Cases reported "Streptococcal Infections"

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1/48. Febrile lady with acute renal failure and desquamating erythema.

    A 63-year-old woman developed acute renal failure and streptococcal toxic shock syndrome caused by streptococcus group G. Initially, an erythema resembling vasculitis was misleading. The subsequent clinical course, however, was typical for streptococcal toxic shock syndrome and met the criteria put forward by The Working Group on Severe streptococcal infections. In patients infected with streptococcus group G, toxic shock syndrome is rare. The streptococcus group G strains isolated from this patient did not produce pyrogenic exotoxins. Instead they produced an M-like protein related to group C and G streptococci that do not act as superantigens.
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2/48. Characterization of blood culture isolates of Streptococcus dysgalactiae subsp. equisimilis possessing Lancefield's group A antigen.

    For three human blood culture isolates of beta-hemolytic streptococci with Lancefield's serogroup A antigen, phylogenetic analysis of the 16S rRNA genes confirmed biochemical identification as Streptococcus dysgalactiae subsp. equisimilis. Genes encoding M or M-like proteins, which are considered to be major virulence determinants in streptococci, were detected in all of these strains. Our data clearly demonstrate that for beta-hemolytic streptococci, the species assignment should not be based on the results of serogrouping alone.
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3/48. Neutrophil antigen 5b is carried by a protein, migrating from 70 to 95 kDa, and may be involved in neonatal alloimmune neutropenia.

    BACKGROUND: Neutrophil antigen 5b has been described as involved in transfusion reactions and not in neonatal alloimmune neutropenia. CASE REPORT: Anti-5b was found in the serum of a mother of a persistently neutropenic newborn, who had several bacterial infections. The neutropenia responded to treatment with recombinant human granulocyte-colony-stimulating factor. immunoprecipitation experiments performed with this and three other 5b antisera identified a protein, migrating from 70 to 95 kDa, as carrier of 5b. The observed pattern of migration may point to heavy glycosylation of this protein. RESULTS: Six 5b-negative donors were identified among 54 screened white donors, for a 5b gene frequency of 0.66. CONCLUSION: Alloimmunization to 5b in pregnancy is rare. In the patients with neonatal neutropenia analyzed in the last decade, this was the first case discovered.
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4/48. Primary CNS lymphoma associated with streptococcal abscess: an autopsy case.

    This report describes a case of streptococcal abscess in the nodules of a primary central nervous system (CNS) lymphoma. magnetic resonance imaging (MRI) of the brain revealed multiple lesions with ringlike enhancement over the bilateral frontal, right temporal, and left parietal lobes. On admission, acute brain edema occurred following angiography, which resulted in respiratory arrest. autopsy findings showed that the ringlike enhanced lesions on MRI were streptococcal abscesses localized in the lymphoma nodules. The lymphoma was classified as non-Hodgkin, diffuse large cells of B-cell lineage. No other lymphoma mass was found extracranially. An immunohistochemical study showed that the lymphoma cells were positive for leukocyte common antigen, Epstein-Barr virus, bax. and bcl-XL, and negative for L-26 and bcl-2. This case demonstrated that an opportunistic streptococcal abscess developed in primary CNS lymphoma in a patient without acquired immunodeficiency syndrome (AIDS), though a few similar cases have been reported in patients with AIDS.
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5/48. encephalomyelitis-associated antimyelin autoreactivity induced by streptococcal exotoxins.

    OBJECTIVE: After implicating streptococcus pyogenes as causing acute disseminated encephalomyelitis (ADEM) in a child, we wanted to prove that in vivo activation of autoreactive T lymphocytes by superantigens of this Streptococcus contributed to the dramatic demyelination. BACKGROUND: ADEM is a demyelinating disorder of the CNS sharing many similarities with MS. Demyelination in MS is considered to be the result of an autoimmune process mediated by autoreactive T lymphocytes with specificity for myelin antigens. methods: Phenotypic analysis and proliferation assays on blood monocytes, as well as isolation of myelin basic protein (MBP)-reactive T-cell lines/clones; and TCR repertorium analysis by PCR-ELISA and cytokine production. RESULTS: 1) The blood T-cell receptor (TCR) repertoire was compatible with in vivo expansion induced by S. pyogenes exotoxins. 2) TCR expression analysis indicated clonal expansion of CD8 MBP-reactive T cells, suggesting in vivo activation. MBP-reactive T cells showed crossreactivity to S. pyogenes supernatant and exotoxins. 3) Cytokine mRNA quantification of the mononuclear cells revealed a Th2-biased profile. CONCLUSION: In vivo exposure to S. pyogenes may have induced activation of pathogenic myelin reactive T cells, contributing to the dramatic inflammatory demyelination.
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6/48. Reiter's syndrome caused by Streptococcus viridans in a patient with hla-b27 antigen.

