Encephalitozoon cuniculi

Encephalitozoon cuniculi (E. cuniculi) is a mammalian microsporidial pathogen with world-wide distribution. An important cause of neurologic and renal disease in rabbits, E. cuniculi can also cause disease in immunocompromised people. Encephalitozoon cuniculi (E. cuniculi) is a mammalian microsporidial pathogen with world-wide distribution. An important cause of neurologic and renal disease in rabbits, E. cuniculi can also cause disease in immunocompromised people. E. cuniculi is a spore-forming unicellular parasite belonging to the phylum Microsporidia and the kingdom Fungi. The infective form of microsporidia (E. cuniculi) is a resistant spore which can survive for a long 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 a polar tube. Inside the cell, the sporoplasm undergoes extensive multiplication. This multiplication occurs either by merogony (binary fission) or schizogony (multiple fission). Microsporidia develop by sporogony to mature spores in the cytoplasm or inside parasitophorous vacuole. During sporogony, a thick wall is formed around the spore. The thick wall formed provides resistance to adverse environmental conditions. Once the spores increase in number and completely fill the cytoplasm of the host's cell, the cell membrane is disrupted and releases the spores to the surroundings. These free mature spores can infect new cells thus continuing the cycle. Human-to-human transmission is possible via transplantation of solid organs from an infected donor. E. cuniculi is a common infection in rabbits. Most rabbits are subclinical carrriers and show no signs of disease. Occasionally however these parasites rarely migrate to nervous tissue or other organs. On occasions when E. cuniculi do reach nervous tissue, rabbits can experience neurological impairment, characterized by partial or complete paralysis, loss of coordination, seizures, and head tilting. Neurological impairment is thought to occur when E. cuniculi multiply within the rabbit's body inducing the development of granulomas. If infection takes place during fetal development, E. cuniculi can invade the eye lens. There, it will replicate until the lens breaks and the chrystalline fibers protrude into the anterior chamber in a process known as phacoclastic uveitis. As a consequence, these fibers will be encapsulated in a granuloma, and the rabbit will most likely lose complete sight in the affected eye. Phacoclastic uveitis usually takes place when the rabbit is between 3 months and 2 years of age. Antibodies to E. cuniculi can be detected through serology (a blood test). A rabbit who has been exposed to E. cuniculi will produce antibodies as a result of this exposure. Serology is used to detect the level of the antibody to the organism in the blood (this result is known as the titre). A positive titre tells you that the rabbit has been exposed to this parasite at some point in its life. Note that this does not allow one to differentiate between simple exposure and an active infection. By performing serology (with an interval of time in between) and comparing the results, it is possible to determine if the rabbit is mounting an immune response to an active infection or if it was previously infected. However, even with a rising titre, one can't determine for certain that a particular health problem is being caused by E. cuniculi or something else. Head tilt, for example, has many causes other than E. cuniculi, including bacterial or viral infections, trauma, and toxicity. A false negative titre may also result if an infected animal produces an inadequate amount of antibodies. A few studies have shown that fenbendazole, a benzimidazole drug, can prevent and treat naturally acquired and experimentally induced E. cuniculi infections. Unfortunately the elimination of spores from the central nervous system does not always result in resolution of clinical signs. Adverse reactions to benzimidazole drugs, including injury to the small intestine and bone marrow, have been reported in rabbits. Practitioners should strictly adhere to recommended dosages and treatment intervals, and consider monitoring complete blood counts during treatment. Microsporidia are obligate intracellular parasitic fungi infecting many animal groups. Lacking mitochondria and peroxysomes, these unicellular eukaryotes were first considered a deeply branching protist lineage that diverged before the endosymbiotic event that led to mitochondria. The discovery of a gene for a mitochondrial-type chaperone combined with molecular phylogenetic data later implied that microsporidia are atypical fungi that lost mitochondria during evolution. Its genome consists of approximately 2.9-megabases (Mbs) in 11 chromosomes, with a total of 1,997 potential protein-coding genes. Genome compaction is reflected by reduced intergenic spacers and by the shortness of most putative proteins relative to their eukaryote orthologues. The strong host dependence is illustrated by the lack of genes for some biosynthetic pathways and for the tricarboxylic acid cycle. Phylogenetic analysis lends substantial credit to the fungal affiliation of microsporidia. Because the E. cuniculi genome contains genes related to some mitochondrial functions (for example, Fe-S cluster assembly), it is possible that microsporidia have retained a mitochondrion-derived organelle.