| Enterocytozoon bieneusi |
| Scientific classification |
| Kingdom: |
Fungi |
| Class: |
Microsporea |
| Order: |
Microsporida |
| Genus: |
Enterocytozoon |
| Species: |
E. bieneusi |
| Binomial name |
Enterocytozoon bieneusi
|
Enterocytozoon bieneusi, common Name: Microsporidia, is a species of the order microsporida which infects the intestinal epithelial cells. It is an obligate intracellular parasite.[1]
Contents
- 1 Abstract
- 2 Discovering the disease
- 3 Culturing
- 4 Study and detection methods
- 5 Life cycle
- 6 Transmission mode
- 7 Hosts
- 8 Effects on hosts
- 9 Treatment
- 10 How common is the disease
- 11 Economic impact
- 12 Unanswered questions
- 13 Interesting facts
- 14 References
- 15 Notes
Abstract[edit]
Enterocytozoon bieneusi, commonly known as microsporidia, is a unicellular, obligate intracellular eukaryote. Their life cycle includes a proliferative merogonic stage, followed by a sporogonic stage resulting in small, environmentally resistant, infective spores, which is their transmission mode. The spores contain a long, coiled polar tube, which distinguishes them from all other organisms and has a crucial role in host cell invasion. E. bieneusi was first found in an AIDS patient in France in 1985 and was later found in swine in 1996 in fecal samples. It causes diarrhea thus the pigs excrete more spores spreading the disease. As this pathogen is very prevalent throughout the world, E. bieneusi is found in a wide variety of hosts including pigs, humans, and other mammals. E. bieneusi can be studied using TEM, light microscopy, PCR and immunofluorescence and can be cultured for short-term. It has not been known yet whether the pathogen gets any diseases and there seem to be widespread economic implications of this pathogen in the swine industry. Furthermore, several treatment medications such as Fumagilin and albendazole seem promising (Mathis et al. 2005).
Discovering the disease[edit]
The earliest reference to the order microsporida was in the mid-20th century. E. bieneusi was first found in an AIDS patient in France in 1985. The electron microscope studies revealed presence of developmental stages of parasite resembling microsporidia. The investigators then named it as E. bieneusi (Desportes et al. 1985). The presence of E. bieneusi in swine was first detected in fecal samples of pigs in Zurich, Switzerland in 1996 (Deplazes et al. 1996)
Culturing[edit]
Short-term culturing of E. bieneusi was achieved by inoculating duodenal aspirate and biopsy specimens into E6 and HLF monolayers. The short-term cultures lasted up to 6 months. After several weeks of culture, gram-positive spore-like structures measuring 1 to 1.2 um long were observed. Mature spores and sporoblasts with double rows of polar tubule coils were seen (Visvesvara 2002). Long term culturing seems to be unsuccessful.
Study and detection methods[edit]
Light microscopy of stained clinical smears, especially of fecal samples, is used to diagnose microsporidia infections.. Transmission electron microscopy is required to differentiate between species of microsporidia, but it is time consuming and expensive. Immunofluorescence Assays using monoclonal and polyclonal antibodies are used, and PCR has recently been employed for E. bieneusi (CDC).
Life cycle[edit]
- The infective form of E. bieneusi is the resistant spore and it can survive for a long time in the environment.
- The spore extends 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 occurs in direct contact with the host cell cytoplasm. In the cytoplasm, 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 (Desportes 1985).
Transmission mode[edit]
E. bieneusi is transported through environment resistant spores.
Common environmental sources of E. bieneusi include ditch and other surface waters, and several species of microsporidia can be isolated from such sources indicating that the disease may be waterborne.
The different modes of transmission that may be possible include the fecal-oral or oral-oral route, inhalation of aerosols, or ingestion of food contaminated with fecal material (Mathis et al. 2005). Furthermore, there seem to be a close relationship between E. bieneusi strains from humans and pigs, suggesting the absence of transmission barrier between pigs and humans for this parasite (Rinder et al. 2000).
Animals, particularly pigs may play a role of zoonotic reservoir in transmitting the disease to other organisms (Abreu-Acosta et al. 2005), (Lores et al. 2002). Both vertical and horizontal transmissions are possible.
Hosts[edit]
Pigs, Fish, Birds, Cattle, Human, Other mammals such as monkeys
Effects on hosts[edit]
E. bieneusi is a common parasite in pigs and it causes diarrhea, from self-limited to severe forms. This is documented by the lack of intestinal lesions in pigs experimentally infected with E. bieneusi (Mathis et al. 2005). The pigs that were infected with this disease excreted more spores.
Treatment[edit]
Inhibitors of chitin synthase enzymes seem to be effective against this pathogen. Fumagilin and albendazole treatments seem promising in swine (Mathis et al. 2005)
How common is the disease[edit]
It is very common in pigs and seems to be a natural pathogen in animals such as pigs (Lores et al. 2002). In some communities of pigs, the prevalence rates of E. bieneusi reached 37% (Mathias et al. 2005). There are no recorded large epidemics yet. PCR Analysis in Czech Republic revealed existence of E. bieneusi in 94% of the samples indicating the large presence of E. bieneusi in swine, and that they may be naturally occurring (Sak et al. 2008).
