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PubMed1991

Encephalitozoon infection in a still-born foal.

A stud Clydesdale foal was still-born near full term. Macroscopic examination revealed a normal placenta, pulmonary atelectasis and faint white mottling of the kidneys. Microscopically there was severe lymphoplasmacytic interstitial nephritis. Numerous organisms resembling Encephalitozoon cuniculi were present in the affected kidneys. The organisms occurred in the areas of inflammation as well as in the renal glomeruli and intracellular cysts in the renal tubular epithelial cells and exhibited Gram positive staining. Ultrastructurally the organisms possessed a polar vacuole and a spiral filament typical of Microsporidia. The organisms were not detected in sections of the other organs examined.

Animals↗
PubMed1991

The pathology of subclinical infection of Encephalitozoon cuniculi in canine dams producing pups with overt encephalitozoonosis.

The macroscopic, microscopic and clinical pathology and the serology of 2 clinically normal Staffordshire Bull Terrier bitches, both of whom produced pups with confirmed encephalitozoonosis, is described. Mild histopathological changes, similar to those seen in the infected pups, were observed. The spores of Encephalitozoon cuniculi were seen in the renal tubules of the kidney of one of the bitches. The serum urea concentrations of one of the bitches was elevated. A positive titre against E. cuniculi was obtained in both of the bitches. A 10-year-old girl who had had close contact with one of the infected litters of pups, seroconverted to E. cuniculi. Her two siblings were serologically negative.

Animals↗
PubMed1989

Serologic evidence of Encephalitozoon cuniculi infection in a colony of squirrel monkeys (Saimiri sciureus).

Five hundred seventeen serum samples obtained during 3 years from a collection of 250 squirrel monkeys were examined by indirect immunofluorescence and dot-ELISA for antibodies to Encephalitozoon cuniculi. One hundred seventy-nine monkeys were positive at least once and fifty six monkeys were positive three or more times. Older animals were more likely to be positive than young animals, but the proportion of serologically positive monkeys did not change appreciably over the 3 years. As judged by the serological evidence, infection with E. cuniculi is distributed widely in this collection of squirrel monkeys.

Animals↗
PubMed1986

The immune response in a dog to Encephalitozoon cuniculi infection.

The immune response to Encephalitozoon cuniculi infection in a dog was investigated by means of the indirect fluorescent antibody test, the leucocyte migration inhibition test and the radial immunodiffusion test for serum IgG and IgM levels. Specific antibodies were detected within 7 days of infection and they persisted for 370 days. A cell-mediated immune response was detected from Day 13 following infection until Day 97. Histopathological examination showed plasma cell infiltration of the kidneys, meninges, lung, bladder, smooth muscle and spleen.

Animals↗
PubMed1986

Can Encephalitozoon cuniculi cross the placenta?

Laboratory rabbits and mice were challenged with Encephalitozoon cuniculi at three different stages of gestation to determine whether the parasite crosses the placenta. No transplacental transmission could be demonstrated.

Animals↗
PubMed1988

The relationship in dogs between primary renal disease and antibodies to Encephalitozoon cuniculi.

Fifty-two serum samples from dogs with primary renal failure were tested for antibodies to Encephalitozoon cuniculi. Twelve were positive as compared to two positive samples from a control group of 42 dogs. There was a statistically significant difference between these two groups which suggests an association between infection with E. cuniculi and the development of chronic renal disease.

Animals↗
PubMed1988

Dot enzyme-linked immunosorbent assay (dot ELISA) for antibodies to Encephalitozoon cuniculi.

A dot-ELISA procedure was developed to detect antibodies against Encephalitozoon cuniculi. Sera from 84 rabbits, 22 dogs, 18 squirrel monkeys and 200 mice were tested by dot-ELISA and most also were tested by immunofluorescence. Comparison of the two tests showed that there was excellent agreement of the results (Kappa values greater than or equal to 0.74) in all four species. Dot-ELISA is a simple, quantitative, rapid alternative to immunofluorescence when large numbers of serum samples must be evaluated.

Animals↗
PubMed1988

Encephalitozoon cuniculi infection in MRL/MPJ-LPR (lymphoproliferation) mice.

