Microsporidiosis
| Microsporidiosis | |
|---|---|
| Specialty | Infectious diseases  |
Microsporidiosis 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 microbial (unicellular) fungi.[1]
In HIV infected individuals, microsporidiosis generally occurs when CD4+ T cell counts fall below 150.
Classification
Although it is classified as a protozoal disease in ICD-10, their phylogenetic placement has been resolved to be within the Fungi, and some sources classify microsporidiosis as a mycosis,[2] however, they are highly divergent and rapidly evolving.[3][4][5]
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.[6]
Life cycle
(Coded to image at right).
- The infective form of microsporidia is the resistant spore and it can survive for an extended 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.[6][7]
Another agent used is albendazole.[8]
References
- ^ "Microsporidiosis: Parasitic Infections: Merck Manual Home Health Handbook".
- ^ Microsporidiosis at the U.S. National Library of Medicine Medical Subject Headings (MeSH)
- ^ Didier ES (April 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.
- ^ Keeling PJ, Luker MA, Palmer JD (January 2000). "Evidence from beta-tubulin phylogeny that microsporidia evolved from within the fungi". Mol. Biol. Evol. 17 (1): 23–31. doi:10.1093/oxfordjournals.molbev.a026235. PMID 10666703.
- ^ Keeling PJ; Madhani, Hiten D. (September 2009). Madhani, Hiten D. (ed.). "Five Questions about Microsporidia". PLOS Pathogens. 5 (9): e1000489. doi:10.1371/journal.ppat.1000489. PMC 2742732. PMID 19779558.
{{cite journal}}: CS1 maint: unflagged free DOI (link) - ^ a b Lanternier F, Boutboul D, Menotti J, et al. (February 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.
- ^ Molina JM, Tourneur M, Sarfati C, et al. (June 2002). "Fumagillin treatment of intestinal microsporidiosis". N. Engl. J. Med. 346 (25): 1963–9. doi:10.1056/NEJMoa012924. PMID 12075057.
- ^ Didier ES, Maddry JA, Brindley PJ, Stovall ME, Didier PJ (June 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.
External links
- CDC's microsporidiosis info page.