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Xenoma

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Xenoma

Xenoma on the flatfish Limanda limanda

A xenoma (also known as a 'xenoparasitic complex') is a growth caused by various fish.[1]

In most cases the cell and its structure and can result in polyploid nuclei. This outcome is due to the microsporidian parasite proliferating inside the host cell. This results in a 'symbiotic co-existence' between the parasite and the host cell.[1] This forms the xenoparasitic complex. They tend to contain numerous cellular components as well as microsporidia at different developmental stages and spores.[2]

Not all microsporidia infections result in the formation of xenomas; only a few microsporidia actually cause xenoma formation.[2]

Contents

  • History 1
  • Pathogenesis 2
  • Xenomas in fish 3
    • Xenomas found in other organisms 3.1
  • Treatment 4
  • See also 5
  • References 6

History

Xenoparasitic complex was the term initially devised in the early twentieth century to describe specific type 'tumours' found on various organisms, specific as the infections were caused by multiple subclasses of microsporidia. A paper published in 1922 by Weissenberg came up with the term 'xenon' for the xenoparasitic complexes he observed on sticklebacks caused by Glugea anomala, before eventually changing it to xenoma (xenon was already the name of a newly discovered chemical element).[1][3]

  1. ^ a b c d e f g h i j k l m n o p q r s t u v Lom J, Dyková I. "Microsporidian xenomas in fish seen in wider perspective". Folia Parasitologica 52: 69–81.  
  2. ^ a b c d e Matos E, Corral L, Azevedo C. "Ultrastructural details of the xenoma of Loma myrophis (phylum Microsporidia) and extrusion of the polar tube during autoinfection". Diseases of Aquatic Organisms 54: 203–207.  
  3. ^ Weissenberg R. "Mikrosporidien und Chlamydozoen als Zellparasiten von Fischen". Verh. Dtsch. Zool. Ges. 27: 41–43. 
  4. ^ Chatton E. "Un complexe xéno-parasitaire morphologique et physiologique Neresheimeria paradoxa chez Fritillaria pellucida". C. R. Acad. Sci. Paris 171: 55–57. 
  5. ^ Chatton E, Courrier R. "Formation d’un complexe xénoparasitaire géant avec bordure en brosse, sous l'influence d'une Microsporidie, dans le testicule de Cottus bubalis". C. R. Soc. Biol. (Paris) 89: 579–583. 
  6. ^ Schröder O. "Thelohania chaetogastris, eine neue in Chaetogaster diaphanus Gruith schmarotzende Microsporidienart". Arch. Protistenkd. 14: 119–133. 
  7. ^ Ramsay JM, Speare DJ, Dawe SC, Kent ML. "Xenoma formation during microsporidial gill disease of salmonids caused by Loma salmonae is affected by host species (Oncorhynchus tshawytscha, O. kisutch, O. mykiss) but not by salinity". Diseases of Aquatic Organisms 48: 125–131.  
  8. ^ a b Mansour L, Prensier G, Jemaa SB, Hassine OKB, Méténier G, Vivarès CP, Cornillot E. "Description of a xenoma-inducing microsporidian, Microgemma tincae n. sp., parasite of the teleost fish Symphodus tinca from Tunisian coasts". Diseases of Aquatic Organisms 65: 217–226.  
  9. ^ Lee SJ, Yokoyama H, Ogawa K. "Modes of transmission of Glugea plecoglossi (Microspora) via the skin and digestive tract in an experimental infection model using rainbow trout, Oncorhyncus mykiss (Walbaum)". J. Fish Dis. 27: 435–444.  
  10. ^ Lee SJ, Yokoyama H, Ogawa K. "Rapid in situ hybridisation technique for the detection of fish microsporidian parasites". Fish Pathol. 38: 117–119.  
  11. ^ Sánchez JG, Speare DJ, Markham RJF, Wright GM, Kibenge FSB. "Localization of the initial developmental stages of Loma salmonae in rainbow trout (Oncorhynchus mykiss)". Vet. Pathol. 38: 540–546.  
  12. ^ Lom J. "A catalogue of described genera and species of microsporidians parasitic in fish". Syst Parasitol 53: 81–99.  
  13. ^ Lom J, Nilsen F. "Fish microsporidia: fine structural diversity and phylogeny". International Journal for Parasitology 33: 107–127.  
  14. ^ a b Wang TC, Nai YS, Wang CY, Solter LF, Hsu HC, Wang CH, Lo CF. "A new microsporidium, Triwangia caridinae gen. nov., sp. Nov. parasitizing fresh water shrimp, Caridina formosae (Decapoda: Atyidae) in Taiwan". Journal of Invertebrate Pathology 112: 281–293.  
  15. ^ Dyková I, Tyml T, Kostka M. "Xenoma-like formations induced by Soricimyxum fegati (Myxosporea) in three species of shrews (Soricomorpha: Soricidae), including records of new hosts". Folia Parasitologica 58: 249–256.  
  16. ^ a b Speare DJ, Markham RJF, Guselle NJ. "Development of an Effective Whole-Spore Vaccine To Protect against Microsporidial Gill Disease in Rainbow Trout (Oncorhyncus mykiss) by Using a Low-Virulence Strain of Loma salmonae". Clinical and Vaccine Immunology 14: 1652–1654.  

