GRAM-POSITIVE SEPSIS : Mechanisms and Differences from Gram-Negative Sepsis - 08/09/11
Résumé |
In modern intensive care settings, gram-positive bacteria account for up to 50% of severe sepsis or septic shock cases, yet the pathogenesis of gram-positive shock is poorly understood.36, 45 This contrasts with the well-researched field of gram-negative sepsis, where the role of bacterial endotoxin is known to be central to development of septic shock. In this article, we attempt to review the mechanisms by which a range of clinically important gram-positive bacteria cause septic shock (Table 1) and, where appropriate, highlight contrasts and similarities with gram-negative pathogenesis.
Clinical differentiation of gram-positive and gram-negative sepsis is often attempted but seldom successful. There are situations, however, where it is possible to predict the type of infecting organism. Septic shock may be related to a focal infection, such as necrotizing fasciitis, which is known to be associated with a particular bacterial species, in this case Streptococcus pyogenes. Similarly, there may be clues from pathognomonic rashes, for example, streptococcal and staphylococcal toxic shock syndromes and meningococcemia. Finally, particular groups of patients may be particularly susceptible to septic shock caused by certain types of bacteria; urology patients with septic shock are likely to have gram-negative infection, and asplenic patients are more likely to suffer pneumococcal shock. Predicting the bacterial causes of septic shock may present an academic challenge, but in practice, broad-spectrum antibiotics will be used empirically until the laboratory isolates a causative pathogen.
The broad mechanisms by which both gram-positive and gram-negative organisms cause shock involve bacterial factors (cell wall, soluble/secreted products) and host factors (susceptibility, primary (immune) response, secondary (tissue) response). There are, however, many contrasts in the ways in which bacteria apply these mechanisms, and this will affect the success of any novel empiric therapeutic approaches to sepsis.
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| Address reprint requests to Shiranee Sriskandan, MD, PhD, Dept of Infectious Diseases, Imperial College School of Medicine, at Hammersmith Hospital, Du Cane Road, London W12 ONN, UK This work was supported by the Medical Research Council (U.K.) through a Career Development Award to Shiranee Sriskandan |
Vol 13 - N° 2
P. 397-412 - juin 1999 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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