Microsporidiosis

The class or order Microsporidia was elevated in to the phylum Microspora by Sprague and Vavra (1997) and Sprague and Becnel (1998) subsequently suggested that the term Microsporidia instead be used for the phylum name. Miicrosporidia, i.e. Nosema bombycis, were first described about 150 years ago as the cause of the disease pebrine in silkworms. In 1922, there were descriptions of gram-positive spores consistent with microspordiosis in the brain of rabbits that were being used for investigations on poliomyelitis (Wright and Craighead 1922). From 1923 to 1926, Levaditi and colleagues studied the organisms seen by Wright and Craighead, which they named Encephalitozoon cuniculi, recognizing them as Microsporidia and demonstrating their lack of host specificity by transmitting infections from rabbits to mice, rats and dogs (Levaditi et al. 1923). Microsporidia were clearly confirmed of being a cause of human disease in 1959 (Matsubayashi et al. 1959), when they were isolated from the cerebrospinal fluid of a 9 year old boy with encephalitis with seizures, coma, and fever lasting about 25 days. Bergquist et al. (1984) reported a 2 year old child with encephalitis and seizures who had Encephalitozoon spores in urine and Margileth et al. (1973) isolated the microsporidium Anncaliia (Nosema) connori from a 4 month old athymic male infant who died with severe diarrhoea and malabsorption. Microsporidia can produce a wide range of clinical diseases. A diarrhoeal syndrome associated with microsporidiosis and HIV infection was reported by Desportes et al. (1985) and the number of articles describing human disease increased rapidly after 1990. In addition to gastrointestinal tract involvement, it has been recognized that Microsporidia can infect virtually any organ system; and patients with encephalitis, ocular infection, sinusitis, myositis, and disseminated infection are well described in the literature.