Open Access Articles- Top Results for Microsporidia


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The microsporidia constitute a phylum (Microspora) of spore-forming unicellular parasites. They were once thought to be protists but are now known to be fungi. Loosely 1500 of the probably more than one million[citation needed] species are named now. Microsporidia are restricted to animal hosts, and all major groups of animals host microsporidia. Most infect insects, but they are also responsible for common diseases of crustaceans and fish. The named species of microsporidia usually infect one host species or a group of closely related taxa. Several species, most of which are opportunistic, also infect humans.

Approximately 10 percent of the species are parasites of vertebrates — including humans, in which they can cause microsporidiosis.

After infection they influence their hosts in various ways and all organs and tissues are invaded, though generally by different species of microsporidia. Some species are lethal, and a few are used in biological control of insect pests. Parasitic castration, gigantism, or change of host sex are all potential effects of microsporidian parasitism (in insects). In the most advanced cases of parasitism the microsporidium rules the host cell completely and controls its metabolism and reproduction, forming a xenoma. .[1]

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.[citation needed] Microsporidia that infect mammals are 1.0-4.0 μm.[2] They also have the smallest eukaryotic genomes.

Microsporidium was once the vernacular name for a member of the class Microsporidea in the protozoan subphylum Cnidospora.[3]

File:Glugea stephani.jpg
Xenoma on flatfish caused by Glugea stephani


File:Parasite140027-fig5 Dictyocoela diporeiae Winters & Faisal, 2014 transmission electron micrographs.tif
Dictyocoela diporeiae.[4] A, meront and spore; B, spore wall; C, polar filament

Microsporidia lack mitochondria, instead possessing mitosomes. They also lack motile structures, such as flagella.

Microsporidia produce highly resistant spores, capable of surviving outside their host for up to several years. Spore morphology is useful in distinguishing between different species. Spores of most species are oval or pyriform, but rod-shaped or spherical spores are not unusual. A few genera produce spores of unique shape for the genus.

The spore is protected by a wall, consisting of three layers:

  • an outer electron-dense exospore
  • a median, wide and seemingly structureless endospore, containing chitin
  • a thin internal plasma membrane

In most cases there are two closely associated nuclei, forming a diplokaryon, but sometimes there is only one.
The anterior half of the spore contains a harpoon-like apparatus with a long, thread-like polar filament, which is coiled up in the posterior half of the spore. The anterior part of the polar filament is surrounded by a polaroplast, a lamella of membranes. Behind the polar filament, there is a posterior vacuole.[1]


In the gut of the host the spore germinates, it builds up osmotic pressure until its rigid wall ruptures at its thinnest point at the apex. The posterior vacuole swells, forcing the polar filament to rapidly eject the infectious content into the cytoplasm of the potential host. Simultaneously the material of the filament is rearranged to form a tube which functions as a hypodermic needle and penetrates the gut epithelium.

Once inside the host cell, a sporoplasm grows, dividing or forming a multinucleate plasmodium, before producing new spores. The life cycle varies considerably. Some have a simple asexual life cycle,[5] 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).

Medical implications

In animals and humans, 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.[6][7][8][9]

Microsporidia, specifically the mosquito-infecting Vavraia culicis, are being explored as a possible 'evolution-proof' malaria-control method.[10] Microsporidian infection of Anopheles gambiae (the principal vector of Plasmodium falciparum malaria) reduces malarial infection within the mosquito, and shortens the mosquito lifespan.[11] As the majority of malaria-infected mosquitoes naturally die before the malaria parasite is mature enough to transmit, any increase in mosquito mortality through microsporidian-infection may reduce malaria transmission to humans.


