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PubMed1980

The course of infection of Encephalitozoon cuniculi in immunodeficient and immunocompetent mice.

A humoral and cellular response was detected in C57BL mice 14-21 days after experimental infection with Encephalitozoon cuniculi. In athymic (nu/nu) mice a severely limited cellular response and no antibodies were detected, but masses of spores were found in the liver and other viscera. These spores were probably responsible for the death of the nude mice. Antibodies in C57BL mice remained at high levels for at least 17 months after infection.

Animals↗
PubMed1980

A survey of Encephalitozoon cuniculi in laboratory animal colonies in the United Kingdom.

Of 38 animal colonies serologically examined for Encephalitozoon cuniculi, 1 mouse, 2 rat and 4 guineapig colonies were positive. A further survey showed that the prevalence within mouse, rat, guineapig and rabbit colonies varied between 25 and 95%. Guineapigs housed with infected rabbits are at a greater risk of being infected than those housed separately. Nephritis was a common feature, but cerebral granulomata were not seen.

Animals↗
PubMed1999

Encephalitozoon intestinale infection in an AIDS patient--a case report.

The first case of one of the most frequent intestinal microsporidians, Encephalitozoon intestinale, is reported from an AIDS patient in the Czech Republic. The patient experienced diarrhoea and was found to have microsporidia spores in stool. Species determination by electron microscopy confirmed the diagnosis of the microsporidian, E. intestinale. The CD4-count at the time of the diagnosis was 73 cells/mm3, IRI = 0.21. Only after symptomatic therapy and rehydration the patient stopped the complaining, and although he refused an antimicrosporidial therapy, the CD4-count one month later increased to 200 cells/mm3 and patient didn't suffered from diarrhoea. Six months after the first finding of microsporidia, the patient was admitted to the hospital care for progressive encephalopathy and developing wasting syndrome again with the intermittent diarrhoea. The patient was treated with albendazole at that time. Nevertheless, after 14 days of albendazole therapy, he still remained positive for E. intestinale spores in the stool (urine specimens remained negative for all the time). The patient died after a two-month hospitalisation and the apparent cause of death was purulent bronchopneumonia, wasting syndrome with microsporidiosis, and HIV encephalopathy. Generalised mycobacteriosis (MAC) was also found from the autopsy material.

AIDS-Related Opportunistic Infections↗
PubMed1979

Animal infectivity of Encephalitozoon cuniculi.

Rabbits, mice, rats and Rhesus monkeys were infected experimentally with a rabbit isolate of the mammalian microsporidan Encephalitozoon cuniculi. The lesions produced were typical of those occurring in spontaneous encephalitozoonosis in rabbits, mice, and rats, respectively. Viable E. cuniculi were recovered from tissues of injected animals with and without lesions. Titration of rabbit, mouse, and hamster isolates of E. cuniculi in mice and in rabbit choroid plexus cell cultures showed that the rabbit isolate was equally infectious for mice and cell cultures. Mouse and hamster isolates were less infectious for cell cultures than for mice. The results provide further evidence that the mouse, hamster, and rabbit isolates of E. cuniculi are identical.

Animals↗
PubMed1979

The biology of Encephalitozoon cuniculi.

Encephalitozoon cuniculi is a widespread and often sub-clinical microsporidian parasite of homeothermic animals, including man. The biology, pathology and taxonomy of the organism is reviewed and the available diagnostic methods discussed. Transmission is almost invariably via the oral route either by ingestion of contaminated tissues and other foods or by ingestion of infected urine, perhaps on food, or when animals lick the coats of others. Transplacental transmission does not seem common but can probably occur when susceptible animals are infected during pregnancy. It has been demonstrated once in mice and once in rabbits. The possibility of arthropod vector transmission awaits thorough investigation but this is unlikely to be as important as the oral route. No drugs have yet been found to be effective against E. cuniculi but control of the spread of encephalitozoonosis in laboratory animals, at least, can probably be achieved by maintaining laboratory hygiene.

Animals↗
PubMed1977

Application of immunofluorescence to the establishment of an Encephalitozoon cuniculi-free rabbit colony.

