The Microsporidian Polar Tube and Its Role in Invasion

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Abstract

The Microsporidia are a phylum of small unicellular eukaryotes comprising more than 150 genera and 1200 species. They are obligate intracellular parasites which are able to form environmentally resistant spores. Historically, Nosema bombycis, was the first described species in this phylum and is the etiological agent of “pébrine” disease that nearly destroyed the silk-worm industry in the nineteenth century. Although the majority of microsporidia that have been described are found in arthropods and fishes, being responsible of important economic losses in the apiculture and fish farms, there are several species of medical and veterinary significance which infect animals and humans.1,2 Cerebral microsporidian infections attributed to Encephalitozoon cuniculi were initially described in 1922 in rabbits with granulomatous encephalitis and several infections were then reported in most vertebrate groups. The first case of microsporidiosis in a human was identified in 1959 in a nine-year-old boy suffering from neurological disorders.3 While reports of humans infected with microsporidia were extremely rare before the AIDS epidemic, these organisms are now recognized as significant emerging pathogens in immunocompromised hosts (HIV-infected patients with AIDS and organ transplant recipients) and is a cause of intestinal, ocular, muscular and systemic diseases.2 Some clinical manifestations have been also reported in immunocompetent hosts. Serological studies with blood donors and pregnant women revealed a prevalence of about 8%,4 suggesting that infections by microsporidia may be common in humans. So far, species belonging to seven different genera Brachiola (recendy renamed Anncaliia), Encephalitozoon, Enterocytozoon, Nosema, Pleistophora, Trachipleistophora and Vittaforma have been found in human infections. Although the origin of infection and epidemiology still remain to be documented for human microsporidiosis, horizontal transmission of most microsporidia occurs by oral ingestion of spores, with the site of initial infection being the gastrointestinal tract.5