Experiments were conducted to determine (a) whether mice bearing the single autosomal recessive gene lpr (lymphoproliferation) are more susceptible to encephalitozoonosis than syngeneic mice without the lpr gene and (b) whether infection with Encephalitozoon cuniculi in autoimmune MRL/MPJ mice accelerates and/or exacerbates the development of hypergammaglobulinemia, a manifestation of encephalitozoonosis in dogs and foxes. The results suggested that the lpr gene does not influence susceptibility to murine encephalitozoonosis. Infection with E. cuniculi changed neither the onset nor the severity of the spontaneous, age-related hypergammaglobulinemia in MRL/MPJ mice. Hypergammaglobulinemic lpr mice with encephalitozoonosis did not develop more severe lesions than lpr mice without encephalitozoonosis nor was their death accelerated.

Animals↗
PubMed1988

The influence of Encephalitozoon cuniculi on neural tissue responses to implanted biomaterials in the rabbit.

Laboratory rabbits are commonly used for testing the tissue response of neural device biomaterials. Rabbits of many colonies in the U.S. are infected by the intracellular microsporidian parasite, Encephalitozoon cuniculi, with rates of infection ranging from 15 to 76% (1). Several authors have suggested that infection by this parasite may alter immune system response and experimental results. We report that infection by E. cuniculi made the interpretation of results more difficult and altered the animals' responsiveness to implanted platinum wires coated with various polymers such as glow discharge methane, Parylene C, or polyimide. Edema, neuronal and glial reaction, and inflammatory responses to the coated wires were quantitated at four sites in each animal. Inconsistency of response in all measured parameters was found, both between animals and between sites in infected animals. Infected animals showed the greatest variability, primarily in the degree of inflammatory reaction. Parylene C was found to induce the most severe inflammatory reaction, an unexpected finding. No consistent reaction to any of the coating materials was found in this study. We believe that this variability in response was primarily due to infection by E. cuniculi. Our results suggest that rabbits should not be used for tissue compatibility testing of neural device biomaterials until the animals are free of E. cuniculi infestation as demonstrated by serologic screening.

Animals↗
PubMed1984

Mechanisms of resistance to the intracellular protozoan Encephalitozoon cuniculi in mice.

Mechanisms of resistance to the obligate intracellular protozoan Encephalitozoon cuniculi were studied in BALB/c mice. Resistance to lethal disease was T cell-dependent because transfer of T-enriched, but not T-depleted, spleen cells from sensitized BALB/c donors would protect infected BALB/c-nu mice. A modified focus-forming assay was utilized to measure effects on E. cuniculi infectivity in vitro. The results show that antibodies exert an opsonization effect and may block parasite entry into nonphagocytic cells. No cytotoxic T cells were demonstrated. Supernatants from E. cuniculi-sensitized spleen cells incubated with E. cuniculi in vitro could induce adherent PEC to kill E. cuniculi.

Animals↗
PubMed1982

Infections with Encephalitozoon cuniculi and Leptospira interrogans, serovars grippotyphosa and ballum, in a kennel of foxhounds.

Leptospira interrogans serovars grippotyphosa and ballum were isolated from kidney and urine of an American Foxhound pup. The pup was from a litter of 12, all of which were unthrifty. Titers for serovar grippotyphosa in pups from the litter ranged from 200 to 6,400 and 23 of 36 adult dogs in the kennel had titers to that serovar. None of the sera was tested for antibodies to serovar ballum. Leptospires were not isolated from or observed in 2 littermates and 1 penmate, but gram-positive organisms morphologically compatible with Encephalitozoon cuniculi were detected in their brains and kidneys.

Animals↗
PubMed1993

Prophylactic and therapeutic immune reconstitution of SCID mice infected with Encephalitozoon cuniculi.

Severe combined immunodeficient (SCID) mice develop lethal infections, resembling opportunistic microsporidiosis of immunocompromised patients, after intraperitoneal (i.p.) inoculations of spores of Encephalitozoon cuniculi. In the present study, SCID mice reconstituted i.p. with 5 x 10(7) spleen cells from naive adult BALB/c mice 14 days prior to the i.p. injection of 10(7) spores were completely resistant to the infection, whereas control infected SCID mice developed clinical disease and died within 17 days post infection (DPI). In another experiment, SCID mice infected i.p. with 10(7) spores of E. cuniculi and after that (on DPI 7) injected i.p. with 5 x 10(7) spleen lymphocytes isolated from immune adult BALB/c mice were partially protected against the parasite (40% of the reconstituted mice survived). In both experiments, high levels of parasite-specific serum antibodies (mostly of the IgG-isotype) were detected in the infected immunocompetent BALB/c mice, whereas virtually no antibodies were found in the infected SCID mice. However, SCID mice reconstituted with either naive spleen cells or immune lymphocytes revealed humoral immune responses comparable with those of immunocompetent mice.

