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)

An in vitro model was employed to study the potential role of streptococcal extra-cellular products, rich in streptolysin O, in cellular injury as related to streptococcal infections and post-streptococcal sequelae. Extra-cellular products (EXPA) rich in streptolysin O were isolated from type 4, group A hemolytic streptococci grown in a chemostat, in a synthetic medium. EXPA induced moderate cytopathogenic changes in monkey kidney epithelial cells and in rat heart cells pre-labeled with 3H-arachidonate. However very strong toxic effects were induced when EXP was combined with oxidants (glucose oxides generated H2O2, AAPH-induced peroxyl radical (ROO.), NO generated by sodium nitroprusside) and proteinases (plasmin, trypsin). Cell killing was distinctly synergistic in nature. Cell damage induced by the multi-component cocktails was strongly inhibited either by micromolar amounts of gamma globulin, and Evan's blue which neutralized SLO activity, by tetracycline, trasylol (aprotinin), epsilon amino caproic acid and by soybean trypsin inhibitor, all proteinase inhibitors as well as by a non-penetrating PLA2 inhibitor A. The results suggest that fasciitis, myositis and sepsis resulting from infections with hemolytic streptococci might be caused by a coordinated 'cross-talk' among microbial, leukocyte and additional host-derived pro-inflammatory agents. Since attempts to prolong lives of septic patients by the exclusive administration of single antagonists invariably failed, it is proposed that the administration of 'cocktails' of putative inhibitors against major pro-inflammatory agonizes generated in inflammation and infection might protect against the deleterious effects caused by the biochemical and pharmacological cascades which are known to be activated in sepsis.
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PMID:Gamma globulin, Evan's blue, aprotinin A PLA2 inhibitor, tetracycline and antioxidants protect epithelial cells against damage induced by synergism among streptococcal hemolysins, oxidants and proteinases: relation to the prevention of post-streptococcal sequelae and septic shock. 984 86

The clinical picture with, among other things, muscular swelling, fever and nocturnal sweating in three males aged 30, 37 and 52 years, suggested a neoplasm and sepsis. Ultimately, they were found to suffer from focal myositis, localized nodular myositis and polymyositis, respectively. The ESR and leukocyte counts were increased, the serum creatinine kinase (CK) activity was normal or slightly increased. The symptoms decreased after prednisone treatment. Both localized and generalized inflammatory muscular diseases may be present without the serum CK activity being raised.
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PMID:[Myositis in the presence of slightly elevated creatine kinase values]. 1036 12

Group A streptococcal infections, ranging from necrotizing fasciitis and myositis to toxic shock syndrome, have increased over the last 10 years. We developed the first primate model of necrotizing fasciitis and myositis. Thirteen baboons were inoculated intramuscularly with group A streptococci (GAS). Eleven animals survived for > or = 11 days before sacrifice, and two animals died within 2 days. The site of inoculation of the survivors exhibited an intense neutrophilic influx (stage I), followed by a lymphoplasmacytic influx (stages II and III). This was accompanied by the appearance of markers of an acute and then a chronic systemic inflammatory response. In contrast, the site of inoculation of the two nonsurvivors exhibited intravascular aggregates of neutrophils at its margin with no influx of neutrophils and with extensive bacterial colonization. We conclude that GAS inoculation induces a local and systemic acute neutrophilia followed by a chronic lymphoplasmacytic response; failure, initially, of neutrophilic influx into the site of inoculation predisposes to systemic GAS sepsis and death; and this three-stage primate model approximates the human disease.
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PMID:Staging of the baboon response to group A streptococci administered intramuscularly: a descriptive study of the clinical symptoms and clinical chemical response patterns. 1091 29

