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PubMed1975

Interactions between Encephalitozoon cuniculi and macrophages. Parasitophorous vacuole growth and the absence of lysosomal fusion.

Encephalitozoon cuniculi grow within ever-increasing parasitophorous vacuoles (PV) in peritoneal macrophages. The PV boundary membrane conforms to a rich arrangement of blebs; similar, but free vesicles were observed within the PV space. An iron dextran-concanavalin A marker was used to express visually clustered distributions of Con A receptors on the PV boundary blebs and free vesicles; no marker was observed on other membrane surfaces within the PV. These results, combined with the observation that the PV grows while the host cytoplasm decreases in mass, implicate the PV boundary blebs of interiorizing into vesicles by a pinocytic mechanism. Phagocytic vacuoles, secondary lysosomes and pinocytic vesicles were labeled by incubating infected macrophages in minimum essential medium with ferritin. Ferritin readily accumulated in secondary lysosomes and phagocytic vacuoles; however, ferritin was excluded from parasitophorous vacuoles containing E. cuniculi. Acid phosphatase cytochemical reaction product was observed in lysosomes and phagocytic vacuoles; however, parasitophorous vacuoles with vegetative E. cuniculi were always negative.

Acid Phosphatase↗
PubMed1981

The ultrastructure of Encephalitozoon cuniculi growing in renal tubules of rabbits.

A wild type rabbit infected orally with cell culture-grown Encephalitozoon cuniculi. Twelve weeks after infection the rabbit was killed and blocks of kidney tissue were fixed for histology and electron microscopy. E. cuniculi were observed within kidney collecting tubule cells. The ultrastructure and development of E. cuniculi in these cells was similar to that described in cultured cells and peritoneal macrophages.

Animals↗
PubMed2004

Phylogenetic analysis of the complete genome sequence of Encephalitozoon cuniculi supports the fungal origin of microsporidia and reveals a high frequency of fast-evolving genes.

Microsporidia are unicellular eukaryotes living as obligate intracellular parasites. Lacking mitochondria, they were initially considered as having diverged before the endosymbiosis at the origin of mitochondria. That microsporidia were primitively amitochondriate was first questioned by the discovery of microsporidial sequences homologous to genes encoding mitochondrial proteins and then refuted by the identification of remnants of mitochondria in their cytoplasm. Various molecular phylogenies also cast doubt on the early divergence of microsporidia, these organisms forming a monophyletic group with or within the fungi. The 2001 proteins putatively encoded by the complete genome of Encephalitozoon cuniculi provided powerful data to test this hypothesis. Phylogenetic analysis of 99 proteins selected as adequate phylogenetic markers indicated that the E. cuniculi sequences having the lowest evolutionary rates preferentially clustered with fungal sequences or, more rarely, with both animal and fungal sequences. Because sequences with low evolutionary rates are less sensitive to the long-branch attraction artifact, we concluded that microsporidia are evolutionarily related to fungi. This analysis also allowed comparing the accuracy of several phylogenetic algorithms for a fast-evolving lineage with real rather than simulated sequences.

Animals↗
PubMed1980

An investigation of Encephalitozoon cuniculi in the wild rabbit Oryctolagus cuniculus in Victoria, Australia.

Sera from 823 wild rabbits (Oryctolagus cuniculus) collected from a number of geographic regions of Victoria, Australia over the past eight years were examined for antibodies to Encephalitozoon cuniculi, along with sera from 46 hares (Lepus europaeus) (Pallas) and 57 New Zealand wild rabbits. No sera were positive, implying that this common laboratory rabbit parasite is absent from wild rabbits in these areas. However, wild rabbits were found to be readily infected by the oral route with small numbers of tissue-culture-grown spores of E. cuniculi. A possible explanation for the absence of encephalitozoonosis in wild rabbits is that E. cuniculi infection places them at a biological disadvantage for survival. The natural hygiene habit of wild rabbits may also significantly decrease post-natal infection.

Animals↗
PubMed1997

Diagnosis of infections caused by Enterocytozoon bieneusi and Encephalitozoon intestinalis using polymerase chain reaction in stool specimens.

