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Results for “Encephalitozoonosis”

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At least 19 recordsLinked to original sources

PubMed1999

Lethal encephalitozoonosis in cyclophosphamide-treated rabbits.

Encephalitozoonosis is an opportunistic infection in animals and humans. Its clinical form is observed in immunosuppressed hosts. We studied the occurrence of the manifest form of rabbit microsporidiosis under cyclophosphamide immunomodulation in 40 New Zealand rabbits. The experimental animals were intraperitoneally infected with 5 x 10(7) Encephalitozoon cuniculi spores. Two weeks after infection the animals were treated intraperitoneally with cyclophosphamide, first with 50 mg/kg and then with 15 mg/kg weekly during the 12-week experimental period. Positive controls were either E. cuniculi-infected or cyclophosphamide-immunosuppressed animals. The negative control rabbits remained untreated. Both clinical signs of encephalitozoonosis and depression of peripheral blood cell count developed between weeks 4 and 6 in the experimental animals which died during week 6 of the experiment. No clinical signs compatible with encephalitozoonosis were observed in any of the controls. The results suggest that immunosuppression induced by cyclophosphamide can give rise to a lethal form of encephalitozoonosis.

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PubMed1997

Bovine leukemia virus-induced clinical signs and morphological changes of encephalitozoonosis in rabbits.

Fourteen three-month-old rabbits spontaneously-infected with the microsporidium Encephalitozoon cuniculi Levaditi, Nicolau et Schoen, 1923 were inoculated intravenously with lymphocytes (Ly) from seropositive bovine leukemia virus infected cattle (Ly/BLV) or with fetal lamb kidney cells infected with bovine fetal leukemia (FLK/BLV). Thirteen rabbits were seropositive to BLV at least for a period of three months. Six rabbits died of pulmonary lesions. Chronic inflammatory lesions of encephalitozoonosis were found in six rabbits killed between 454 and 548 days of the observation period. Five animals bore subcutaneous granulomas. Immunohistochemically, E. cuniculi was demonstrated in the inflammatory lesions of rabbits studied. Control animals also spontaneously infected with E. cuniculi did not show clinical signs of encephalitozoonosis. Morphological changes were found incidentally in the form of small glial foci and focal interstitial nephritis in these animals. The combined action of BLV-E. cuniculi on the bodies of rabbits is proposed as a suitable model for the study of encephalitozoonosis in man with human immunodeficiency virus (HIV) infection.

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PubMed2002

Serological investigation of canine encephalitozoonosis in Norway.

Encephalitozoon cuniculi, a microsporidian parasite of vertebrates, is considered a health risk to AIDS patients and other immunocompromised human beings. In most hosts, infection with the parasite runs a subclinical course. In some carnivore species, however, clinical disease affecting whole litters arises from intrauterine transmission of the parasite. In both blue foxes ( Alopex lagpus) and dogs ( Canis familiaris), outbreaks of encephalitozoonosis can be severe. Canine encephalitooonosis has been reported from various parts of the world, including South Africa and the United States. In Norway, there have been large outbreaks of the disease in blue fox farms, affecting also mink, but there have been no reports of encephalitozoonosis in dogs. Infection in dogs would represent a zoonotic problem, due to the close social relationship between dog and man. The purpose of the present study was to investigate the possible occurrence of E. cuniculi infection in Norwegian dogs by serological methods. In the study, 1,104 canine serum samples, originally submitted for biochemical analysis by veterinary practitioners throughout Norway, were screened by enzyme-linked immunosorbent assay for antibodies to E. cuniculi. Samples from 237 of the dogs were tested also by the indirect fluorescent antibody test. All samples were concluded as negative. The results indicate that the likelihood of occurrence of E. cuniculi infection in Norwegian dogs is small.

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PubMed2006

Diagnosis and manifestation of encephalitozoonosis in mice after experimental infection with different species and application of dexamethasone.

