Microsporidiosis
| Microsporidiosis | |
|---|---|
| Specialty | Infectious diseases  |
Microspridiosis is an opportunistic intestinal infection that causes diarrhea and wasting in immunocompromised individuals (HIV, for example). It results from different species of microsporidia, a group of protozoal parasites.[1]
In HIV infected individuals, microsporidiosis generally occurs when CD4+ T cell counts fall below 100.
Classification
Although it is classified as a protozoal disease in ICD-10, there has been recent evidence that the causative agent is more fungal than protozoal,[2][3] and some sources classify microsporidiosis as a mycosis.[4]
Causative agents
At least 14 microsporidian species have been recognized as human pathogens, spread across eight genera:
- Brachiola
- B. algerae, B. connori, B. vesicularum
- Encephalitozoon
- E. cuniculi, E. hellem, E. intestinalis
- Enterocytozoon
- E. bieneusi
- Microsporidium
- M. ceylonensis, M. africanum
- Nosema
- N. ocularum
- Pleistophora sp.
- Trachipleistophora
- T. hominis, T. anthropophthera
- Vittaforma
- V. corneae.
The primary causes are Enterocytozoon bieneusi and Encephalitozoon intestinalis.[5]
Life cycle
(Coded to image at right).
- The infective form of microsporidia is the resistant spore and it can survive for an exteneded period of 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. bieneusi) or inside a vacuole called a parasitophorous vacuole (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.
Treatment
Fumagillin has been used in the treatment.[5][6]
Another agent used is albendazole.[7]
References
- ^ "Microsporidiosis: Parasitic Infections: Merck Manual Home Edition".
- ^ Didier ES (2005). "Microsporidiosis: an emerging and opportunistic infection in humans and animals". Acta Trop. 94 (1): 61–76. doi:10.1016/j.actatropica.2005.01.010. PMID 15777637.
{{cite journal}}: Unknown parameter|month=ignored (help) - ^ Keeling PJ, Luker MA, Palmer JD (2000). "Evidence from beta-tubulin phylogeny that microsporidia evolved from within the fungi". Mol. Biol. Evol. 17 (1): 23–31. PMID 10666703.
{{cite journal}}: Unknown parameter|month=ignored (help)CS1 maint: multiple names: authors list (link) - ^ Microsporidiosis at the U.S. National Library of Medicine Medical Subject Headings (MeSH)
- ^ a b Lanternier F, Boutboul D, Menotti J; et al. (2009). "Microsporidiosis in solid organ transplant recipients: two Enterocytozoon bieneusi cases and review". Transpl Infect Dis. 11 (1): 83–8. doi:10.1111/j.1399-3062.2008.00347.x. PMID 18803616.
{{cite journal}}: Explicit use of et al. in:|author=(help); Unknown parameter|month=ignored (help)CS1 maint: multiple names: authors list (link) - ^ Molina JM, Tourneur M, Sarfati C; et al. (2002). "Fumagillin treatment of intestinal microsporidiosis". N. Engl. J. Med. 346 (25): 1963–9. doi:10.1056/NEJMoa012924. PMID 12075057.
{{cite journal}}: Explicit use of et al. in:|author=(help); Unknown parameter|month=ignored (help)CS1 maint: multiple names: authors list (link) - ^ Didier ES, Maddry JA, Brindley PJ, Stovall ME, Didier PJ (2005). "Therapeutic strategies for human microsporidia infections". Expert Rev Anti Infect Ther. 3 (3): 419–34. doi:10.1586/14787210.3.3.419. PMID 15954858.
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External links
- CDC's microsporidiosis info page.