OBJECTIVE: To study the usefulness of polymerase chain reaction (PCR) for the species identification of microsporidia in stool specimens obtained from HIV-infected patients with Enterocytozoon bieneusi or Encephalitozoon intestinalis infections. SETTING: Infectious disease clinic in a university hospital. PATIENTS: Thirty-seven stool specimens from 29 HIV-infected patients with microsporidiosis were tested. The diagnosis of microsporidian infection was made by light microscopy of stool specimens and species identification was made by transmission electron microscopy of duodenal biopsies. Sixty-one stool specimens from 45 HIV-infected patients without microsporidiosis served as controls. METHODS: PCR was performed using DNA extracted from stools with two primers sets, one specific for E. bieneusi and one specific for E. intestinalis. RESULTS: A 1265 base-pair fragment of the small subunit ribosomal RNA (rrs) gene could be amplified from all 31 stool specimens infected with E. bieneusi. In addition, a 930 base-pair fragment of the rrs gene could be amplified from all six stool specimens infected with E. intestinalis. The 61 control stools were negative with both primers. CONCLUSIONS: These results suggest that a PCR based assay using species-specific primers sets can be used successfully for microsporidian species differentiation from stool specimens, thus obviating the need for invasive biopsy procedures.

AIDS-Related Opportunistic Infections↗
PubMed1975

Encephalitozoon sp. in the blue-masked lovebird, Agapornis personata (Reichenow): first confirmed report of microsporidan infection in birds.

A microsporidan tentatively classified as Encephalitozoon sp. on the basis of structure and tinctorial qualities was identified in tissues from a group of blue-masked lovebirds. Agapornis personata (Reichenow). The organism was present in renal tubular epithelial cells, hepatocytes, bile duct epithelial cells, and intestinal epithelial cells. Focal hepatic necrosis occurred around clusters of the organisms but inflammation was minimal or absent in the other infected tissues. Attempts to infect laboratory mice with the organism were unsuccessful. Ultrastructural features were compared with those of E. cuniculi of mammals.

Animals↗
PubMed1979

An investigation of the route and progression of Encephalitozoon cuniculi infection in adult rabbits.

Rabbits infected either orally or intratracheally with cell culture-grown Encephalitozoon cuniculi were monitored regularly for serum antibody levels and E. cuniculi in the urine. Their responses were compared with intravenously inoculated and uninoculated control rabbits. All rabbits receiving E. cuniculi developed serum antibodies, generally within 3 weeks, and excreted E. cuniculi by 6 weeks. In the acute stage of infection, the organs most affected were lung, kidney and liver; the brain and gut were unaffected. However, during chronic infection, the brain, kidney, and heart were the only organs found to be involved. Antibody levels were very high at this stage. Thus both the oral and tracheal routes may be normal routes of infection with E. cuniculi in adult rabbits.

Animals↗
PubMed1980

Effect of fumagillin on in vitro multiplication of Encephalitozoon cuniculi.

Encephalitozoon cuniculi (Levaditi, Nicolau & Schoen) is an obligate intracellular pathogenic parasite of rabbits, carnivores, laboratory rodents, and a variety of other mammals. Cell cultures of rabbit and canine cells were infected with rabbit and dog isolates of E. cuniculi. Four days later 5 microgram/ml of fumagillin was introduced into the culture medium. The multiplication of the parasite was inhibited within 48 h and this effect was maintained as long as the antibiotic remained in the medium. There was no effect when spores and proliferative forms of the parasite were incubated with fumagillin before being used for infecting host cells. No infection occurred, however, if the antibiotic was added to the culture medium before introduction of E. cuniculi. On electron-microscopic examination, the treated parasites were found to have severe cytoplasmic swelling, vesicular distortion of the plasma membrane, and marked reduction in cytoplasmic ribosomes. it was concluded that fumagillin blocks multipliation of E. cuniculi in vitro. The drug may be useful for the treatment or prevention of spontaneous encephalitozoonosis.

Animals↗
PubMed1977

Altered immune responsiveness associated with Encephalitozoon cuniculi infection in rabbits.

