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

We present four cases of diffuse fasciitis (DF) associated with peripheral eosinophilia in which spirochetal organisms were identified. Two patients had borderline positive results on serologic evaluation for Borrelia burgdorferi. Deep biopsy showed dermal sclerosis associated with variable degrees of perivascular mononuclear inflammation. Diffuse fasciitis, septal panniculitis, and myositis with mononuclear cell infiltrates and varying numbers of eosinophils were observed. All cases showed a striking lymphocytic vasculopathy associated with atypical reactive endothelial cells. Using modified Dieterle and Steiner silver stains, multiple organisms were seen in one specimen, a single unequivocal organism detected in two specimens. In one case, no organisms were detected on silver stain; however, organisms were demonstrated using rabbit polyclonal antibodies against B. burgdorferi. B. burgdorferi-specific DNA was identified in one patient by the polymerase chain reaction. These results indicate that some cases of eosinophilic fasciitis are an expression of Lyme disease. We have previously proposed the more specific term "borrelial fasciitis" to describe such lesions.
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PMID:Borrelial fasciitis: diffuse fasciitis and peripheral eosinophilia associated with Borrelia infection. 890 92

Since the 1980s there has been a marked increase in the recognition and reporting of highly invasive group A streptococcal infections with or without necrotizing fasciitis associated with shock and organ failure. Such dramatic cases have been defined as streptococcal toxic-shock syndrome. Strains of group A streptococci isolated from patients with invasive disease have been predominantly M types 1 and 3 that produce pyrogenic exotoxin A or B or both. In this paper, the clinical and demographic features of streptococcal bacteremia, myositis, and necrotizing fasciitis are presented and compared to those of streptococcal toxic-shock syndrome. Current concepts in the pathogenesis of invasive streptococcal infection are also presented, with emphasis on the interaction between group A Streptococcus virulence factors and host defense mechanisms. Finally, new concepts in the treatment of streptococcal toxic-shock syndrome are discussed.
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PMID:Streptococcal toxic-shock syndrome: spectrum of disease, pathogenesis, and new concepts in treatment. 890 67

The incidence of group A Streptococcus (GAS) invasive infections has been increasing worldwide, and there is no obvious explanation for this phenomenon. In 1993, a working group on severe GAS infections was established to define accurately what constitutes an invasive infection. Three types of infection are particularly feared: necrotizing fasciitis, myositis and a newly defined entity, named streptococcal toxic shock syndrome (STSS) because of a certain analogy with its staphylococcal counterpart. GAS produces many toxins responsible for its clinical manifestations. Some of them, labelled streptococcal pyrogenic exotoxins, have been characterized as superantigens. These proteins play a key role in initiating the immune response to GAS and are mostly responsible for the precipitous course of invasive infections. Death rates are high in streptococcal invasive infections, ranging from about 20% for necrotizing fasciitis to almost 100% for myositis. Therapy consists mainly of high doses of antibiotic combinations, aggressive surgery, and intravenous administration of immunoglobulins for STSS.
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PMID:Group A Streptococcus invasive infections: a review. 903 79

Proliferative myositis, a reactive lesion similar to proliferative fasciitis and nodular fasciitis, has only been cytogenetically described in one other report to date. This previously described case showed trisomy 2. Cytogenetic analysis and fluorescence in situ hybridization (FISH) of a proliferative myositis lesion in the present study did not reveal trisomy 2 but the following clonal translocation was observed: 46,XX,t(6;14)(q23;q32).
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PMID:Chromosomal anomalies in a case of proliferative myositis. 933 81

While the plain film and nuclear medicine bone scan are still the traditional imaging modalities used in the evaluation of musculoskeletal infection, the cross-sectional imaging modalities, computed tomography (CT) and magnetic resonance imaging (MRI), have become critical in the delineation of many types of musculoskeletal infection. In particular, the evaluation of soft tissue infections, including cellulitus, myositis, fasciitis, abscess, and septic arthritis are often best evaluated by MRI or CT due to their excellent anatomic resolution and soft tissue contrast. Even in osseous infection, CT and MRI can give better anatomic delineation of the extent of infection. In cases where the plain film and nuclear medicine bone scan findings are complicated due to previous surgery, trauma, or underlying illness, the anatomic resolution and soft tissue contrast provided by MRI and CT are often necessary to determine if underlying infection exists. MRI's visualization of the bone marrow allows for the sensitive detection of osteomyelitis, although specificity for the diagnosis of osteomyelitis is aided by other findings, including cortical destruction. The CT and MRI findings in the spectrum of musculoskeletal infections are discussed and contrasted, and pitfalls in their evaluation of musculoskeletal infection are described.
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PMID:CT and MRI evaluation of musculoskeletal infection. 944 78

