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Query: UMLS:C0027121 (myositis)
 4,538 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A high-passage laboratory strain of coxsackievirus B1 produced a unique myositis that predominantly and profoundly affected hip extensors and, to a lesser extent, hindquarter knee flexors when inoculated into a strain of random-bred newborn mice of Swiss origin (COH mice). The effect was not observed in BALB/c or C3H mice similarly inoculated. In addition to the differences in susceptibility of the mouse strains, it was found that six different low-passage "field" isolates of coxsackie-virus B1 isolated from infected patients varied considerably in their capability to induce these lesions. Thus, selective myositis which is muscle group-specific can be induced in a mouse model with coxsackievirus B1, and both genetic factors of the host and characteristics of the virus strain play a significant role in the pathogenesis of the myositis.
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PMID:Selective polymyositis inducted by coxsackievirus B1 in mice. 22 92

A case of polymyositis in a 15 year old girl demonstrating the clinical course of an infectious disease is presented. The Coxsackie virus B2 was isolated from the stools, and serum antibodies were detected. Histologic examination of muscle showed signs of myositis. The patient was treated with cortisone and recovered completely. Possible viral etiology of the polymyositis is suggested.
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PMID:Polymyositis accompanying coxsackie virus B2 infection. 63 1

Mice infected with coxsackievirus B1 (CVB1) develop a chronic hindquarter muscle weakness which resembles human polymyositis. In this study, we used in situ hybridization to screen for persistent viral RNA in hamstring and quadriceps muscles from mice that displayed various degrees of clinical weakness. At 28 to 31 days postinfection, when chronic myositis is well developed but infectious virus can no longer be recovered, persistent CVB1 RNA was found in hindquarter skeletal muscle of all 12 infected animals examined. Persistent CVB1 showed a multifocal distribution within muscle and was associated with three different histopathology patterns (HPPs). These three HPPs (HPP-1, HPP-2, and HPP-3) represent potentially different stages in the mechanism of persistence. They are based on the pattern of grains, the location of hybridization signal within the muscle, and the accompanying histopathology. In HPP-1, virus persisted in nonnecrotic muscle fibers and was not directly associated with foci of inflammatory cells. HPP-2 consisted of virus contained within necrotic myocytes that were surrounded by inflammatory cells. HPP-3 was rare and showed virus inside infiltrating mononuclear cells in a region where muscle tissue had been extensively destroyed. Persistent CVB1 occurred more frequently in severely diseased animals and in tissue sections displaying intense inflammation. Moreover, HPP-2 showed a stronger association with tissue inflammation and hindquarter weakness than did HPP-1. These data demonstrate that CVB1 persists in skeletal muscle for at least 28 to 31 days postinfection and support the concept that this persistence plays a role in the development of murine polymyositis.
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PMID:Viral persistence during the developmental phase of Coxsackievirus B1-induced murine polymyositis. 194 49

The idiopathic inflammatory myopathies are a heterogeneous group of uncommon diseases. The incidence rate of IIM is approximately 5 cases per million population, but there appears to be an increase in the rate over the last two decades, particularly in black females. This may be a true increase or due to renewed interest and awareness of the disease and improvement in our ability to diagnose mild disease. There has also been progress in decreasing the mortality rate in IIM perhaps secondary to better treatment and/or the diagnosis of mild disease. The discovery of anti-Jo-1 antibodies has renewed the investigation of a possible viral etiology of IIM. Studies of quantitative slot blot hybridization with coxsackievirus probes and RNA from IIM muscle biopsies and in situ hybridization of biopsies with a Theiler's virus probe have revealed a few positive hybridizations in each study. Although there are some fundamental problems with these studies, these intriguing results bear confirmation. These results continue to implicate picornaviruses as the primary suspects in the pathogenesis of IIM. HIV has now been associated with a number of rheumatologic syndromes, including a polymyositis that is indistinguishable from IIM, and we can expect additional changes in the epidemiology of this family of disorders in coming years. Study of these patients may provide insight into the etiopathogenesis of IIM.
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PMID:Idiopathic inflammatory myopathies. 221 63

Dermatomyositis in childhood is an uncommon disease, affecting muscle and skin. The disease usually has an insidious onset; the proximal muscle groups are classically more affected than the distal group. If left untreated, the disease will either spontaneously arrest or will progress until the child is completely bedridden, with death secondary to hypoventilation and aspiration. For a definitive diagnosis 3 or 4 of the following criteria (plus rash) are required: 1) symmetrical limb girdle weakness; 2) muscle biopsy evidence of myositis and muscle necrosis; 3) elevation of muscle enzymes; 4) electromyographic changes of myositis. The main pathologic feature of juvenile dermatomyositis is vasculitis affecting small arteries and veins of muscle, skin and gastrointestinal tract. Whether muscle from patients with polymyositis contains a specific auto antigen or is contaminated with an immunogenic infectious agent such as a virus (coxsackie virus, for instance) remains unclear. Childhood dermatomyositis is almost uniformly responsive to steroid treatment; there is a good chance of remission with minimal risk of secondary complications with an initial low dosage of prednisone (1 mg/kg/day). The use of additional drugs such as azathioprine, methotrexate or cyclophosphamide is reserved for patients who are either not completely responsive to steroids or difficult to wean off steroids. Cyclosporine A has been proposed to achieve a reduction in steroid dosage.
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PMID:[Dermatomyositis in children]. 271 39