The possible role played by streptolysin S (SLS) of group A streptococci in the pathophysiology of streptococcal infections and in post-streptococcal sequelae is discussed. The following properties of SLS justify its definition as a distinct virulence factor: 1) its presence on the streptococcus surface in a cell-bound form, 2) its continuous and prolonged synthesis by resting streptococci, 3) its non-immunogenicity, 4) its extractability by serum proteins (albumin, alpha lipoprotein), 5) its ability to become transferred directly to target cells while being protected from inhibitory agents in the milieu of inflammation, 6) its ability to bore holes in the membrane phospholipids in a large variety of mammalian cells, 7) its ability to synergize with oxidants, proteolytic enzymes, and with additional host-derived proinflammatory agonists, and 8) its absence in streptococcal mutants associated with a lower pathogenicity for animals. Because tissue damage in streptococcal and post-streptococcal sequelae might be the end result of a distinct synergism between streptococcal and host-derived proinflammatory agonists it is proposed that only cocktails of anti-inflammatory agents including distinct inhibitors of SLS (phospholipids), gamma globulin, inhibitors of reactive oxygen species, proteinases, cationic proteins cytokines etc., will be effective in inhibiting the multiple synergistic interactions which lead to fasciitis, myositis and the flesh-eating syndromes, and often develop into sepsis, septic shock and multiple organ failure. The creation of mutants deficient in SLS and in proteases will help shed light on the specific role played by SLS in the virulence of group A hemolytic streptococci.
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PMID:Is streptolysin S of group A streptococci a virulence factor? 1066 Jan 34

Skin and soft tissue infections are the most common cause for hospital admission of injection drug users. Cutaneous and subcutaneous abscesses are the most frequent type of SSTI and occur most commonly when drug users are no longer able to inject intravenously and resort to injection directly into skin or muscle. Abscesses may be difficult to differentiate from uncomplicated cellulitis or may be confused with pseudoaneurysms, hematoma, phlegmon, or thrombosed vein. Special studies, including ultrasonography; CT scans, and MR imaging; or careful incision and inspection may be necessary to clarify the extent of infection and the presence of abscess. These procedures may also help differentiate a subcutaneous abscess from a vascular structure. Uncomplicated cellulitis most commonly responds to antibiotic therapy directed toward Staphylococcus aureus and Streptococcus spp. In several recent studies, cutaneous and subcutaneous abscesses have been found to be caused by polymicrobial infections and to include anaerobic organisms as well as aerobic gram-positive cocci in a little more than 50% of cases. Complete, often repeated, incision and drainage is a prerequisite for successful outcome in these cases. Complications of SSTI are many and are potentially life threatening. They include direct extension of subcutaneous abscess into vital areas or structures, necrotizing fasciitis and myositis, bacteremia, and sepsis. An outbreak of a highly lethal SSTI that recently occurred in Scotland, Ireland, and England seems to have resulted from infection with Clostridia spp, including C. novyi and C. perfringens. A rare but well-documented SSTI in injection drug users is pyomyositis, an abscess-forming infection of skeletal muscle. More than 20 cases have been reported in temperate climates to date. Although not life-threatening, chronic cutaneous venous ulcers of the lower extremities are common and debilitating, requiring long-term multidisciplinary care for successful healing.
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PMID:Skin and soft tissue infections in injection drug users. 1237 Nov 23

We report the case of an ABO-incompatible kidney transplant recipient who died suddenly following a good transplant course of 12 years. For 10 years after transplantation, the graft function had been stable (s-Cr: 1.0-1.5 mg/dL), although chronic hepatitis C had developed, with elevation of transaminase. In the 11th year, he was admitted into the hospital with low-grade fever and general fatigue. Jaundice and anaemia progressed, and he died 2 months after admission. The autopsy diagnosis was: (1) post-renal transplantation state, (2) phlegmonous enterocolitis with septic infarction, (3) cellulitis and necrotic myositis, and (4) sepsis. The transplanted kidney graft showed well-preserved glomeruli and tubules, corresponding to chronic allograft nephropathy (CAN) grade Iota (ci1, ct1, cv1), according to the Banff classification. The pathological changes observed in this long-surviving ABO-incompatible kidney graft were similar to those of an ABO-compatible graft, although its degree was milder.
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PMID:An autopsy case of bacterial septic shock 12 years following ABO-incompatible renal transplantation. 1519 73