Economic impact[edit]
Since this is a relatively new finding in pigs, the economic impact has not been studied yet. Pig farming in the US has annual revenue of $18 billion and US has about 75000 pig farms. Infection in even few pigs can be devastating as the disease is easily spread. Moreover, these pigs can serve as zoonotic reservoirs for E. bieneusi so transmission to other animals and humans is possible. Since the transmission from swine to other humans and animals is not studied yet, this may cause a major impact on the health of this country. Moreover, in other parts of the world such as China where the pig industry is major economic component and where humans and pigs live in crowded conditions, the disease can be very easily spread and can have a potentially major impact on the economy.
Unanswered questions[edit]
Much more work needs to be done in characterizing this pathogen as this was discovered relatively recently. Moreover, work needs to be done in studying effects in a broad range of species such as swine (not just humans) as this will reveal the multi-faceted nature of E. bieneusi. Furthermore, a concrete plan on treatment in pigs needs to be developed and its effects on specific stages of lifecycle should be measured to see where it can be effectively controlled. Also, it is not known whether E. bieneusi gets any diseases itself, and while the morbidity effects are known, the effects of this pathogen on reproduction are not known.
Interesting facts[edit]
Did you know that in the mid-19th century, microsporidia almost destroyed the silk industry in Europe?
Louis Pasteur studied the disease in silkworm for 5 years and showed the farmers that the plague could be successfully overcome by microscopic examination of silkworms and ova with elimination of all those found to be diseased (Franzen 2008). Though we do not know what species of microsporidia infected the silkworm, E. bieneusi or other closely related species are possible.
This work was the main influence on Pasteur for his Germ Theory of Disease.
Microsporidia are currently under debate as an organism to be studied by mycologists or by other eukaryotic scientists. They are basal to fungi and the animal kingdoms as evidence from microsporidia's extremely puny genome.
References[edit]
- Abreu-Acosta, N., Lorenzo-Morales, J., Leal-Guio, Y., Coronado-Alvarez, N., Foronda, P., Alcoba-Florez, J., Izquierdo, F., Batista-Diaz, N., Del Aguila, C., & Valladares, B. (2005). Enterocytozoon bieneusi (microsporidia) in clinical samples from immunocompetent individuals in tenerife, canary islands, Spain. Transactions of the Royal Society of Tropical Medicine and Hygiene, 99(11), 848-855. doi:10.1016/j.trstmh.2005.05.010
- Breitenmoser, A. C., Mathis, A., Burgi, E., Weber, R., & Deplazes, P. (1999). High prevalence of enterocytozoon bieneusi in swine with four genotypes that differ from those identified in humans. Parasitology, 118 ( Pt 5)(Pt 5), 447-453.
- Deplazes, P., Mathis, A., Muller, C., & Weber, R. (1996). Molecular epidemiology of encephalitozoon cuniculi and first detection of enterocytozoon bieneusi in faecal samples of pigs. The Journal of Eukaryotic Microbiology, 43(5), 93S.
- Desportes, I., Le Charpentier, Y., Galian, A., Bernard, F., Cochand-Priollet, B., Lavergne, A., Ravisse, P., & Modigliani, R. (1985). Occurrence of a new microsporidan: Enterocytozoon bieneusi n.g., n. sp., in the enterocytes of a human patient with AIDS. The Journal of Protozoology, 32(2), 250-254.
- Keeling, P. J., & Fast, N. M. (2002). Microsporidia: Biology and evolution of highly reduced intracellular parasites. Annual Review of Microbiology, 56, 93-116. doi:10.1146/annurev.micro.56.012302.160854
- Lores, B., del Aguila, C., & Arias, C. (2002). Enterocytozoon bieneusi (microsporidia) in faecal samples from domestic animals from galicia, Spain. Memorias do Instituto Oswaldo Cruz, 97(7), 941-945.
- Mathis, A., Weber, R., & Deplazes, P. (2005). Zoonotic potential of the microsporidia. Clinical Microbiology Reviews, 18(3), 423-445.2005
- Pagornrat, W., Leelayoova, S., Rangsin, R., Tan-Ariya, P., Naaglor, T., & Mungthin, M. (2009). Carriage rate of enterocytozoon bieneusi in an orphanage in bangkok, Thailand. Journal of Clinical Microbiology, 47(11), 3739-3741.
- Rinder, H., Thomschke, A., Dengjel, B., Gothe, R., Loscher, T., & Zahler, M. (2000). Close genotypic relationship between enterocytozoon bieneusi from humans and pigs and first detection in cattle. The Journal of Parasitology, 86(1), 185-188.
- Sak, B., Kucerova, Z., Kvac, M., Kvetonova, D., Rost, M., & Secor, E. W. (2010). Seropositivity for enterocytozoon bieneusi, Czech Republic. Emerging Infectious Diseases, 16(2), 335-337.
- Sak, B., Kvac, M., Hanzlikova, D., & Cama, V. (2008). First report of enterocytozoon bieneusi infection on a pig farm in the Czech Republic. Veterinary Parasitology, 153(3-4), 220-224.
- Visvesvara, G. S. (2002). In vitro cultivation of microsporidia of clinical importance. Clinical Microbiology Reviews, 15(3), 401-413.
Notes[edit]
- ^ 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.