Animals↗
PubMed1994

[Natural transmission of microsporidia (Encephalitozoon cuniculi) by way of the chicken egg].

100 chicken embryos were examined for naturally occurring infections with Encephalitozoon cuniculi (E.c.). Two embryos were found to be dead, the others were killed at an age of 18 days. Samples from the oesophagus, intestine, liver, kidneys, heart and brain were collected and examined by immunohistochemical methods. E.c. was found in about 40% of the embryos. This microsporidian was observed in all organs, particularly, however, in the oesophagus, intestine, brain and heart. The number of E.c. was significantly larger in the two embryos that died than in the others. The investigations demonstrated, that E.c. may be transmitted naturally to the chicken egg. Further, the results suggested that E.c. may be a cause of death in chicken embryos. In most cases, however, E.c. infections are inapparent in embryos. Such inapparent infections may be an important way of contamination of chicken production units with E.c.

Animals↗
PubMed1993

[Naturally-acquired microsporidia (Encephalitozoon cuniculi) infections in hens].

During a short period of time, four approximately ten months old chickens from an egg production (group A) unit developed symptoms of apathy, lameness, mild diarrhoea and loss of weight. The layers were killed and submitted for necropsy. For the first time, microsporidia infection, probably Encephalitozoon cuniculi (E.c.) was diagnosed in chickens. The diagnosis was mainly based on immunohistochemical methods. E.c. was found particularly in the cells of the cutaneous mucous membrane of the crop and in epithelial cells, the cells of the propria mucosae and the smooth muscle cells of the small intestine. E.c. also frequently occurred in the fibres of the skeletal muscle. Intracellularly, E.c. and its development stages were located primarily in the cytoplasm and less frequently in the nucleus of cells. Retrospective investigations on tissue samples from a domestic cock and 9 hens by immunohistochemical methods also revealed occurrence of this microsporidian. The results showed that in chickens E.c. infections can cause multi-symptomatic illness but may also be clinically inapparent.

Animals↗
PubMed1995

[A case of disseminated Encephalitozoon intestinalis microsporidiosis in an AIDS patient in Nîmes].

The pathogene's role importance of the microsporidia in nature is considerable. The human being, easily in contact, presents clinical manifestations only with some of them and in a very occasional manner. The increased frequency of the immunodepression has permitted to describe recently a new protozoon, Encephalitozoon intestinalis (alias Septata intestinalis) of the family of the Glugeidae and the human illness of which it is the agent. This parasitose is interesting to be presented because of its rarity and its circulation to organs far from one another. The diagnostic has been done thanks to the only optic microscope and confirmed from its visible efficacity of one cure of albendazole. The pyrimethamine could present a relative efficiency on a relapse of the sinusitis.

Acquired Immunodeficiency Syndrome↗
PubMed1996

Specific detection of the microsporidia Encephalitozoon intestinalis in AIDS patients.

The microsporidia Encephalitozoon intestinalis is an opportunistic pathogen responsible for severe gastrointestinal diseases and disseminated infection in AIDS patients. No light-microscopical method allows the specific detection of this unicellular parasite and up to this date, only electron microscopy could confirm the diagnosis of the species. We propose a method combining the non specific labelling of microsporidian spores by the fluorochrome Uvitex 2B and an indirect immunofluorescent assay with a polyclonal antibody specifically directed against E. intestinalis. Preliminary data demonstrate the specificity of this antibody. This method enables the distinction between E. intestinalis and Enterocytozoon bieneusi an other microsporidian also associated with gastrointestinal infection. Due to the precocious detection of E. intestinalis patients will be treated earlier with albendazole which is potentially active against this species.

Acquired Immunodeficiency Syndrome↗
PubMed1995

Septata intestinalis and Encephalitozoon cuniculi: cross-reactivity between two microsporidian species.

An infection with Septata intestinalis was diagnosed in a 35-year-old AIDS patient without diarrhoea. The diagnosis was based on morphological examinations of a duodenal biopsy specimen. Serum antibodies were detected reacting with spores of Encephalitozoon cuniculi. Spores of S. intestinalis and E. cuniculi stained with Brown Hopps Gram stain showed a red colour (Gram negative) and not a blue/black colour which was described for microsporidian spores in tissue.

AIDS-Related Opportunistic Infections↗