Twenty-eight BALB/c mice were infected with different strains of Encephalitozoon species (Encephalitozoon cuniculi II - mouse type, E. cuniculi III - dog type, Encephalitozoon hellem, Encephalitozoon intestinalis). Five of them were infected with E. cuniculi II (mouse type) and simultaneously immunosuppressed with dexamethasone. Clinical signs of encephalitozoonosis were not remarkable. Ascites was found in two mice of dexamethasone-treated group 14 days post-infection (p.i.). The histopathological changes were found mainly in spleen and liver in the form of lymphoepithelioid granuloma. Spores were found in faeces since day 14 p.i. and visualized by Calcoflour White M2R. After cultivation on cellular cultures (VERO E6 - monkey kidney cells, RK-13 - rabbit kidney fibroblasts), the species differentiation was performed by PCR using panmicrosporidial primers (PMP1, PMP2) and specific primers (ECUN-F, ECUN-R, V1, SI-500). The differences were recorded in the immune response of immunocompetent and immunosuppressed mice. At day 60 p.i., the titres of specific antibodies measured by indirect immunofluorescence antibody test were lower (1:4096) in dexamethasone-treated mice when compared with non-immunosuppressed animals (1:8196). The significant increases of antibody titres were recorded in particular infected groups within the experiment (P < 0.01 between day 14 p.i. and day 30 p.i., P < 0.001 between day 14 p.i. and day 60 p.i.). Experimental encephalitozoonosis in non-immunosuppressed and immunosuppressed mice provides a useful model for the study of immune response and lesions associated with these protozoans.

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PubMed2006

Disseminated encephalitozoonosis in captive, juvenile, cotton-top (Saguinus oedipus) and neonatal emperor (Saguinus imperator) tamarins in North America.

Disseminated encephalitozoonosis was diagnosed in 2 sibling, juvenile, cotton-top tamarins (Saguinus oedipus) and 3 sibling, neonatal, emperor tamarins (S. imperator) by use of histologic examination, histochemical analysis, electron microscopy, and polymerase chain reaction (PCR) analysis with nucleotide sequencing. All tamarins were captive born at zoos in North America and died with no premonitory signs of disease. The main pathologic findings were myocarditis (4/5), hepatitis (3/5), interstitial pneumonia (3/5), skeletal myositis (3/5), meningoencephalitis (2/5), adrenalitis (2/5), tubulointerstitial nephritis (1/5), myelitis (1/5), sympathetic ganglioneuritis (1/5), and retinitis (1/5). Central nervous system lesions were the most prominent findings in cotton-top tamarins. The inflammation was predominantly lymphocytic and suppurative in cotton-top tamarins, whereas emperor tamarins had granulomatous or lymphoplasmacytic lesions. Intralesional periodic acid-Schiff-, gram-, or acid-fast (or all 3)-positive, oval-to-elliptical shaped organisms were found in 1 cotton-top and the 3 emperor tamarins. By electron microscopy, these organisms were consistent with microsporidia of the genus Encephalitozoon. E. cuniculi genotype III was detected by PCR analysis and sequencing in paraffin-embedded brain, lung, and bone marrow specimens from the cotton-top tamarins. Although PCR results were negative for one of the emperor tamarins, their dam was seropositive for E. cuniculi by ELISA and Western blot immunodetection. These findings and recent reports of encephalitozoonosis in tamarins in Europe suggest that E. cuniculi infection may be an emerging disease in callitrichids, causing high neonatal and juvenile mortality in some colonies. The death of 2 less than 1-day-old emperor tamarins from a seropositive dam supports the likelihood of vertical transmission in some of the cases reported here.

Adrenal Glands↗

PubMed1977

Diagnosis of experimental encephalitozoonosis in rabbits by complement fixation.

A complement-fixation (CF) test has been developed for detection of experimental encephalitozoonosis in rabbits. The antigen consisted of disrupted homogenates of Encephalitozoon cuniculi spores grown in and released from rabbit choroid plexus tissue culture cells. The test was sensitive and capable of detecting experimental encephalitozoonosis in rabbits as early as 15 days after intracerebral infection. The test was specific for infected animals, and no cross-reactivity was demonstrated between E. cuniculi antigen and Nosema apis, Trypanosoma congolese, Trypanosoma cruzi, rabbit liver powder, rabbit brain powder, and rabbit choroid plexus cell culture. Sera from rabbits infected with Toxoplasma gondii, Eimeria stiedai, and Eimeria perforans did not exhibit antibodies to E. cuniculi. No CF-inhibition activity was detected.

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PubMed1977

The india-ink immunoreaction: a method for the rapid diagnosis of encephalitozoonosis.

Sera from 37 rabbits were assayed for antibodies against Encephalitozoon cuniculi (Nosema cuniculi) by the india-ink immunoreaction and the indirect fluorescent antibody tests: all animals seropositive to the former were also positive to the latter test. 27 of the rabbits were also tested for skin hypersensitivity and then autopsied. Animals positive to the skin test were also positive to the serological tests. At autopsy 18 of 22 rabbits positive in the immunological tests showed lesions typical of encephalitozoonosis. Sera from 200 rabbits originating from 6 institutes were assayed by the india-ink test: seropositive rabbits were found from all institutes (9.1 to 81.9% incidence), with serum titres ranging from 1:125 to 1:5000. The india-ink test appears to be a rapid and convenient method for diagnosis of encephalitozoonosis in rabbits.