The variation in immune response of two unrelated colonies of laboratory rabbits to high doses of heat-killed Brucella abortus strain 19 was investigated. One was a mixed-breed, multicolored colony in which a high prevalence of encephalitozoonosis had been recorded, whereas the other rabbits were derived from a colony of Dutch-marked specific-pathogen-free rabits. Although considerable variation in the immune response between individual rabbits was noticed at all bleeds, rabbits infected with Encephalitozoon cuniculi showed, on comparison with uninfected rabbits from either colony, a depressed immunoglobulin G response from week 5 of the antigen injection schedule and, from week 8, an elevated immunoglobulin M response.

Animals↗
PubMed1978

Encephalitozoon cuniculi antibodies in a specific-pathogen-free rabbit unit.

We describe our discovery of Encephalitozoon cuniculi antibodies in a specific-pathogen-free rabbit colony. Small-sized samples had failed to reveal the presence of infection with a prevalence of about 5%. Using an India ink immunoreaction test by which we were able to visualize both negative and positive reactions, we were able to undertake a 100% screen of the colony of more than 700 rabbits and to repeat this 4 weeks later when we had culled the positive reactors. By collating the results of those tests with the results of tests on previously collected samples, we have been able to discuss and observe age and sex susceptibilities and the mode of transmission of the naturally occurring disease.

Aging↗
PubMed1980

Role of antibody and complement in the control of Encephalitozoon cuniculi infections by rabbit macrophages.

The capacity of mononuclear peritoneal macrophages to phagocytose Encephalitozoon cuniculi was tested in vitro. Normal rabbit serum or cell culture medium had little effect on the rate of removal of organisms by rabbit peritoneal macrophages. Treatment with immune rabbit serum or immune rabbit immunoglobulin G significantly (P less than 0.001) increased phagocytosis of E. cuniculi. Guinea pig complement was found to significantly (P less than 0.001) enhance the phagocytosis of antibody-treated E. cuniculi. With few exceptions, induced (peritoneal exudate) macrophages were no more effective than unstimulated (resident) macrophages in the phagocytosis of E. cuniculi. Secondary lysosomes labeled with ferritin were seen fusing with phagosomes containing immune rabbit serum-treated parasites. Phagosome-lysosome fusion was not observed when parasites were treated with either normal rabbit serum or culture medium. The results of the present study suggest a role for antibody enhancement of phagocytosis and intracellular killing as a mechanism of resistance to encephalitozoonosis in rabbits.

Animals↗
PubMed1991

Enteric infection with an obligate intracellular parasite, Encephalitozoon cuniculi, in an experimental model.

Rabbits were intrarectally infected with 3 doses (5 x 10(3), 5 x 10(5), and 5 x 10(7] of an obligate intracellular parasite, Encephalitozoon cuniculi, with or without prior colonic lavages. Although chronic administration of enemas seems to interfere to some degree with the intestinal translocation of the parasite, systemic infection was observed in both manipulated and nonmanipulated animals. The animals responded with antibodies of immunoglobulin A (IgA) and IgG isotypes, reflecting the route of infection. They also produced significant amounts of circulating immune complexes composed of IgA and IgG antibodies and E. cuniculi antigens. Lesions compatible with encephalitozoonosis were seen in the liver, kidney, lung, and brain. In all instances, nonmanipulated animals had more severe lesions than manipulated rabbits given the same dose of parasites. Levels of serum antibodies, circulating immune complexes, and histopathologic changes were associated with the infection dose. The presented data suggest that human microsporidiosis may also be transmitted via the rectal route. It is, therefore, of clinical relevance in view of several reports of microsporidian infections in patients with acquired immunodeficiency.

Administration, Rectal↗
PubMed1995

Disseminated Encephalitozoon (Septata) intestinalis infection in a patient with AIDS: novel diagnostic approaches and autopsy-confirmed parasitological cure following treatment with albendazole.