    A 26-year-old male patient with mitral valve prolapse and hla-b27 antigen received endodontic treatment for dental caries. Two weeks later fever, dysuria, diarrhea, sterile inflammatory arthritis of lower limbs, enthesitis, dactylitis, conjunctivitis, and uveitis consecutively developed. blood culture performed at the time of active arthritis yielded Streptococcus viridans. He did not have any history of psoriasis, acute infectious diarrhea, chronic inflammatory bowel diseases, or sexually transmitted diseases. Laboratory studies also excluded the possibility of infections by human immunodeficiency virus, hepatitis b or C virus, chlamydia, and streptococci from the upper airway. This report indicates that Streptococcus viridans can be the triggering microorganisms of Reiter's syndrome in some circumstances.
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7/48. Infection-triggered anorexia nervosa in children: clinical description of four cases.

    BACKGROUND: anorexia nervosa (AN) is a serious illness with no definitive treatment. Clinical and research evidence led to the hypothesis that some children with AN may have a pediatric autoimmune neuropsychiatric disorder associated with streptococcus (PANDAS), similar in pathogenesis to other hypothesized PANDAS disorders. methods: Four youngsters (ages, 11-15 years) with PANDAS AN were treated with an open trial of antibiotics, in addition to conventional treatment. They were evaluated for eating disorder and obsessive-compulsive symptoms, and for weight gain. Evidence of streptococcal infection came from clinical evaluation, throat cultures, and two serological tests: anti-deoxyribonuclease B (anti-DNase B) and anti-streptolysin O (ASO) titers. The "rheumatic" marker D8/17 was also measured. This B-cell alloantigen is associated, in several publications, with poststreptococcal autoimmunity: rheumatic fever (RF), Sydenham's chorea (SC), and possibly PANDAS obsessive compulsive disorder (OCD) and tic disorders. RESULTS: There was clinical evidence of possible antecedent streptococcal infection in all four patients, two of whom had comorbid OCD, with possible infection-triggered AN. All four had the rheumatic marker: A percentage of D8/17-positive B cells of 28-38%, with a mean of 33% (12% or more is considered positive for the marker). The patients responded to conventional treatment plus antibiotics with weight restoration and decreased eating disorder and obsessive-compulsive symptoms. Three needed to gain weight and did so. CONCLUSIONS: There may be a link between infectious disease and some cases of AN, which raises the possibility of new treatment.
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8/48. Pustular psoriasis elicited by streptococcal antigen and localized to the sweat pore.

    A woman, aged 39 years, presented with a localized, painful, pustular eruption of the neck, scalp, and finger of five years' duration. A diagnosis of pustular psoriasis was made clinically and histologically. It was possible to reproduce the disease by the intradermal injection of killed Group A streptococcal organisms. The induced pustules, as well as those appearing clinically, were intraepidermal and indistinguishable from the Kogoj spongiform abscess, and on serial sectioning showed a distinctive localization to the acryosyringium. Immunosuppressant as well as antistreptococcal therapy in the form of cyclophosphamide and clindamycin was of help. The process is classified as a nonvasculitic pustular bacterid, and as a prototype for antigen localization of lesions to the occluded epidermal sweat duct unit.
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9/48. Streptococcal toxic shock syndrome revealed by a peritonitis. Case report and review of the literature.

    Group A streptococcus (GAS) or streptococcus pyogenes cause a variety of life-threatening infectious complications including necrotizing fasciitis, purpura fulminans and streptococcal toxic shock syndrome (STSS). exotoxins that act as superantigens are felt to be responsible for STSS. These exotoxins are highly destructive to skin, muscle and soft tissue. This syndrome has a rapid and fulminant course with frequently fatal outcome. GAS remains sensitive to penicillin but in serious infection a combination of clindamycin and ceftriaxone or meropenemum is recommended. Several studies have shown that mortality was dramatically reduced in STSS patients treated with immunoglobulin g given intravenously (IVIG). Early recognition of this most rapidly progressive infection and prompt operative debridement are required for successful management. This report presents a female patient at two month post-partum with a peritonitis and multi-organ failure.
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10/48. Invasive Group C Streptococcus infection associated with rhabdomyolysis and disseminated intravascular coagulation in a previously healthy adult.

    Infections with Group C Streptococci can lead to severe disease, particularly in individuals with underlying illnesses such as cardiovascular disease, malignancy or immunosuppression. We report the first case of rhabdomyolysis and disseminated intravascular coagulation secondary to Group C Streptococcus in a previous healthy male. A toxic shock-like syndrome associated with Group C and Group G Streptococci has been reported. However, unlike with Group A Streptococci, production of endotoxins by these organisms is less well defined. We tested the patient's isolate for its ability to produce superantigenic toxins and to induce a mitogenic response. Although it is not known whether Group C Streptococci require special growth conditions for the production of superantigens, we could not demonstrate either the production of exotoxins or the induction of a mitogenic response.
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