Main article: Microsporidiosis

Microsporidian infections of humans sometimes cause a disease called microsporidiosis. At least 14 microsporidian species, spread across eight genera, have been recognized as human pathogens. These include Trachipleistophora hominis.[12]

Microsporidia as hyperparasites

File:Parasite140019-fig4 Nosema podocotyloidis - Hyperparasitic Microsporidia.tif
A hyperparasitic microsporidian, Nosema podocotyloidis, a parasite of a digenean which is itself a parasite of a fish [13]

Microsporidia can infect a variety of hosts, including hosts which are themselves parasites. In that case, the microsporidian species is an hyperparasite, i.e. a parasite of a parasite. As an example, more than eighteen species are known which parasitize digeneans (parasitic flatworms). These digeneans are themselves parasites in various vertebrates and molluscs. Eight of these species belong to the genus Nosema.[13]


Microsporidia have the smallest known (nuclear) eukaryotic genomes. The parasitic lifestyle of microsporidia has led to a loss of many mitochondrial and Golgi genes, and even their ribosomal RNAs are reduced in size compared with those of most eukaryotes. As a consequence, the genomes of microsporidia are much smaller than those of other eukaryotes. Currently known microsporidial genomes are 2.5 to 11.6 Mb in size, encoding from 1,848 to 3,266 proteins which is in the same range as many bacteria.[14]

Horizontal gene transfer (HGT) seems to have occurred many times in microsporidia. For instance, the genomes of Encephalitozoon romaleae and Trachipleistophora hominis contain genes that derive from animals and bacteria, and some even from fungi.[14]


For some time microsporidia were considered as very primitive eukaryotes, especially because of the lack of mitochondria, and placed along with the other Protozoa such as diplomonads, parabasalia and archamoebae in the protist-group Archezoa. More recent research has falsified this theory of early origin (for all of these). Yet microsporidia are proposed to be highly developed and specialized organisms, which just dispensed functions that are needed no longer, because they are supplied by the host.[15] Furthermore, spore-forming organisms in general do have a complex system of reproduction, both sexual and asexual, which look far from primitive.

Nowadays microsporidia are placed within the Fungi or as a sister-group of the Fungi with a common ancestor.[16][17][18][19]

Forming of clades is largely based on habitat and host. Three classes of Microsporidia are proposed by Vossbrinck and Debrunner-Vossbrinck, based on the habitat: Aquasporidia, Marinosporidia and Terresporidia.[20]

One classification could be:

