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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An outbreak of infection due to Streptococcus pyogenes occurred in a geriatric rehabilitation unit between February and September 1981, affecting 10 patients and two staff. The severity of the illness ranged from asymptomatic throat carriage, through skin and soft-tissue sepsis, to fulminant septicaemia and necrotising fasciitis: two patients died of their infection. Streptococcus pyogenes infection may present in a variety of ways, and may be dangerous. Recently developed serological tests have been found useful in the surveillance of an outbreak. Although Streptococcus pyogenes is sensitive to penicillin and other antibiotics, good ward hygiene is still essential for controlling such an outbreak in an institution.
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PMID:Virulent Streptococcus pyogenes: outbreak and spread within a geriatric unit. 635 Apr 76

Two autopsy cases of fulminant-type infection associated with necrotizing fasciitis were analyzed clinicopathologically. Both cases involved 57-year-old alcohol abusers. The former was a woman with group A (beta) hemolytic Streptococcus pyogenes infection, and the latter was a man with Vibrio vulnificus infection. The sudden onset of shock with high fever resulted in sepsis, decreased clotting, and hepatorenal symptoms, followed by death within a few days. Post-mortem examination showed widespread congestion and bleeding, and alcoholic liver cirrhosis was observed. Necrotizing fasciitis was identified in both cases. Bacteria from the pharynx or intestinal tract invaded the blood, and marked bacterial proliferation produced sepsis, resulting in necrotizing fasciitis. Despite the presence of sepsis, bilateral pulmonary congestion and bleeding were observed without pneumonia. Due to the rapid progression of sepsis, there was no time for granulocyte migration from the bone marrow. It seems that almost all mature granulocytes which had already existed in the bone marrow accumulated at the focus of necrotizing fasciitis because the bone marrow had few mature granulocytes and lacked hypercellularity. The cause of death in each case was circulatory collapse due to septic shock. It was difficult to distinguish the type of infection on histopathology. Cultures were necessary to determine the bacterial agents involved.
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PMID:Autopsy cases of fulminant-type bacterial infection with necrotizing fasciitis: group A (beta) hemolytic Streptococcus pyogenes versus Vibrio vulnificus infection. 1825 85

Platelets contribute to inflammation however, the role of platelet activation during the pathophysiological response to invasive bacterial infection and sepsis is not clear. Herein, we have investigated platelet activation in a mouse model of invasive Streptococcus pyogenes infection at 5, 12, and 18 hours post infection and correlated this to parameters of infection. The platelet population in ex-vivo blood samples showed no increased integrin activation or surface presentation of CD62P, however platelet-neutrophil complex formation and plasma levels of CD62P were increased during bacterial dissemination and the progression of sepsis, indicating that platelet activation had occurred in vivo. Platelet-neutrophil complex formation was the most discriminatory marker of platelet activation. Platelet-neutrophil complexes were increased above baseline levels during early sepsis but decreased to significantly lower levels than baseline during late sepsis. The removal of these complexes from the circulation coincided with a significant increase in organ damage and the accumulation of platelets in the liver sinusoids, suggesting that platelet activation in the circulation precedes accumulation of platelets in damaged organs. The results demonstrate that monitoring platelet activation using complementary methods may provide prognostic information during the pathogenesis of invasive S. pyogenes infection.
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PMID:The Dynamics of Platelet Activation during the Progression of Streptococcal Sepsis. 2765 98