Microsporidia
Microsporidia | ||||||
---|---|---|---|---|---|---|
Fibrillanosema crangonycis
| ||||||
Scientific classification | ||||||
| ||||||
Subclasses | ||||||
Microsporidiosis Microchapters |
Diagnosis |
---|
Treatment |
Case Studies |
Microsporidia On the Web |
American Roentgen Ray Society Images of Microsporidia |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Microsporidia are parasites of animals, now considered to be extremely reduced fungi. Most infect insects, but they are also responsible for common diseases of crustaceans and fish, and have been found in most other animal groups, including humans and other mammals which can be parasitized by species of Encephalitozoon. Replication takes place within the host's cells, which are infected by means of unicellular spores. These vary from 1-40 μm, making them some of the smallest eukaryotes. They also have the shortest eukaryotic genomes.
Microsporidia are unusual in lacking mitochondria and in having mitosomes. They also lack motile structures such as flagella. The spores are protected by a layered wall including proteins and chitin. Their interior is dominated by a unique coiled structure called a polar tube (not to be confused with the polar filaments of Myxozoa). In most cases there are two closely associated nuclei, forming a diplokaryon, but sometimes there is only one.
During infection, the polar tube penetrates the host cell (the process has been compared by Patrick J. Keeling to "turning a garden hose inside out"), and the contents of the spore are pumped through it. Keeling likens the system to a combination of "harpoon and hypodermic syringe", adding that it is "one of the most sophisticated infection mechanisms in biology".
Once inside the host cell, the sporoplasm grows, dividing or forming a multinucleate plasmodium before producing new spores. The life cycle varies considerably. Some have a simple asexual life cycle, while others have a complex life cycle involving multiple hosts and both asexual and sexual reproduction. Different types of spores may be produced at different stages, probably with different functions including autoinfection (transmission within a single host). The Microsporidia often cause chronic, debilitating diseases rather than lethal infections. Effects on the host include reduced longevity, fertility, weight, and general vigor. Vertical transmission of microsporidia is frequently reported. In the case of insect hosts, vertical transmission often occurs as transovarial transmission, where the microsporidian parasites pass from the ovaries of the female host into eggs and eventually multiply in the infected larvae. Amblyospora salinaria n. sp. which infects the mosquito Culex salinarius Coquillett, and Amblyospora californica which infects the mosquito Culex tarsalis Coquillett, provide typical examples of transovarial transmission of microsporidia (Andreadis and Hall 1979a,b; Jahn et al. 1986; Becnel and Andreadis 1998).
Because they are unicellular, Microsporidia were traditionally treated as protozoa, and like other amitochondriate eukaryotes were considered to have diverged very early on. However, other genes place them alongside or within the Fungi, and this is supported by several chemical and morphological features. In particular, they appear to be allied with the Zygomycota or Ascomycota.
Microsporidium was once the vernacular name for a member of the class Microsporea (Corliss and Levine 1963).
Classification
- Subclass: Dihaplophasea
- Order: Meiodihaplophasida
- Superfamily Thelohanioidea
- Family Thelohaniidae
- Family Duboscqiidae
- Family Janacekiidae
- Family Pereziidae
- Family Striatosporidae
- Family Cylindrosporidae
- Superfamily Burenelloidea
- Family Burenellidae
- Superfamily Amblyosporoidae
- Family Amblyosporidae
- Superfamily Thelohanioidea
- Order Dissociodihaplophasida
- Superfamily Nosematoidea
- Family Nosematidae
- Family Ichthyosporidiidae
- Family Caudosporidae
- Family Pseudopleistophoridae
- Family Mrazekiidae
- Superfamily Culicosporoidea
- Family Culicosporidae
- Family Culicosporellidae
- Family Golbergiidae
- Family Spragueidae
- Superfamily Ovavesiculoidea
- Family Ovavesiculidae
- Family Tetramicridae
- Superfamily Nosematoidea
- Order: Meiodihaplophasida
- Subclass Haplophasea
- Order Glugeida
- Family Glugeidae
- Family Pleistophoridae
- Family Encephalitozoonidae
- Family Abelsporidae
- Family Tuzetiidae
- Family Microfilidae
- Family Unikaryonidae
- Order Chyridiopsida
- Family Chytridiopsida
- Family Buxtehudiidae
- Family Enterocytozoonidae
- Family Burkeidae
- Order Glugeida
Microsporidia causing human disease
Although phylum microsporidia has more than 1000 species and over 100 genres, Only 14 species were associated with human disease.
- Anncaliia (formerly Brachiola)[2]
- A. algerae, A. connori, A. vesicularum
- Encephalitozoon
- E. cuniculi, E. hellem, E. intestinalis (formerly Septata intestinalis)
- Enterocytozoon
- E. bieneusi
- Microsporidium
- M. ceylonensis, M. africanum
- Nosema
- N. ocularum
- Pleistophora sp.
- Trachipleistophora
- T. hominis, T. anthropophthera
- Vittaforma
- V. corneae.
- Tubulinosema
- T. acridophagus
Diseases caused by the different species
The clinical manifestations vary according to the causative species with diarrhea being the most common presentation.[3]
Microsporidian species | Clinical manifestation |
Anncaliia 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), Anncaliia connori | Ocular infection |
Pleistophora sp. | Muscular infection |
Trachipleistophora anthropophthera | Disseminated infection |
Trachipleistophora hominis | Muscular infection, stromal keratitis, (probably disseminated infection) |
Tubulinosema acridophagus | 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.
See also
- List of Microsporidian Genera
- Nosema apis, a microsporidian parasite of bees
References
- ↑ Balbiani, G. (1882). "Sur les microsporides ou psorospermies des Articulés". Comptes rendus de l’Académie des Sciences, Paris. 95: 1168–1171.
- ↑ Didier ES, Weiss LM (2006). "Microsporidiosis: current status". Curr Opin Infect Dis. 19 (5): 485–92. doi:10.1097/01.qco.0000244055.46382.23. PMC 3109650. PMID 16940873.
- ↑ "CDC - DPDx - Microsporidiosis".
- Andreadis, T. G., and Hall, D. W. 1979a. Development, ultrastructure, and mode of transmission of Amblyospora sp. (Microspora) in the mosquito. J. Protozool. 26, 444–452.
- Andreadis, T. G., and Hall, D. W. 1979b. Significance of transovarial infections of Amblyospora sp. (Microspora: Thelohaniidae) in relation to parasite maintenance in the mosquito Culex salinarius. J. Invertebr. Pathol. 34, 152–157.
- Becnel, J. J. and Andreadis, T. G. 1998. Amblyospora salinaria n. sp. (Microsporidia: Amblyosporidae): parasite of Culex salinarius (Diptera: Culicidae), its life stages in an intermediate host and establishment as a new species. J. Invertebr. Pathol. 71:258-262.
- Corliss, J.O. and Levine, N.D. 1963. Establishment of the Microsporidia as a new class in the protozoan subphylum Cnidospora.. J. Protozool., 10 (Suppl.), 26-27.
- Jahn, G. C., Hall, D.W., and Zam, S. G. 1986. A comparison of the life cycles of two Amblyospora (Microspora: Amblyosporidae) in the mosquitoes Culex salinarius and Culex tarsalis Coquillett. J. Florida Anti-Mosquito Assoc. 57, 24–27.
- Patrick J. Keeling et al. (2000). Evidence from Beta-Tubulin Phylogeny that Microsporidia Evolved From Within the Fungi. Molecular Biology and Evolution 17:23-31.
- Nature 414, 401 - 402 (22 November 2001); doi:10.1038/35106666