Encephalitozoon cuniculi | |
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Scientific classification | |
Kingdom: | |
Phylum: | |
Suborder: | Apansporoblastina |
Family: | Unikaryonidae |
Genus: | Encephalitozoon |
Species: | E. cuniculi |
Binomial name | |
Encephalitozoon cuniculi C. Levaditi, Nicolau & R. Schoen, 1923 [1] | |
Encephalitozoon cuniculi is a microsporidial parasite of mammals with world-wide distribution. An important cause of neurologic and renal disease in rabbits, E. cuniculi can also cause disease in immunocompromised people.
Its current accepted name is Nosema cuniculi. [2]
E. cuniculi is a microsporidial, unicellular, obligate intracellular, eukaryotic, parasite. It belongs to the phylum Microsporidia. Microsporidia are parasitic fungi infecting many animal groups. [3] Lacking mitochondria and peroxysomes, they 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.
The genome consists of approximately 2.9-megabases (Mbs) in 11 chromosomes, with a total of 1,997 potential protein-coding genes. [4] Genome compaction is reflected by reduced intergenic spacers and by the shortness of most putative proteins relative to their eukaryote orthologues. [5] At the time of publication (2001), only 44% of the proteins had a function assigned to them. the latest reference proteome in Uniprot (2021) lists 2041 proteins with ~620 proteins annotated as "uncharacterized", about 200 without annotation (e.g. "UPF0329 protein ECU06_1620") and another ~150 or so that are annotated as having some "domain" (including domains of unknown function) and numerous proteins of "probable" and "putative" function plus dozens with "similarity" to characterized proteins. [6] Hence, even 20 years after the genome sequence was published, about 50% of the E. cuniculi proteome remains uncharacterized or poorly understood.
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. [5]
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.
E. cuniculi has undergone an evolutionary process of genome reduction that has affected all major DNA repair pathways. [7] DNA double-strand breaks are one of the most detrimental forms of DNA damage, as they can cause genome fragmentation if not repaired. More than half of the proteins that ordinarily participate in the two double strand break repair pathways, homologous recombinational repair and non-homologous end joining, are absent in E. cuniculi compared to other related species. [7] The remaining proteins are all involved in additional cellular functions (such as meiosis). [7]
First identified in rabbits, E. cuniculi infections have been reported worldwide in over 20 mammalian species, including humans. Prevalence in pet rabbits is high, with 23–75% having antibodies to the disease. Studies of healthy dogs have found a 0–38% prevalence. Cats appear to be relatively resistant to the organism, although experimental infections in kittens with feline leukemia virus have been described. E. cuniculi also infects rodents, and the organism has been detected in the feces of 13% of pet birds. A small percentage of healthy people have antibodies to the organism, indicating previous exposure. Seroprevalence rates are higher in immunocompromised people, and in those who live in or have visited tropical countries. Most infections do not result in clinical disease. [8]
E. cuniculi spores are usually shed in urine, but can also be found in the feces and respiratory secretions of infected animals. Spores can be detected in urine 38 to 63 days after infection, with intermittent shedding thereafter. Ingestion of spores is the main route of transmission, although inhalation of spores can also occur. Transplacental and intrauterine infections have been documented in rabbits. [8]
Up to 80% of rabbits in the United States and Europe are serologically positive for E. cuniculi, which indicates that they have been exposed to the organism. Most of these animals will remain asymptomatic and never show signs of disease. Only a small minority of infected rabbits develop the disease encephalitozoonosis. The most common clinical signs associated with this disease involve the central nervous system, eyes, and kidneys. [9]
Most rabbits with neurologic signs show vestibular dysfunction only. Symptoms often appear suddenly, and include head tilt, ataxia, nystagmus, and circling. Most of these animals are still aware of their surroundings and are eating despite their loss of balance. More severely affected rabbits, such as those which can no longer stand, have a worse prognosis. [10]
E. cuniculi infections in the eye cause cataract formation, white intraocular masses, and uveitis. Symptoms usually occur in young rabbits, and only one eye is generally affected. Rabbits with ocular lesions related to encephalitozoonosis are usually otherwise healthy, and tolerate vision loss well. [10]
E. cuniculi has a predilection for the kidneys and can cause chronic or acute kidney failure. Symptoms of renal impairment include increased water consumption, increased urine output, loss of appetite, weight loss, lethargy, and dehydration. Milder cases do not cause symptoms, and signs of infection may be an incidental finding on necropsy. [10]
It is currently difficult to definitively diagnose E. cuniculi infections in live rabbits. A presumptive diagnosis is often made based on consistent clinical signs and high antibody levels. Serology tests that look for IgG antibodies are commonly run, and can be used to rule out the disease if negative. However, a positive IgG titer cannot differentiate an active infection from a previous infection or an asymptomatic carrier state. [11] Tests for IgM antibodies are also available, but again positive results cannot distinguish between active and latent infections. [10]
Polymerase chain reaction (PCR) has long been established as the standard technique for detection of microsporidia in humans, and attempts to apply this to rabbits are ongoing. Studies have found that PCR of liquified lens material is a reliable means of diagnosing E. cuniculi uveitis in rabbits, but PCR testing of rabbit urine and cerebrospinal fluid is not reliable. [10]
A few studies have shown that albendazole, 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. [10]
E. cuniculi is an important opportunistic pathogen in people, particularly those immunocompromised by HIV/AIDS, organ transplantation, or CD4+ T-lymphocyte deficiency. As this organism is more common in animals than people it is likely a zoonotic disease. Three different strains of E. cuniculi have been identified, and are classified as I (rabbit), II (mouse), and III (dog). [8] Human-to-human transmission is possible via transplantation of solid organs from an infected donor. [12]
Toxoplasmosis is a parasitic disease caused by Toxoplasma gondii, an apicomplexan. Infections with toxoplasmosis are associated with a variety of neuropsychiatric and behavioral conditions. Occasionally, people may have a few weeks or months of mild, flu-like illness such as muscle aches and tender lymph nodes. In a small number of people, eye problems may develop. In those with a weak immune system, severe symptoms such as seizures and poor coordination may occur. If a person becomes infected during pregnancy, a condition known as congenital toxoplasmosis may affect the child.
