Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027121 (myositis)
4,538 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nine puppies suffered from progressive paresis with muscle wasting, hyporeflexia and extensor rigidity. CK-activity in serum was elevated and electrodiagnostic findings were indicative of lower motor neuron disease. Although lesions were also found in the CNS, additional neurological signs were rare, but CSF examination revealed the presence of inflammatory lesions. On pathologic examination, all animals had a disseminated necrotizing myositis. In addition, a disseminated encephalomyelitis was found as well as, in 2 cases, a neuritis. In the lesions of 6 animals protozoal organisms were found which were immunocytochemically identified as Neospora caninum. Our results show that the protozoal myositis-encephalitis syndrome in puppies can be diagnosed in the clinic with high probability. A clinical differentiation between toxoplasmosis and Neospora caninum infection is presently difficult.
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PMID:[The clinical diagnosis of protozoal myositis syndrome (Neospora caninum) of puppies]. 188 44

The occurrence is reported of acute myositis in a man with meningoencephalitis due to toxoplasmosis. The ultrastructure and immunohistochemistry of a muscle biopsy of the patient were investigated. Toxoplasma organisms were not found in the muscle biopsy. The perivascular inflammatory cells in the muscle were mainly CD4+ T cells and the inflammatory cells in and around the muscle fibres were chiefly macrophages. Expression of major histocompatibility complex class I and II antigens was observed in the infiltrating cells and endothelial cells of the blood vessels. A small proportion of the infiltrating cells expressed interferon-gamma. A possible role of the immune mechanism in the evolution of myositis is discussed.
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PMID:Acute toxoplasma myositis: an immunohistochemical and ultrastructural study. 208 60

Four litters of German Shorthaired Pointers from one owner developed a toxoplasmosis-like illness. According to the records, 29 of 39 dogs had hind limb paralysis. Six dogs from 2 litters were necropsied and had generalized encephalomyelitis. Tachyzoites and tissue cysts of Neospora caninum were found in the brain and spinal cord of each dog. Lesions were found in the eyes, extraocular muscles, or both in all of the dogs, and N caninum was detected microscopically in the eyes (retina and choroid in 1 dog), extraocular muscles, or both in 5 of the 6 dogs. Ocular lesions consisted of focal retinitis, choroiditis, mild nonspecific iridocyclitis, and myositis of extraocular muscles. Organisms stained with anti-N caninum serum, but not with anti-Toxoplasma gondii serum in an immunohistochemical test, except in 1 dog. In one dog, aged thick-walled N caninum tissue cysts reacted mildly with anti-T gondii serum.
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PMID:Repeated transplacental transmission of Neospora caninum in dogs. 222 66

A 55-year-old Japanese male who developed acute polymyositis and chorioretinitis due to toxoplasmosis is described. The patients was well until one month prior to the present admission, when he had an onset of painful swelling of lymphnodes in the posterior cervical region, proximal muscle weakness, myalgia and a partial defect in the visual field of the right eye. He admitted that he had had a chance to eat half-cooked mutton while he had visited Saudi Arabia 40 days before. He was unable to go up and down the stairs at the peak of the illness. Serum CPK was 2050 u/l (N = 5-50) on January 11, 1989. These symptoms improved spontaneously except for the visual field defect. He was admitted to our hospital on January 31, 1989. On admission, neurological examination was unremarkable except for retinal exudate in the right eye which appeared consistent with the clinical diagnosis of toxoplasma chorioretinitis. Serum CPK was 103 u/l, and EMG showed myogenic changes. The IgM-immunofluorescent (IFA) anti-Toxoplasma gondii antibody titer was elevated to 640, and IgG-immunofluorescent antibody to 20480 after IgM-IFA. These clinical and serological findings indicate acute and recent Toxoplasma gondii infection. It appeared likely that Toxoplasma gondii directly caused acute myositis and chorioretinitis. Clinical manifestations of toxoplasma myositis may mimic those of idiopathic polymyositis, however, the clinical course of the former is usually self-limited probably because of generation of antibodies which will inhibit the growth of the organism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute acquired toxoplasmosis presenting as polymyositis and chorioretinitis in a Japanese male]. 260 34

Clinical symptoms of the central and peripheral nervous system occur in about 40% of patients wit HIV infection. At autopsy, CNS lesions can be demonstrated in even higher percentages. Primary sequelae of HIV infection--either due to direct viral effects or the immunopathologic response of the human host--are acute aseptic meningitis or mengingo-encephalitis, HIV encephalopathy, myelopathy, neuropathy, and myositis. Secondary consequences of immunodeficiency in AIDS are opportunistic infections with other viruses, bacteria, fungi, and protozoa, e.g. CMV, HSV and HZV encephalitis, mycobacterial CNS infections, neurosyphilis, cryptococcal meningitis, and last but not least cerebral toxoplasmosis. The main secondary malignoma of the CNS is lymphoma. Together these disorders form a complex spectrum of central and peripheral neurological symptoms.
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PMID:[Neurologic complications of AIDS]. 304 48