Encephalitozoon intestinalis is a recently described microsporidian which causes intestinal and disseminated infections in severely immunocompromised patients with AIDS. Preliminary data suggest that albendazole can be an effective therapy for patients with E. intestinalis infection. However, relapses have been reported following treatment in some cases. These results were based upon examination of cytologic, biopsy, or stool samples with an inherent sampling bias. This report documents the first postmortem evaluation of a patient with E. intestinalis infection treated with albendazole. Antemortem microsporidial diagnosis was performed on nasal mucosal smear and duodenal biopsy specimens by electron microscopy and a newly developed indirect fluorescent-antibody method based upon in vitro cultivation of the organism. This case represents the initial report of using nasal cytologic specimens for ultrastructural and antibody-based species-level diagnosis of microsporidiosis. Following successful treatment of this infection with albendazole, the patient died of other causes. A thorough autopsy examination failed to reveal the presence of E. intestinalis in any tissue, providing confirmatory evidence for a complete parasitological cure with albendazole.

Acquired Immunodeficiency Syndrome↗
PubMed1977

Isolation of Encephalitozoon cuniculi from urine samples.

Encephalitozoon cuniculi was isolated from the urine of infected rabbits using human and canine tissue cultures. The organism was isolated from 7 of 11 contaminated urines from seropositive animals. The advantages of urine over tissue as a source of E. cuniculi are that it is obtainable from living animals, can be examined for the presence of organisms, and is essentially free of cells likely to overgrow the tissue cultures used for isolation.

Animals↗
PubMed1978

The immunoperoxidase test diagnosis of Encephalitozoon cuniculi in rabbits.

Sera collected from both naturally and artificially infected rabbits were found to show excellent correlation when examined for the presence of Encephalitozoon cuniculi antibodies using the immunoperoxidase and immunofluorescence tests. Out of 85 randomly selected rabbits, 21 were found to be serologically positive using both the tests. However, lesions which could be attributed to E. cuniculi infection were only demonstrated in 16.

Animals↗
PubMed1978

Humoral immune response to infection with Encephalitozoon cuniculi in rabbits.

Parenteral administration of Encephalitozoon cuniculi induced an antibody response within 7--11 days. Peroral administration was less effective since only 2 of 6 animals showed seroconversion; they became seropositive within 14--21 days. Sera from animals which became seropositive had high antibody titres during the whole test period. Immune sera from 3 animals were fractionated by gel filtration. With the india-ink immunoreaction test, antibodies to E. cuniculi were found only in the 7S fractions, while the indirect fluorescent-antibody test detected them in fractions 19S and 7S. The 7S fractions were identified as IgG and the 19S fractions as IgM. A program for eradication of encephalitozoonosis, based on these results, is discussed.

Animals↗
PubMed1979

Sensitivity of Encephalitozoon cuniculi to various temperatures, disinfectants and drugs.

Spores of Encephalitozoon cuniculi were exposed to various temperature or to disinfectants, and their infectivity was then tested on monolayer cultures of canine kidney cells. The maximum survival time for spores suspended in medium 199 was 1 day at -20 degrees C, 98 days at 4 degrees C, 6 days at 22 degrees C, and 2 days at 37 degrees C. Only 2.5% survived 30 min at 56 degrees C. Boiling for 5 min or autoclaving at 120 degrees C for 10 min killed all spores. Dry spores survived less than a week at 4 degrees C but at least 4 weeks at 22 degrees C. Exposure for 30 min to recommended working concentrations of 9 of the 11 disinfectants tested killed all spores. The growth-inhibition effect of 7 antibiotics and chemotherapeutics was studied on canine kidney cell culture inoculated with E. cuniculi. None could completely inhibit growth. The most effective was chloroquine phosphate which, at a concentration of 12.5 mg per 1000 ml culture medium and during a test period of 8 weeks, reduced the harvest of E. cuniculi to 31% of that from inoculated, untreated cultures.

Animals↗
PubMed1979

Simple focus assay for Encephalitozoon cuniculi.

In this is vitro infectivity assay for Encephalitozoon cuniculi, lesions due to the organism appeared as macroscopically distinct foci. The number of such foci was used as a direct measure of the number of infectious units in the original sample. The expected correlation between focus-forming units and 50% infectious doses was observed in limit dilution experiments.

Cell Line↗