Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.2.3.23 (GAS)
 957 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Some patients with Group A Streptococcal toxic shock syndrome (StrepTSS) develop a unique form of cardiomyopathy characterized by global hypokinesia and reduced cardiac index. Here we investigated the immune responses of cardiomyocytes to Group A Streptococcus both in vivo and in vitro. Our data demonstrate that cardiomyocyte-derived cytokines are produced following both direct GAS stimulation and after exposure to GAS-activated inflammatory cells. These locally produced, cardiomyocyte-derived cytokines may mediate cardiac contractile dysfunction observed in patients with StrepTSS-associated cardiomyopathy and may hold the key to our ability to attenuate this severe complication.
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PMID:Do cardiomyocytes mount an immune response to Group A Streptococcus? 2137 78

Streptococcal toxic shock syndrome (STSS) is a systemic, life-threatening illness usually caused by invasive respiratory tract or skin and soft tissue infections of Streptococcus pyogenes (group A streptococcus, GAS). We report the case of an adult woman with lactational amenorrhea and GAS vulvovaginitis progressing to STSS. She was admitted to our hospital because of fever, lethargy, and a 2-week history of vaginal discharge; she also had hypotension and multiple organ failure. Blood and urine cultures yielded gram-positive cocci and GAS. After 14 days of antimicrobial therapy, she fully recovered without any complications. The vulvovaginitis was most likely the portal of entry for GAS, which is rarely recognized as a causative pathogen of vulvovaginitis. Lactational amenorrhea is thought to be a risk factor for GAS vulvovaginitis. It is important for clinicians to recognize the possibility of GAS vulvovaginitis in breastfeeding women with vaginal symptoms and consider the necessity of prompt antibiotic treatment.
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PMID:Streptococcal toxic shock syndrome following group A streptococcal vulvovaginitis in a breastfeeding woman. 3115 10

Streptococcal toxic shock syndrome (STSS) is caused mainly by Streptococcus pyogenes (Group A Streptococci, GAS), and it has a fatality rate of 25%. Mutations in CsrRS and RopB, which suppress the transcription of many virulence factors, were recently found in clinical isolates from STSS patients, but it is not fully understood when and where GAS acquires the mutations in the host. To resolve this question, we used our mouse model of human STSS to recover GAS strains from injections sites, spleens and blood of moribund mice with STSS-like symptoms, and analyzed the sequence of the covR/covS genes and ropB gene that encode CsrRS and RopB. Fifteen out of twenty mice that were inoculated transdermally into muscles with GAS organisms became moribund with STSS-like symptoms after more than 20 days after inoculation. We found that all the disseminated GAS strains recovered from the blood and spleens of the moribund mice had mutations in either the covR genes or the covS genes. The mutation sites in the GAS strains recovered from the blood and spleen were identical in each mouse, whereas the strains recovered from the muscles included a mix of disseminated strains, other mutant strains, and the parent strain. The mutant strains killed mice significantly earlier than the parent strain. Our data indicated that GAS organisms remained at the injection site, and various mutants appeared there, among which the strain that acquires the mutation in the covR/S gene is expected to overexpress various virulence factors simultaneously and cause systemic infection such as STSS.
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PMID:Acquisition of genetic mutations in Group A Streptococci at infection site and subsequent systemic dissemination of the mutants with lethal mutations in a streptococcal toxic shock syndrome mouse model. 3213 23