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PubMed1990

Brain and spinal cord lesions in encephalitozoonosis in mink.

Central nervous system lesions were studied by light microscopy in 43 farmed mink, aged 5 months to 2 1/2 years, with spontaneous encephalitozoonosis and showing cataractous eye changes. Lesions were found in the brain and spinal cord of all animals examined but were generally mild and chronic. The lesions were consistent with those previously described in spontaneous encephalitozoonosis in other carnivores. Parasites in parasitophorous vacuoles and free or phagocytosed in necrotic and granulomatous lesions were demonstrated in animals aged 5 months to 1 year. The occurrence of arterial lesions of the polyarteritis nodosa type found in the youngest animals probably indicates fetal infection. In animals aged 1 1/2 and 2 1/2 years active lesions were usually lacking and the changes were characterized by arterial sclerosis, sometimes with aneurysmal formations, small perivascular lympho-plasmacytic cuffings and focal gliosis.

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PubMed1986

Evaluation of kidney function in dogs suffering from canine encephalitozoonosis by standard clinical pathological and radiopharmaceutical techniques.

Canine encephalitozoonosis can be responsible for a severe renal disease in dogs which may develop into progressive, irreversible kidney failure. Three pure-bred Boxer littermates with confirmed encephalitozoonosis were subjected to sequential clinical pathological tests and renal biopsies. The endogenous serum creatinine and urea levels showed an initial temporary reduction but later increased steadily. The phenolsulphonphthalein retention test confirmed this end-stage renal disease. Initial hyper-gamma globulinaemia showed a rapid decline. Urinalysis was an indicator of chronic renal disease and the kidney biopsies confirmed progressive irreversible kidney lesions. Evaluation of sequential tests are advocated for the setting of a prognosis. The radiopharmaceutical techniques employed proved to be sensitive indicators of renal dysfunction and a means of evaluating the function of the left and right kidney separately.

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PubMed1977

Diagnosis of encephalitozoonosis in experimentally infected rabbits by intradermal and immunofluorescence tests.

The indirect immunofluorescence antibody test was performed on serial blood samples from eight young New Zealand White rabbits with experimental encephalitozoonosis. The test showed seroconversion in six of the eight infected rabbits by the 8th day after inoculation and in all rabbits by the 15th day. Antibody titers reached a peak by about the 36th day after inoculation and remained significantly elevated until the termination of the experiment at 84 days after inoculation. None of four sham-inoculated rabbits showed an immunofluorescence response by the 60th day after inoculation. Immunofluorescence and intradermal test responses were compared before infection and at the 60th day after inoculation in a total of 32 experimentally infected rabbits. Both tests were equally effective (100%) in detecting infected animals. Six of eight (first group) and 22 of 24 (second group) experimentally infected rabbits were confirmed histologically to have lesions compatible with encephalitozoonosis. No cross reactions were observed between Encephalitozoon cuniculi and Toxoplasma gondii, Eimeria perforans, or Eimeria stiedai by intradermal test or immunofluorescence test.

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PubMed1978

Serological and histological studies on adult rabbits with recent, naturally acquired encephalitozoonosis.

Twenty adult rabbits were killed two to 12 weeks after antibodies to Encephalitozoon cuniculi were first detected in their sera. Specimens of urine were examined for E cuniculi and sections of kidneys and brains were examined both for organisms and lesions consistent with encephalitozoonosis. Organisms were observed in the kidneys from two weeks after the appearance of antibodies, and histological lesions in the kidneys were observed after five weeks. However, organisms were rarely seen in the brain and lesions in this organ were infrequent and, generally, not present until at least eight weeks after the first detectable antibody. The results indicate the course of natural infection of encephalitozoonosis in rabbits and show that serology is the most sensitive procedure for its early diagnosis.

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PubMed1978

Light and electron microscopical studies on canine encephalitozoonosis: cerebral vasculitis.

