GRAM-POSITIVE SEPSIS: Mechanisms and Differences from Gram-Negative Sepsis
Section snippets
BACTERIAL FACTORS
Gram-positive infections often arise from infected foci at, or just under, the body surface (e.g., skin infections, wound infections, muscle). Infection is often associated with an influx of host neutrophils, and the bacteria have an array of tools that allow, first, invasion of the outer host layers and, second, evasion of neutrophil-mediated phagocytosis. The processes of invasion and killing of phagocytes contribute to the inflammatory cascade leading to septic shock. In contrast,
Host Susceptibility Factors
Certain patient groups are more likely to sustain infection owing to particular groups of pathogens. Patients with surgical or traumatic wounds distant from the abdomen are more likely to develop wound infections and septic shock from gram-positive bacteria. In addition, certain groups of patients respond to infection in a distinct fashion. One example is the “alpha strep shock syndrome,” characteristically seen in neutropenic patients who have undergone bone marrow transplantation and who
SUMMARY
This article has reviewed the mechanisms by which gram-positive bacteria lead to septic shock, with regard to bacterial structure and toxicology and the host responses elicited both in animal models and in the clinical setting. Gram-positive organisms are better suited to invade host tissues and elicit, in general, a brisker phagocytic response than gram-negative organisms. The lack of endotoxin in the outer cell wall is compensated for by the presence of exposed peptidoglycan and a range of
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2020, International Journal of PharmaceuticsCitation Excerpt :In general, Gram positive and Gram negative bacteria are able to start the infection and promote the evolution for a more complicate case, as the sepsis. However, the fact that gram-positive bacteria are better suited to invade tissues than Gram-negative bacteria is known (Minasyan, 2017; Sriskandan and Cohen, 1999). The reason is based in the fact that the lack of endotoxin in the outer cell wall is compensated for by the presence of exposed peptidoglycan and a range of other toxic secreted products.
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
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Department of Infectious Diseases, Imperial College School of Medicine at Hammersmith Hospital, London, United Kingdom