos , Dados de Sequência Molecular , Polimorfismo Genético , Polimorfismo de Fragmento de RestriçãoRESUMO
A spontaneous model of Purkinje cell degeneration in rats is described. Breeding data indicate that the condition is hereditary and not sex linked. The breeding colony has remained free of common murine pathogens, including parvovirus. In older rats with pronounced ataxia, the major lesions consisted of greatly reduced numbers or complete absence of Purkinje cells (PCs), particularly in the anterior lobe of the cerebellum. There was a decreased thickness and increased cellular density of the molecular layer and degeneration of the inferior olivary nuclei. Morphometric analysis indicated that the anterior lobes of affected rats were 52% smaller than those of normal rats. In young rats, before severe signs of ataxia had developed, microscopic changes were minimal. The preliminary findings are discussed in relationship to human cerebellar ataxias and mouse models of Purkinje cell degeneration.