References

See also

Studies have shown it is possible to vaccinate against xenomas. One study showed that developing a vaccine using a 103 to 105 dose of killed spores from a low-virulence strain of Loma salmonae resulted in rainbow trout producing 85% less xenomas in their gills after experimental infection (compared to the control). This ultimately offers much improved protection to microsporidial gill disease which is common amongst rainbow trout.[16] Therapeutic drugs have proved ineffective at treating this disease and harvesting whole-spores is a relatively easy technique.[16]

The host can eventually destroy the xenoma. Proliferative inflammation occurs in mature xenomas and transforms them into granulomas. Granuloma involution then ensues where phagocytosis kills the spores.[1]

Treatment

Whilst xenomas are more highly characteristic of hepatopancreas.[14] Xenoma-like formations have also been found in species of shrew caused by Soricimyxum fegati, a type of myxosporea, showing they can also occur in mammals.[15]

Xenomas found in other organisms

Recently fish-infecting microsporidia have been grouped into five classes depending on their molecular traits, a higher level of classification using SSU (small subunit) rDNA analysis. However molecular data is still lacking for several genera of microsporidia.[13]

  • Xenomas with a thick wall [1]
  • Xenomas without a thick wall and where the complete volume of the original cell is converted into a xenoma [1]
  • Xenomas without a thick wall and where the complete volume of the original cell is not converted into a xenoma [1]

[1] that cause xenomas can therefore be quite diverse and so are characterised more comprehensively into several groups depending on their morphology:genera Microsporidia [8] induce xenoma formation.genera however only ten of these [12][2]

Xenomas in fish

Transmission of such hybridizationin situ that the microsporidia Loma salmonae enters the mucosal epithelium in the intestine and migrates to the lamina propria before arriving at the gills, where it eventually resides, via infecting blood cells.[11] Other transport vehicles are thought to include T cells, lymphocytes, and other migratory cells including monocytes where they succumb to infection by means of either phagocytosis of the parasite in the lamina propria or by infiltration by sporoplasms using their polar tube. It is also very possible that these transport cells might themselves develop into a xenoma.[1]

While it is generally accepted that the xenoma prevents spread of the species that cause xenomas are spore-forming, it is possible that their spores may release their sporoplasms which penetrate the xenoma wall, infiltrating and infecting surrounding cells. In microsporidia this is mediated by a unique and highly specialised protein: the polar tube. This specialised protein is found inside the spore and is in contact with the sporoplasm. Specific environmental stimulation causes the spore to discharge the polar tube which penetrates the xenoma membrane and provides an exit route for the sporoplasm. This is thought to be a form of autoinfection.[1] Rupture of the xenoma may also result in dispersal of the infectious spores.[1] This can lead to the formation of other and more persistent forms of xenomas.[2]

[1] In microsporidian xenomas the whole

Once a host cell is infected with the microsporidian (or protist) parasite, a complete restructuring of the host cell ensues. This occurs as the parasite seeks to take control of the metabolism of the cell, in order to survive and exploit the host cell's resources and reproduction. It provides the parasite with optimal growth conditions and protection from the host's immune response. The parasite proliferates within the host cell where its mass replaces most of the host cell's cytoplasm, with the rest being taken up by microvillus structures and rhizoids. Other structures may be present inside the infected host cell including vesicles, fat globules and bundles of fibril. The nucleus may be in varying locations including the centre of the cell and may also vary in structure i.e. lobed, branched or divided into multiple fragments, but it will always be hypertrophic.[1] The host also commonly envelops the proliferating parasite and the host cell itself in layers of membranes and cells.[2]

Xenomas are provoked in various types of organisms, depending on the species of the annelid Chaetogaster diaphanus,[6] whereas other species of microsporidia will target other tissue types. Another example is microsporidial gill disease in different species of fish caused by Loma salmonae. It was found that certain species had a higher prevalence of xenoma formation following infection with the same parasite i.e. xenomas per gill filament in chinook salmon was 8 to 33 times greater than in rainbow trout, showing differences in host cell susceptibility.[7]

Pathogenesis

[5][1] where a dense microvillus layer is present for improved nutrient absorption.Taurulus bubalis of testes infection of the Microsporidium cotti This can be contrasted to the [4][1].Fritillaria pellucida appendicularian in the absorption extend into the cytoplasm for nutrient rhizoids nuclei formation whilst forming a thick-walled hyposome where polyploid, hypertrophy induces Sphaeripara catenata protist dinoflagellate For example the [1]

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