Treatment and experimental therapeutics of blastomycosis

Abstract

In 1894, blastomycosis (Gilchrist’s disease) was first described by Gilchrist as a protozoan infection [1,2]. However, in 1896, Gilchrist and Stokes [3] identified the pathogen as a fungus and named it, Blastomyces dermatitidis. Two years later, the disease was successfully transferred by inoculation of material from a human lesion to a dog [4]. Later, other cases of blastomycosis were reported by physicians, mainly from the Chicago area, and their keen interest in this mycosis led to its recognition at one time as the ‘Chicago disease’. Blastomycosis was originally believed to be endemic to North and Central America (U.S., Canada, Mexico, and Central America) until 1952, when a case was reported from Tunisia in which the pathogen was identified as Scopulariopsis americana, a synonym of B. dermatitidis [5,6]. Later, other cases of blastomycosis in Africa, South America and Asia followed [7-131. In 1968, McDonough and Lewis [14] discovered the ascomycetous state (Ajellomyces dermatitidis) of B. dermatitidis and provided a method for testing further the identity of fungi from North American and African blastomycosis. Recently, some of the clinical features, diagnosis and treatment of blastomycosis in Africa, have been reviewed [15]. The exact incidence and epidemiology of blastomycosis is not well understood mainly because of the lack of a reliable immunologic marker from previous infections. Blastomyces (Ajellomyces) dermatitidis is a dimorphic fungus that grows in mammalian tissues as budding cells (yeast phase), and in cultures as a dry, white mold (mycelial form) bearing spherical or ovoid conidia (arthrospores), 2 to 10 pm in diameter [16-l 81. The arthrospores represent the infectious particles of the parasite [19]. Inhalation of these conidia results in primary infection in the