Giardia duodenalis, also known as Giardia intestinalis and Giardia lamblia, is a flagellated parasitic protozoan microorganism of the genus Giardia that colonizes the small intestine, causing a diarrheal condition known as giardiasis. The parasite attaches to the intestinal epithelium by an adhesive disc or sucker, and reproduces via binary fission. Giardiasis does not spread to other parts of the gastrointestinal tract, but remains confined to the lumen of the small intestine. The microorganism has an outer membrane that makes it possible to survive even when outside of its host, and which can render it tolerant to certain disinfectants. Giardia trophozoites are anaerobic, and absorb their nutrients from the intestinal lumen. If the organism is stained, its characteristic pattern resembles the familiar "smiley face" symbol.
Cryptosporidiosis, sometimes informally called crypto, is a parasitic disease caused by Cryptosporidium, a genus of protozoan parasites in the phylum Apicomplexa. It affects the distal small intestine and can affect the respiratory tract in both immunocompetent and immunocompromised individuals, resulting in watery diarrhea with or without an unexplained cough. In immunosuppressed individuals, the symptoms are particularly severe and can be fatal. It is primarily spread through the fecal-oral route, often through contaminated water; recent evidence suggests that it can also be transmitted via fomites contaminated with respiratory secretions.
Virulence is a pathogen's or microorganism's ability to cause damage to a host.
Trichomonas vaginalis is an anaerobic, flagellated protozoan parasite and the causative agent of a sexually transmitted disease called trichomoniasis. It is the most common pathogenic protozoan that infects humans in industrialized countries. Infection rates in men and women are similar but women are usually symptomatic, while infections in men are usually asymptomatic. Transmission usually occurs via direct, skin-to-skin contact with an infected individual, most often through vaginal intercourse. The WHO has estimated that 160 million cases of infection are acquired annually worldwide. The estimates for North America alone are between 5 and 8 million new infections each year, with an estimated rate of asymptomatic cases as high as 50%. Usually treatment consists of metronidazole and tinidazole.
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Coccidia (Coccidiasina) are a subclass of microscopic, spore-forming, single-celled obligate intracellular parasites belonging to the apicomplexan class Conoidasida. As obligate intracellular parasites, they must live and reproduce within an animal cell. Coccidian parasites infect the intestinal tracts of animals, and are the largest group of apicomplexan protozoa.
Microsporidia are a group of spore-forming unicellular parasites. These spores contain an extrusion apparatus that has a coiled polar tube ending in an anchoring disc at the apical part of the spore. They were once considered protozoans or protists, but are now known to be fungi, or a sister group to fungi. These fungal microbes are obligate eukaryotic parasites that use a unique mechanism to infect host cells. They have recently been discovered in a 2017 Cornell study to infect Coleoptera on a large scale. So far, about 1500 of the probably more than one million species are named. Microsporidia are restricted to animal hosts, and all major groups of animals host microsporidia. Most infect insects, but they are also responsible for common diseases of crustaceans and fish. The named species of microsporidia usually infect one host species or a group of closely related taxa. Approximately 10 percent of the species are parasites of vertebrates —several species, most of which are opportunistic, can infect humans, in whom they can cause microsporidiosis.
Francisella tularensis is a pathogenic species of Gram-negative coccobacillus, an aerobic bacterium. It is nonspore-forming, nonmotile, and the causative agent of tularemia, the pneumonic form of which is often lethal without treatment. It is a fastidious, facultative intracellular bacterium, which requires cysteine for growth. Due to its low infectious dose, ease of spread by aerosol, and high virulence, F. tularensis is classified as a Tier 1 Select Agent by the U.S. government, along with other potential agents of bioterrorism such as Yersinia pestis, Bacillus anthracis, and Ebola virus. When found in nature, Francisella tularensis can survive for several weeks at low temperatures in animal carcasses, soil, and water. In the laboratory, F. tularensis appears as small rods, and is grown best at 35–37 °C.
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Microsporidiosis is an opportunistic intestinal infection that causes diarrhea and wasting in immunocompromised individuals. It results from different species of microsporidia, a group of microbial (unicellular) fungi.
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Encephalitozoon intestinalis is a parasite. It can cause microsporidiosis.
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Hamiltosporidium is a genus of Microsporidia, which are intracellular and unicellular parasites. The genus, proposed by Haag et al. in 2010, contains two species; Hamiltosporidium tvaerminnensis, and Hamiltosporidium magnivora. Both species infect only the crustacean Daphnia magna (Waterflea).
Enterospora nucleophila is a microsporidian infecting the gilt-head bream. It develops primarily within the nuclei of rodlet cells and enterocytes, at the intestinal epithelium. It can also be found in cytoplasmic position within other cell types, including phagocytes, at subepithelial layers. It is the causative agent of emaciative microsporidiosis of gilthead sea bream, a chronic condition manifested as a severe growth arrestment, normally accompanied by trickling mortality.