Histologic sections and case histories from 23 dogs with proven fatal toxoplasmosis-like illness at the Angell Memorial Animal Hospital were reviewed. Toxoplasma gondii was identified in 13 dogs. A newly identified parasite, Neospora caninum, structurally distinct from T gondii, was found in 10 dogs. The newly discovered organism, belonging to a new genus and new species, formed meronts in many tissues of the dogs, especially the brain and spinal cord. Neospora caninum was located directly in the host cell cytoplasm without a parasitophorous vacuole; it divided by endodyogeny, contained more than 11 rhoptries, and did not react with the anti-T gondii serum in the immunoperoxidase test. Meningoencephalomyelitis and myositis were the main lesions associated with N caninum. Ulcerative and fistulous dermatitis was the major lesion in 1 dog.
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PMID:Newly recognized fatal protozoan disease of dogs. 339 51

Toxoplasma serology was performed in 28 patients with hairy-cell leukaemia and was positive in eight patients (29%). In two patients (7%) reactivated toxoplasmosis was proven by either isolation of Toxoplasma gondii or by significant antibody titre rise with generation of specific IgM-antibodies. In four patients (14%), a clinical diagnosis of active toxoplasmosis was based on signs and symptoms, serologic tests, and response to specific treatment. The high proportion of patients in which active toxoplasmosis was proven or probable (six; 21%) may be related to the presence of severe monocytopenia. In patients with hairy-cell leukaemia developing fever of unknown origin and myositis, toxoplasma serology should be performed, particularly because treatment of active toxoplasmosis usually is successful.
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PMID:Toxoplasmosis in hairy-cell leukaemia. 394 97

Extensive severe polymyositis in a patient with toxoplasmosis was presented. Toxoplasmosis was serologically substantiated by a serial two tube rise in a toxoplasma-antibody titer by a hemagglutination test. When appeared to be toxoplasma gondii was detected in areas of myositis. Toxoplasma gondii was found in a single small area of hepatic necrosis, but no other organ or tissue was involved. Thus, the present case was peculiar in respect that skeletal muscles were the major target of toxoplasmosis. A causal relationship between toxoplasmosis and polymyositis was discussed and the literatures were reviewed. Serological investigation and histopathological search for toxoplasma gondii should be done in every case of polymyositis not only for the appropriate therapy but also for the further elucidation of the relationship between toxoplasmosis and polymyositis.
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PMID:Polymyositis and toxoplasmosis. 728 66

The most important cyst-forming coccidian parasites in human and veterinary medicine belong the genera of Toxoplasma, Neospora and Sarcocystis. Toxoplasma gondii shows its clinical relevance in congenital infections and opportunistic infections in immunodeficient patients. In veterinary medicine the parasite is predominantly the cause of important economic loss in livestock production. Neospora causes diseases resembling toxoplasmosis; neosporosis is one of the most important causes of bovine abortion in the US. Neospora caninum leads to myositis and paralysis in dogs. The potential implication of Neospora in toxoplasmosis-like diseases in humans is not yet known. Sarcocystis is usually a relatively harmless intestinal parasite in humans. Recent data from tropical areas suggest that man can also become an intermediate host for certain Sarcocystis species, which potentially represents a source of opportunistic infection and disease in areas with increasing HIV prevalence. In veterinary medicine, Sarcocystis causes muscle diseases and also abortion or myeloencephalitis with lethal outcome in certain animal species. Molecular-epidemiological investigations have resulted in a new understanding of biological and population-genetic mechanisms relevant to the disease. Recently developed molecular techniques, such as transfection in protozoan parasites, are presently used not only to elucidate molecular-pathogenetic events in the course of disease, but also to prepare potential new immuno-therapeutic tools for future vaccination against infection or disease.
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PMID:[Cyst-forming Coccidia: Toxoplasma, Neospora, Sarcocystis]. 777 Jul 50

Twenty-four 5-month-old battery-hatched Japanese quail were inoculated orally with 10(5) (ME 49 strain, group A, 6 birds), 10(3) (ME 49 strain, group B, 6 birds), 10(5) (GT-1 strain, group C, 6 birds), and 10(3) (GT-1 strain, group D, 6 birds) Toxoplasma gondii oocysts. All birds in group C died or were euthanized within 8 days after inoculation (DAI). Five of the 6 birds in group D died or were euthanized 8, 9, 15, 19, and 23 DAI. One of the 6 quail in group A died 9 DAI, and 1 of the 6 birds in group D died 16 DAI. The 11 quail (1 from group D and 10 from groups A and B) were euthanized 63 DAI; T. gondii was isolated by bioassays in mice from the brains of 10, hearts of 10, and skeletal muscles of all 11 quail. Quail that survived marked small intestinal and splenic toxoplasmosis lived long enough to develop severe protozoal pneumonia, myocarditis, or meningoencephalitis. The quail that survived only to be examined at 63 DAI had moderate multifocal nonpurulent encephalitis and myositis and had a hypertrophic spleen that contained hemosiderin-laden macrophages. Toxoplasma gondii antibodies were found in the sera of all quail examined 63 DAI. Antibody titers to T. gondii in the modified agglutination test were higher than in the indirect hemagglutination and latex agglutination tests. Antibodies were not detected in quail sera examined by the Sabin-Feldman dye test.
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PMID:Experimental toxoplasmosis in Japanese quail. 806 54


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