Brain lesions in 2 natural cases of canine encephalitozoonosis were studied by light and electron microscopy. Granulomatous reactions, associated with small vessels and capillaries, partly originated from extensive perithelial cell proliferation which ultimately produced the epithelioid cell component. Diffuse glial reactions apparently occurred in relation to the vasculitis. Lymphoid cells infiltrated the epithelioid and glial cell inflammation. Encephalitozoon in all its reproductive stages was identified as the aetiological agent, and ultrastructurally differentiated from Nosema on the basis that a single nucleus was observed. Viable organisms were present only within endothelial cells. Macrophages containing dead spores were usually seen around parasitized vessels and, less frequently, in the neuropil. Organisms, whether viable or non-viable, were never seen extracellularly at the ultrastructural level. Selected histochemical stains and electron microscopy were used to differentiate between viable and non-viable spores. Vasculitis is demonstrated as the underlying lesion of canine encephalitozoonosis affecting the brain and is suggested to be the basic factor in the pathogenesis of this disease.

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PubMed1997

Catecholamines and encephalitozoonosis in rabbits.

Twenty four rabbits (Oryctolagus cuniculus f. domestica) were used to detect specific anti-Encephalitozoon cuniculi antibodies. To identify microsporidian infection, a haemolytic test in agar gel was carried out. Blood samples of animals with and without spontaneous encephalitozoonosis were evaluated, and compared for the presence of epinephrine (EPI), norepinephrine (NE), and dopamine (DA). Rabbits infected spontaneously with E. cuniculi had significantly lower levels of catecholamines than healthy animals. This decrease in catecholamines is of special interest because of their role as factors modifying the immune response. These neuromediators also have different influences on the function of immune cells.

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PubMed2002

Fox encephalitozoonosis: isolation of the agent from an outbreak in farmed blue foxes (Alopex lagopus) in Finland and some hitherto unreported pathologic lesions.

The farmed blue fox (Alopex lagopus) is particularly susceptible to congenital infections of the microsporidian species Encephalitozoon cuniculi. This report is based on an outbreak of the disease in Finland with high mortality. Five pups (four males and one female) with prolonged disease were examined. The pups had moderate pathological alterations in the kidneys and mild lesions were found in the brains, hearts, salivary and prostatic glands. Diagnosis of E. cuniculi infection was made from serological tests (ELISA, CIA, IFAT), and by in vitro isolation of the parasite from the brain of all five pups investigated. The identity was confirmed by molecular means as E. cuniculi strain II ('mouse strain'). Novel histopathological lesions not described as yet in fox encephalitozoonosis are presented. These include cerebral infarction and necrotizing inflammation of the renal pelvis. The sources and mechanisms of spreading of E. cuniculi to blue foxes are discussed.

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PubMed2001

Isolation of Encephalitozoon cuniculi using primary tissue culture techniques from a rabbit in a colony showing encephalitozoonosis.

Encephalitozoon spores were isolated in a primary tissue culture of the kidneys from an encephalitozoonosis-suspected rabbit in a municipal zoo in Hokkaido. The isolated spores were morphologically characteristic of microsporidial ones in chromotrope stain, and proven to be E. cuniculi by a polymerase chain reaction (PCR) with a species-specific primer set and by direct DNA sequencing of the PCR products.

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PubMed1992

Extraglomerular lesions in kidneys of mink with encephalitozoonosis.

Extraglomerular renal lesions were studied by light and electron microscopy in 13 farmed mink which showed cataractous eyes associated with spontaneous encephalitozoonosis. The extraglomerular renal lesions consisted of multiple renal cysts, multifocal-to-coalescing interstitial nephritis and vasculitis. Tubular cysts of varying size were present in the corticomedullary junction and medulla. The inflammatory infiltrates were composed mostly of lymphocytes and plasma cells and usually accompanied an interstitial fibrosis. Vasculitis, perivasculitis and sclerotic arteries were frequently seen.

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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.

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PubMed1993

Mesangioproliferative glomerulonephritis in mink with encephalitozoonosis.

Renal specimens from 6 mink with encephalitozoonosis were studied by light and electron microscopy and immunohistochemistry. The glomeruli of affected kidneys had a mesangioproliferative glomerulonephritis which was characterized by an increase in mesangial cells and matrix in most glomeruli. Some glomeruli were partially or completely sclerosed. There were protein or granular casts in the cortical and medullary tubules. Interstitial nephritis, vasculitis and tubular cysts were found. Electron microscopy demonstrated extensive matrix and increased cellularity in the mesangial areas. Glomeruli showed segmentally thickened or wrinkled capillary basement membranes. Electron dense deposits were found in the glomerular basement membranes and mesangium. Peroxidase-anti-peroxidase immunohistochemistry demonstrated that IgG and IgM positive material was present as granular deposits in the glomerular basement membrane and occasionally in the mesangium.

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