Hematogenous focal infections are a rare complication of bacteremia or sepsis caused by viridans-group streptococci. We describe two patients with acute leukemia who developed myositis during alpha-hemolytic streptococcal bacteremia. Children complaining of severe muscle pain associated with viridans streptococcal infections should be carefully evaluated for the presence of focal pyogenic complications and rhabdomyolysis. The severity of infectious myositis is highly variable, depending on the etiologic organism and host immunity, making individualized treatment the most effective approach.
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PMID:Myositis complicating viridans streptococcal sepsis in childhood leukemia. 1546 4

Azathioprine, an analog of 6-mercaptopurine has been used as a steroid-sparing agent in the treatment of inflammatory bowel disease for over 30 years. Hypersensitivity reactions to azathioprine including fever, myalgia, arthralgia, rash are well documented in the literature. Here, we report 2 cases of azathioprine hypersensitivity in patients with inflammatory bowel disease manifesting with the unusual symptom of profound muscular weakness resulting in inability to perform simple tasks such as lifting even light objects, sitting upright, and walking a few steps. Development of severe weakness raised concern about myositis, rhabdomyolysis, myopathy, and sepsis in these patients. Discontinuation of azathioprine resulted in prompt improvement of muscular weakness, and rechallenge led to recurrence of similar symptoms within hours. These observations suggest that the development of muscular weakness in patients on azathioprine should be considered as an adverse effect of the drug. Failure to recognize this adverse outcome can lead to prolonged periods of muscular weakness in this group of patients.
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PMID:Severe muscular weakness: an unusual adverse effect of azathioprine therapy. 1691 6

Infectious muscle diseases have very different aetiologies. The viral myositides are proved by clinical and laboratory evidences in various etiologic settings (Influenza A and B, Coxsackie and HIV). The bacterial myositis was considered in the near past a tropical disease, but in our days with migration of people from South to North and the endemia of AIDS it became a problem of the "civilized" world. On the other hand, tuberculous endemia in Central-Eastern Europe, including Romania, results in quite high incidence of osteoarticular tuberculosis. In this section the authors take into consideration some clinical entities, such as psoas abscess, postanginal sepsis, beta-haemolytic streptococcus infection and that caused by Koch bacillus. Other rare musculoskeletal infections such as gas gangrene and non-clostridial anaerobic myonecrosis are also reviewed. Immune depression caused by underlying diseases, therapies, alcoholism or old age is often encountered. The parasitic aetiologies include infestations with Trichinella spiralis, Cysticercus cellulosae, Toxoplasma and Amoeba. The contribution of imagistic methods to diagnosis is emphasised. Ultrasonography associated with CT imaging are usually used, while MRI should be reserved for cases in which axial skeleton is involved. The management is based on appropriate antibiotic therapy and surgery.
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PMID:Infectious muscle disease. 1723 94

Streptococcal toxic shock syndrome and associated myositis caused by group A beta-hemolytic streptococcus pyogenes generally have a poor outcome despite aggressive operative treatment. Frequently the diagnosis is missed initially as the clinical features are non-specific. The progression to a toxic state is rapid and unless definitive treatment measures are initiated early, the end result can be catastrophic. We report a previously healthy patient who had features of toxic shock syndrome due to alpha haemolytic (viridans) streptococcus mitis which was treated successfully with antibiotics, aggressive intensive care support including the use of a 'sepsis care bundle', monitoring and continuous multidisciplinary review. Life and limb threatening emergencies due to streptococcus mitis in an immune-competent person are rare and to our knowledge, have not previously been described in the English scientific literature. Successful outcome is possible provided a high degree of suspicion is maintained and the patient is intensively monitored.
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PMID:Surviving streptococcal toxic shock syndrome: a case report. 1796 90


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