Clinical and laboratory data from 1973 to 1988 were retrospectively reviewed to study the microbiology of infection following trauma. A total of 368 specimens obtained from 340 trauma patients showed bacterial growth. The traumas included lacerations (163), blunt trauma (76), penetrating trauma (65), bites (20), and open fractures (10). Anaerobic bacteria only were isolated in 119 (32%) specimens, aerobic bacteria only in 58 (16%), and mixed aerobic-anaerobic flora in 191 (52%). A total of 444 anaerobic (1.2 isolates per specimen) and 267 aerobic or facultative (0.7 per specimen) were recovered. The predominant anaerobic bacteria included Bacteroides fragilis group (119 isolates), Peptostreptococcus spp (113), Clostridium spp (78), Prevotella spp (58), and Fusobacterium spp (23). The predominant aerobic bacteria included Escherichia coli (83), Staphylococcus aureus (61), Streptococcus pyogenes (27), Streptococcus group D (16), and Klebsiella pneumoniae (16). The types of infections included abscesses (109), bacteremia (32), bites (13), empyema (10), osteomyelitis (21), peritonitis (52), thrombophlebitis (12), and wounds (116, including posttraumatic wounds, cellulitis, stump wound, decubitus ulcers, myositis, and fasciitis). S. aureus was isolated at all sites. However, organisms of the oropharyngeal flora predominated in infections that originated from that location (ie, head and neck wounds, and abscesses or bites), and those of the gastrointestinal flora predominated in infections that originated from that site (ie, peritonitis, abdominal abscesses, decubitus ulcers). This study showed the polymicrobial nature of many infections that follow trauma.
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PMID:Aerobic and anaerobic microbiology of infection after trauma. 978 44

We describe a patient with a streptococcal myositis/fasciitis and toxic shock syndrome following an intramuscular injection with diclofenac. A patient complaining of sore throat and headaches for two days and fever up to 38.5 degrees C for one day consulted her family physician. 75 mg of diclofenac were injected intramuscularly for symptomatic treatment. On the next day massive pain at the injection site and a generalized erythema occurs and fever up to 38.5 degrees C persists. She is admitted to the local hospital for suspected abscess formation. Despite rapid antibiotic treatment a septic shock develops. The patient is transferred to a tertiary care hospital. An extensive debridement is performed and the antibiotic regimen changed to high dose penicillin and clindamycin. The association of life threatening diseases due to Group A streptococci and non-steroidal anti-inflammatory drugs (NSAID) is well documented by several case reports. We believe there is no longer any need for intramuscular injections of NSAID. The rare but severe complications preclude further use of the intramuscular dosage in view of the availability of oral alternatives.
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PMID:[Erythema and fever after diclofenac i.m]. 978 79

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

Since the 1980s, there has been a marked increase in the recognition and reporting of highly invasive group A streptococcal (GAS) infections associated with shock and organ failure, with or without necrotizing fasciitis. Such dramatic cases have been defined as streptococcal toxic shock syndrome (StrepTSS). Strains of GAS isolated from patients with invasive disease have been predominantly M types 1 and 3, which produce either pyrogenic exotoxin A or B or both. The clinical and demographic features of streptococcal bacteremia, myositis, and necrotizing fasciitis are presented and compared with those of StrepTSS. Current concepts in the pathogenesis of invasive streptococcal infection will be presented, with emphasis on the interaction between GAS virulence factors and host defense mechanisms. Finally, new concepts in the treatment of StrepTSS will be discussed.
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PMID:The flesh-eating bacterium: what's next? 1008 9

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


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