Murine polymyositis (PM) induced by coxsackievirus B1 (CVB1) has been used as a model of human PM. Our study was undertaken to investigate the role of T cells in CVB1 induced PM by examining disease development in neonatally thymectomized mice. Clinical weakness and histological inflammatory myositis occurred in 42.7% of sham operated animals but only 7.7% of thymectomized mice. These experiments demonstrate the importance of T cells in the pathogenesis of this virus induced autoimmune disorder.
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PMID:T cells are required for coxsackievirus B1 induced murine polymyositis. 283 72

Subgenomic cDNA clones representing defined regions of the genome of Coxsackie B3 virus were used as hybridisation probes to detect RNA of various enteroviruses in cell culture and mouse model systems. Radiolabelled probes were used in slot blots to quantitate the RNA in samples; biotinylated probes were used to localise virus RNA at the cellular level by in situ hybridisation with monolayers of infected cells or thin sections of tissue samples. Probes derived from the 5' or 3' terminal regions of Coxsackie virus RNA, which are highly conserved in the genus Enterovirus, detected RNA of various serotypes in infected cell cultures, but failed to hybridise with hepatitis A virus (HAV) RNA. Although HAV is clearly a Picornavirus, our data support the view that its taxonomic position within the enteroviruses should be reconsidered. The biotinylated probes were also used to detect in situ virus RNA in paraffin-embedded tissue samples from experimental mouse models of Coxsackie B3 virus-induced myocarditis or Coxsackie B1 virus-induced myositis. Since the integrity of the tissues was preserved during the process, and viral RNA was localised in the affected muscle fibres, this has enabled us unequivocally to relate the infecting virus to the underlying tissue injury.
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PMID:Detection of enterovirus RNA in experimentally infected mice by molecular hybridisation: specificity of subgenomic probes in quantitative slot blot and in situ hybridisation. 285 Mar 42

The causes of polymyositis are imperfectly known. The role of Toxoplasma, the myotropism of which is significant in acute myositis, may be suspected on the ground of secondary serological data, but it has not yet been confirmed. On the other hand, the role of coxsackie virus, which until recently had been established only on morphological or serological data, has now been ascertained by molecular biology techniques. The best example of experimental viral polymyositis is the disease induced by inoculation of retrovirus to the monkey. This has led to the identification in man of polymyositis revealing an acquired immunodeficiency syndrome.
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PMID:[Role of toxoplasma and viruses in polydermatomyositis]. 296 56

We report a case of chronic recurrent polymyositis associated with increasing antibody titers of coxsackievirus A9 in serum during clinical exacerbations. Muscle biopsy specimens showed pathologic changes consistent with chronic myositis, including perivascular mononuclear cell infiltration and hyalinization of muscle fibers with cytoplasmic vacuolations. The specific fluorescence was observed in the muscle fibers stained with antiserum for coxsackievirus A9. These findings indicate that this viral subtype as the etiologic agent in this case and virus plays a pathogenic role in some cases of chronic polymyositis.
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PMID:Chronic polymyositis: presence of coxsackievirus A9 antigen in muscle. 301 37

Coxsackievirus B-3 myocardiopathy was induced in weanling mice by intraperitoneal and intracerebral inoculations of the Nancy strain. Acute mortality was 5.5%. The cardiomyopathy is characterized by an early phase lasting about 9 days with myocardial necrosis, associated inflammation, and healing by fibrosis and calcification involving 25 to 50% of the contractile fibers in each affected mouse. Infectious coxsackievirus may be recovered from the heart during this phase. Continuing myocardial inflammatory lesions follow during the later phase, but infectious virus is no longer present. When mice were forced to swim in a preheated pool (33 degrees C) during both phases of their myocardiopathy, virulence was strikingly augmented. Fully half of the mice died of congestive failure, the majority while swimming. Hearts were dilated, hypertrophied, and grossly necrotic. The myocardium was transformed to a completely necrotic, inflammatory, calcifying mass. At the peak of the infectious phase, myocardial replication of coxsackievirus was increased 530 times in nurslings which had been forced to swim. Myositis in hind limbs was more frequent, and inflammatory lesions in perirenal and pericardial fat were more severe in the mice which were forced to swim. When swimming was begun on the 9th day after infection, the virulence and lethality (13.8%) of infection were moderately increased.
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PMID:Augmentation of the virulence of murine coxsackie-virus B-3 myocardiopathy by exercise. 424 39


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