Eukaryotes Genomes - ENCEPHALITOZOON CUNICULI

Encephalitozoon cuniculi is a microsporidian parasite. Microsporidians are primordial eukaryotes lacking mitochondriae, they are intracellular parasites of other eukaryotes, ranging from protozoans to humans. To date, more than 1,200 species belonging to 143 genera have been described as parasites infecting a wide range of vertebrate and invertebrate hosts. Microsporidia, are characterised by the production of resistant spores that vary in size, depending on the species. They possess a unique organelle, the polar tubule or polar filament , which is coiled inside the spore. The microsporidia spores of species associated with human infection measure from 1 to 4m. There are at least 14 microsporidian species that have been identified as human pathogens, Encephalitozoon cuniculi being one of them. Microsporidia are being increasingly recognised as opportunistic infectious agents worldwide. Cases of microsporidiosis have been reported in developed as well as in developing countries.

The involvement of Microsporidians in several human pathologies was discovered during the 1950s. However, it was only in the 1980s, with the emergence of AIDS and the use of immunosuppressors during organ transplants, that the association of microsporidians and several opportunistic infections was demonstrated. Since then, several cases of microsporidial infections in non-immunocomprimised patients have been reported. In humans, Encephalitozoon cuniculi is responsible for various pathologies, affecting the nervous system as well as the respiratory and digestive tracts.

Encephalitozoon cuniculi not only is pathogenic to humans but can infect a wide range of hosts, including laboratory mice and rats and is a major health issue for rabbits. Cerebral microsporidial infection was first described in 1922 in rabbits with granulomatous encephalitis. The parasite causes chronic infections in rabbits that may eventually lead to granulomatous inflammation in various organs. Encephalitis and nephritis are among the most common clinical manifestations.

The primary significance of E. cuniculi in laboratory rodents is as a contaminant of transplantable tumors. In addition to infected tumors, transmission is via exposure to infectious urine. Following ingestion, sporoplasm from infectious spores gains entrance to host intestinal epithelium, where multiplication occurs. Continued multiplication results in eventual host cell rupture, with dissemination to other organs, including the brain, kidneys, liver, and lungs.

Infection with E. cuniculi transiently increases NK (natural killer) cell activity, causes hepatosplenomegaly with ascites, alters brain and kidney architecture, alters host responses to transplanted tumors, and reduces cellular and humoral responses to a variety of immunogens. E. cuniculi infection of mice is used as a model of human microsporidiosis. Natural infection of laboratory mice and rats would compromise studies involving the gastrointestinal, renal, and central nervous system and possibly others.

This organism has a very compact genome (the smallest eukaryotic genome known to date) of 2.9 Mbases. The genome is organised into 11 chromosomes.

E. cuniculi should be included in the expanding spectrum of potentially life-threatening opportunistic pathogens that infect the brain. Detection of the parasite in cerebrospinal fluid may be difficult, since the number of spores may be low. Microscopical examination of urinary sediment, however, appears to be a simple method for the diagnosis of disseminated encephalitozoonosis

References:

Nature 414(6862):450-453(2001
New England Journal of Medicine 336:474-478 (1997)
http://ourworld.compuserve.com/homepages/TheBroons/path15.htm
http://www.genoscope.cns.fr/externe/English/Projets/Projet_AD/AD.html
http://www.dpd.cdc.gov/dpdx/hTML/Microsporidiosis.asp?body=Frames/M-R/Microsporidiosis/body_Microsporidiosis_page1.htm