An Intracellular Parasite Resembling a Microsporidian Associated with Ascites in Swiss Mice

Nelson, John B.

doi:10.3181/00379727-109-27317

Cited by 33 publications

(16 citation statements)

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“…Since 1857, when Nageli first discussed newly identified parasitic agents in silkworms, which he termed Nosema bombycis (140), microsporidia have been recognized as a cause of disease in various animal groups, among them commercially important insects, fish, laboratory rodents, rabbits, fur-bearing animals, and primates (45,82,141,171,194,252). Indeed, their host range is extensive, including most invertebrates and all classes of vertebrates (45,(200)(201)(202)(203).…”

Section: Introductionmentioning

confidence: 99%

Human microsporidial infections

et al. 1994

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Microsporidia are obligate intracellular spore-forming protozoal parasites belonging to the phylum Microspora. Their host range is extensive, including most invertebrates and all classes of vertebrates. More than 100 microsporidial genera and almost 1,000 species have now been identified. Five genera (Enterocytozoon spp., Encephalitozoon spp., Septata spp., Pleistophora sp., and Nosema spp.) and unclassified microsporidia (referred to by the collective term Microsporidium) have been associated with human disease, which appears to manifest primarily in immunocompromised persons. The clinical manifestations of microsporidiosis are diverse and include intestinal, pulmonary, ocular, muscular, and renal disease. Among persons not infected with human immunodeficiency virus, ten cases of microsporidiosis have been documented. In human immunodeficiency virus-infected patients, on the other hand, over 400 cases of microsporidiosis have been identified, the majority attributed to Enterocytozoon bieneusi, an important cause of chronic diarrhea and wasting. Diagnosis of microsporidiosis currently depends on morphological demonstration of the organisms themselves. Initial detection of microsporidia by light microscopic examination of tissue sections and of more readily obtainable specimens such as stool, duodenal aspirates, urine, sputum, nasal discharge, bronchoalveolar lavage fluid, and conjunctival smears is now becoming routine practice. Definitive species identification is made by using the specific fluorescein-tagged antibody (immunofluorescence) technique or electron microscopy. Treatment options are limited, but symptomatic improvement of Enterocytozoon bieneusi infection may be achieved with the anthelmintic-antiprotozoal drug albendazole. Preliminary observations suggest that Septata intestinalis and Encephalitozoon infections may be cured with albendazole. Progress is being made with respect to in vitro propagation of microsporidia, which is crucial for developing antimicrosporidial drugs. Furthermore, molecular techniques are being developed for diagnostic purposes, taxonomic classification, and analysis of phylogenetic relationships of microsporidia.

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Section: Introductionmentioning

confidence: 99%

Human microsporidial infections

et al. 1994

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“…Antibodies alone are probably not protective. Parasitic proliferation in macrophages readily occurs in non-immune animals (Nelson 1962, Weidper 1975. The parasitized macrophages in the preseflt cases might possibly indicate an impaired immunity.…”

Section: Discussionmentioning

confidence: 99%

BRAIN AND SPINAL CORD LESIONS IN ENCEPHALITOZOONOSIS IN BLUE FOXES Transmission and Scanning Electron Microscopic Studies

Bjerkås¹

1987

Acta Pathologica Microbiologica Scandinavica Series A :Patholog

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Bjerkk, I. Brain and spinal cord lesions in encephalitozoonosis in blue foxes. Scanning and transmission electron microscopic studies. Acta path. microbiol. immunol. scand. Sect. A, 95: [269][270][271][272][273][274][275][276][277][278][279] 1987.The brains and spinal cords from 3 young blue foxes suffering from acute to subacute encephalitozoonosis, were examined by transmission and scanning electron microscopy. Parasitophorous vacuoles (PV) were demonstrated more frequently in vascular smooth muscular cells than in endothelial cells. The present study also indicated that the parasite has great affinity for neurons, including their processes. In addition, PV occurred in macrophages and probably also in intravascular monocytes. PV were readily differentiated from phagosomes by the bleb formations of the limiting membrane. An accumulation of host cell mitochondria near the PV in areas where developmental stages were attached, was a most striking feature. The inflammatory lesions, mainly of the granulomatous type, were almost constantly associated with the presence of released parasites, both in vascular walls and the nervous tissue. Phagocytosed parasites were probably killed by the lysosomal enzymes, although the spores were only slowly degraded.

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“…Wright and Craighead (1922) were the first workers to see microsporidian spores in mammals, when they found them in the brains of lab oratory rabbits. Their taxonomic diagnosis was not confirmed until 39 years later when Nelson (1962) observed polar tubes (=polar filaments) extruded from the spores obtained from peritoneal macrophages of mice and Lainson et al (1964) demonstrated by electron microscopy the presence of the polar tube within spores of a strain obtained from rats. Their taxonomic diagnosis was not confirmed until 39 years later when Nelson (1962) observed polar tubes (=polar filaments) extruded from the spores obtained from peritoneal macrophages of mice and Lainson et al (1964) demonstrated by electron microscopy the presence of the polar tube within spores of a strain obtained from rats.…”

Section: Introductionmentioning

confidence: 99%

Microsporidia

Canning¹

1993

Parasitic Protozoa

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An Intracellular Parasite Resembling a Microsporidian Associated with Ascites in Swiss Mice

Cited by 33 publications

References 0 publications

Human microsporidial infections

Human microsporidial infections

BRAIN AND SPINAL CORD LESIONS IN ENCEPHALITOZOONOSIS IN BLUE FOXES Transmission and Scanning Electron Microscopic Studies

Microsporidia

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