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December 5, 2008

Causal Agents

The term microsporidia is also used as a general nomenclature for the obligate intracellular protozoan parasites belonging to the phylum Microsporidia. To date, more than 1,200 species belonging to 143 genera have been described as parasites infecting a wide range of vertebrate and invertebrate hosts. Microsporidia, are characterized by the production of resistant spores that vary in size, depending on the species. They possess a unique organelle, the polar tubule or polar filament, which is coiled inside the spore as demonstrated by its ultrastructure. The microsporidia spores of species associated with human infection measure from 1 to 4 µm and that is a useful diagnostic feature. There are at least 14 microsporidian species that have been identified as human pathogens: Brachiola algerae, B. connori, B. vesicularum, Encephalitozoon cuniculi, E. hellem, E. intestinalis, Enterocytozoon bieneusi Microsporidium ceylonensis, M. africanum, Nosema ocularum, Pleistophora sp., Trachipleistophora hominis, T. anthropophthera, Vittaforma corneae. Encephalitozoon intestinalis was previously named Septata intestinalis, but it was reclassified as Encephalitozoon intestinalis based on its similarity at the morphologic, antigenic, and molecular levels to other species of this genus. Based on recent data it is now known that some domestic and wild animals may be naturally infected with the following microsporidian species: E. cuniculi, E. intestinalis, E. bieneusi. Birds, especially parrots (parakeets, love birds, budgies) are naturally infected with E. hellem. E. bieneusi and V. corneae have been identified in surface waters, and spores of Nosema sp. (likely B. algerae) have been identified in ditch water.

Life Cycle

Life cycle of Microsporidia

The infective form of microsporidia is the resistant spore and it can survive for a long time in the environment . The spore extrudes its polar tubule and infects the host cell . The spore injects the infective sporoplasm into the eukaryotic host cell through the polar tubule . Inside the cell, the sporoplasm undergoes extensive multiplication either by merogony (binary fission) or schizogony (multiple fission) . This development can occur either in direct contact with the host cell cytoplasm (e.g., E. bieneusi) or inside a vacuole termed parasitophorous vacuole (e.g., E. intestinalis). Either free in the cytoplasm or inside a parasitophorous vacuole, microsporidia develop by sporogony to mature spores . During sporogony, a thick wall is formed around the spore, which provides resistance to adverse environmental conditions. When the spores increase in number and completely fill the host cell cytoplasm, the cell membrane is disrupted and releases the spores to the surroundings . These free mature spores can infect new cells thus continuing the cycle.

Geographic Distribution

Microsporidia are being increasingly recognized as opportunistic infectious agents worldwide. Cases of microsporidiosis have been reported* in developed as well as in developing countries, including: Argentina, Australia, Botswana, Brazil, Canada, Czech Republic, France, Germany, India, Italy, Japan, The Netherlands, New Zealand, Spain, Sri Lanka, Sweden, Switzerland, Thailand, Uganda, United Kingdom, United States of America, and Zambia.

* These data account for infections caused by at least one of the microsporidian species listed in the causal agent section.

Clinical Features

Human microsporidiosis represents an important and rapidly emerging opportunistic disease, occurring mainly, but not exclusively, in severely immunocompromised patients with AIDS. Additionally, cases of microsporidiosis in immunocompromised persons not infected with HIV as well as in immunocompetent persons also have been reported. The clinical manifestations of microsporidiosis are very diverse, varying according to the causal species with diarrhea being the most common.

Microsporidian species Clinical manifestation
Brachiola algerae Keratoconjunctivitis, skin and deep muscle infection
Enterocytozoon bieneusi* Diarrhea, acalculous cholecystitis
Encephalitozoon cuniculi and Encephalitozoon hellem Keratoconjunctivitis, infection of respiratory and genitourinary tract, disseminated infection
Encephalitozoon intestinalis (syn. Septata intestinalis) Infection of the GI tract causing diarrhea, and dissemination to ocular, genitourinary and respiratory tracts
Microsporidium (M. ceylonensis and M. africanum) Infection of the cornea
Nosema sp. (N. ocularum), Brachiola connori Ocular infection
Pleistophora sp. Muscular infection
Trachipleistophora anthropophthera Disseminated infection
Trachipleistophora hominis Muscular infection, stromal keratitis, (probably disseminated infection)
Vittaforma corneae (syn. Nosema corneum) Ocular infection, urinary tract infection

* Two reports of E. bieneusi in respiratory samples have also been published, one in 1992 and the other in 1997.

Laboratory Diagnosis

There are several methods for diagnosing microsporidia:


The treatment of choice for ocular microsporidiosis (Brachiola algerae, Encephalitozoon hellem, E. cuniculi, Vittaforma corneae) is oral albendazole* plus topical fumagillin. Corneal infections with V. corneae often do not respond to chemotherapy and may require keratoplasty. Oral fumagillin has been effective to treat Enterocytozoon bieneusi infections, but it has been associated with thrombocytopenia. Albendazole* is the drug of choice to treat gastroenteritis caused by Encephalitozoon intestinalis and to treat disseminated microsporidiosis (E. hellem, E. cuniculi, E. intestinalis, Pleistophora sp., Trachipleistophora sp., Brachiola vesicularum) and skin and deep muscle infection (Brachiola algerae). For additional information, see the recommendations in The Medical Letter (Drugs for Parasitic Infections).

* This drug is approved by the FDA, but considered investigational for this purpose.

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