Serologic screening of a rabbit breeding colony over a 9-month period showed that all 9-week-old rabbits with Encephalitozoon cuniculi infection were born of E cuniculi-infected does. This observation, obtained from studies on 395 young rabbits, suggested that transmission of infection is either transplacental or the result of close contact soon after birth. On this basis, 16 young healthy rabbits, seronegative to E cuniculi, were isolated and tested at 2-week intervals for antibodies to E cuniculi. In the first 2 months, seven rabbits showed indications of developing antibodies to E cuniculi and were immediately removed from the colony. The remaining rabbits along with their 52 offspring were tested for serum antibodies for a further 16 months and no rabbit became seropositive. Eight months after establishment of the colony, three does, one buck and six 12-week-old rabbits were killed. Macroscopic and extensive histologic and immunofluorescence examinations failed to reveal any evidence of infection with E cuniculi. These results showed that serological screening for E cuniculi infection by immunofluorescence is a simple yet adequate procedure for establishing a rabbit colony free of encephalitozoonosis.

Animals↗
PubMed1978

The eradication of Encephalitozoon cuniculi from a specific pathogen-free rabbit colony.

Encephalitozoan cuniculi was discovered in a large specific pathogen-free rabbit colony during routine quality assurance testing. By using a modified India-ink immunoreaction test we were able to test the entire colony for antibodies to Encephalitozoon cuniculi. The prevalence of the disease was approximately 5%. All seropositive animals were culled, and another test of the entire colony, carried out 4 weeks later, revealed one seropositive rabbit which was also culled. Two subsequent screenings of the whole colony have shown no further seropositive animals.

Animals↗
PubMedDate not supplied

Diagnostic approaches for Encephalitozoon infections in patients with AIDS.

In conclusion, at the current time the most important task of the laboratory for proper clinical management of the patient with microsporidiosis is to perform genus-level diagnosis of the agent, i.e. distinguishing Encephalitozoon sp. infection from other microsporidial agents including Septata, Enterocytozoon, Nosema, and Pleistophora. This can be performed in any well-equipped pathology department with access to electron microscopy. If species identification is desired, we currently recommend consultation with one of several laboratories specializing in this area until diagnostic reagents become more widely available.

AIDS-Related Opportunistic Infections↗
PubMed1996

Autopsy verification of Encephalitozoon intestinalis (microsporidiosis) eradication following albendazole therapy.

Microsporidian infections are increasingly recognized as an important cause of morbidity for persons infected with the human immunodeficiency virus. Encephalitozoon (formerly Septata) intestinalis is a recently described microsporidian that causes intestinal and disseminated infections in severely immunocompromised patients with acquired immunodeficiency syndrome. Several studies suggest that albendazole is an effective therapy for E intestinalis infection. However, relapses of symptoms and reappearance of microsporidian spores in diagnostic specimens have been reported following treatment in some cases. Because these results are based on examination of feces or cytologic specimens with an inherent sampling bias, it would be ideal to have autopsy data on the complete tissue evaluation of major organ systems of patients who had antemortem E intestinalis infection treated with albendazole. This report describes an acquired immunodeficiency syndrome patient with diarrhea and wasting syndrome associated with E intestinalis infection. Treatment with albendazole produced relief of his clinical symptoms and eliminated microsporidian spores in his feces. Following his death from other causes, an autopsy was performed. Comprehensive microscopic examination of all major organs revealed no evidence of residual microsporidian infection, suggesting parasitologic cure of E intestinalis with albendazole. The postmortem finding of complete clearance of microsporidia from body tissues is significant for future albendazole treatment of patients infected with E intestinalis and provides strong support for the value of the autopsy in evaluating the therapeutic efficacy of antimicrobials in emerging infections.

Acquired Immunodeficiency Syndrome↗
PubMed2005

Uptake of Encephalitozoon spp. and Vittaforma corneae (Microsporidia) by different cells.

Microsporidia are obligate intracellular parasites infecting a broad range of vertebrates and invertebrates. Various microsporidian species induce different clinical pictures in humans. The reason for this is not clear. It has been speculated that the different microsporidian species are transmitted by various routes, thus causing infections in different organs. Another possibility is that the diverse microsporidia have different tropisms to organ-specific cells, thus causing various diseases. In this study, we investigated the uptake of microsporidian spores by different cells with an immunofluorescence staining technique to investigate whether there is a difference between microsporidian species as well as between different cells. Using this technique, we were able to distinguish between intra- and extracellular microsporidian spores. All examined cell lines were able to internalize microsporidian spores, but the extent of internalization differed significantly between the cells. Although the results showed some patterns that correlate with the distribution of the parasites in humans, the different clinical pictures cannot be sufficiently explained by this phenomenon, so it seems more likely that the various clinical manifestations caused by the different microsporidian species are a consequence of different infection routes rather than of different affinities of the microsporidian species to different cells.

Animals↗