  1. Subclass: Dihaplophasea
  2. Subclass Haplophasea

See also


  1. 1.0 1.1 Ronny Larsson, Lund University (Department of Cell and Organism Biology) Cytology and taxonomy of the microsporidia 2004.
  2. Didier, ES. (Apr 2005). "Microsporidiosis: an emerging and opportunistic infection in humans and animals". Acta Trop 94 (1): 61–76. PMID 15777637. doi:10.1016/j.actatropica.2005.01.010. 
  3. Corliss JO, Levine ND (1963). "Establishment of the Microsporidia as a new class in the protozoan subphylum Cnidospora". The Journal of Protozoology 10 (Suppl.): 26–27. 
  4. Winters, A. D., Faisal, M. 2014. Molecular and ultrastructural characterization of Dictyocoela diporeiae n. sp. (Microsporidia), a parasite of Diporeia spp. (Amphipoda, Gammaridea). Parasite, 21, 26 doi:10.1051/parasite/2014028 open access publication - free to read
  5. Ironside JE (2007). "Multiple losses of sex within a single genus of Microsporidia". BMC Evolutionary Biology 7: 48. PMC 1853083. PMID 17394631. doi:10.1186/1471-2148-7-48. 
  6. Andreadis TG, Hall DW; Hall (August 1979). "Development, ultrastructure, and mode of transmission of Amblyospora sp. (Microspora) in the mosquito". The Journal of Protozoology 26 (3): 444–52. PMID 536933. doi:10.1111/j.1550-7408.1979.tb04651.x. 
  7. Andreadis TG, Hall DW; Hall (September 1979). "Significance of transovarial infections of Amblyospora sp. (Microspora:Thelohaniidae) in relation to parasite maintenance in the mosquito Culex salinarius". Journal of Invertebrate Pathology 34 (2): 152–7. PMID 536610. doi:10.1016/0022-2011(79)90095-8. 
  8. Jahn GC, Hall DW, Zam SG (1986). "A comparison of the life cycles of two Amblyospora (Microspora: Amblyosporidae) in the mosquitoes Culex salinarius and Culex tarsalis Coquillett". Journal of the Florida Anti-Mosquito Association 57 (1): 24–27. 
  9. Becnel JJ, Andreadis TG; Andreadis (May 1998). "Amblyospora salinaria n. sp. (Microsporidia: amblyosporidae), parasite of Culex salinarius (Diptera: culicidae): its life cycle stages in an intermediate host". Journal of Invertebrate Pathology 71 (3): 258–62. PMID 9538031. doi:10.1006/jipa.1998.4729. 
  10. Koella, Jacob C.; Lorenz, Lena; Bargielowski, Irka (2009). "Chapter 12 Microsporidians as Evolution-Proof Agents of Malaria Control?". Advances in Parasitology. Advances in Parasitology 68: 315–327. ISBN 978-0-12-374787-7. PMID 19289199. doi:10.1016/S0065-308X(08)00612-X. Retrieved 2009-12-10. 
  11. Bargielowski I, Koella JC; Koella (2009). Baylis, Matthew, ed. "A Possible Mechanism for the Suppression of Plasmodium berghei Development in the Mosquito Anopheles gambiae by the Microsporidian Vavraia culicis". PLoS ONE 4 (3): e4676. PMC 2651578. PMID 19277119. doi:10.1371/journal.pone.0004676. 
  12. Heinz, E; Williams, TA; Nakjang, S; Noël, CJ; Swan, DC; Goldberg, AV; Harris, SR; Weinmaier, T; Markert, S et al. (Oct 2012). "The genome of the obligate intracellular parasite Trachipleistophora hominis: New insights into microsporidian genome dynamics and reductive evolution". PLoS Pathog 8 (10): e1002979. doi:10.1371/journal.ppat.1002979. 
  13. 13.0 13.1 Toguebaye, B. S.; Quilichini, Y.; Diagne, P. M.; Marchand, B. (2014). "Ultrastructure and development of Nosema podocotyloidis n. sp. (Microsporidia), a hyperparasite of Podocotyloides magnatestis (Trematoda), a parasite of Parapristipoma octolineatum (Teleostei)". Parasite 21: 44. PMC 4150386. PMID 25174849. doi:10.1051/parasite/2014044.  open access publication - free to read
  14. 14.0 14.1 Corradi, N.; Selman, M. (2013). "Latest Progress in Microsporidian Genome Research". Journal of Eukaryotic Microbiology 60 (3): 309–312. PMID 23445243. doi:10.1111/jeu.12030.  edit
  15. Keeling PJ, Slamovits CH; Slamovits (December 2004). "Simplicity and Complexity of Microsporidian Genomes". Eukaryotic Cell 3 (6): 1363–9. PMC 539024. PMID 15590811. doi:10.1128/EC.3.6.1363-1369.2004. 
  16. Fischer WM, Palmer JD; Palmer (September 2005). "Evidence from small-subunit ribosomal RNA sequences for a fungal origin of Microsporidia". Molecular Phylogenetics and Evolution 36 (3): 606–22. PMID 15923129. doi:10.1016/j.ympev.2005.03.031. 
  17. Liu YJ, Hodson MC, Hall BD; Hodson; Hall (2006). "Loss of the flagellum happened only once in the fungal lineage: phylogenetic structure of Kingdom Fungi inferred from RNA polymerase II subunit genes". BMC Evolutionary Biology 6: 74. PMC 1599754. PMID 17010206. doi:10.1186/1471-2148-6-74. 
  18. Gill EE, Fast NM; Fast (June 2006). "Assessing the microsporidia-fungi relationship: Combined phylogenetic analysis of eight genes". Gene 375: 103–9. PMID 16626896. doi:10.1016/j.gene.2006.02.023. 
  19. Lee SC, Corradi N, Byrnes EJ et al. (November 2008). "Microsporidia evolved from ancestral sexual fungi". Current Biology 18 (21): 1675–9. PMC 2654606. PMID 18976912. doi:10.1016/j.cub.2008.09.030. 
  20. Vossbrinck CR, Debrunner-Vossbrinck BA; Debrunner-Vossbrinck (May 2005). "Molecular phylogeny of the Microsporidia: ecological, ultrastructural and taxonomic considerations". Folia Parasitologica 52 (1–2): 131–42; discussion 130. PMID 16004372. doi:10.14411/fp.2005.017. 

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