Management of common bacterial infections of the skin

Bernard, Philippe

doi:10.1097/qco.0b013e3282f44c63

Cited by 95 publications

(63 citation statements)

References 42 publications

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“…They usually occur at new sites after complete resolution of the primary lesion and are thought to be reinfections by manual spread of bacteria from colonized areas such as the nares into casual epidermal microlesions. Accordingly, decolonization is an advocated measure for treatment of recurrent furunculosis (3). Hence, in the context of this study, the number of recurrences is likely to be a measure of the skin's ability to prevent new infection by controlling small inocula of pathogens.…”

Section: Discussionmentioning

confidence: 99%

Severity of Staphylococcus aureus Infection of the Skin Is Associated with Inducibility of Human β-Defensin 3 but Not Human β-Defensin 2

et al. 2010

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Gram-positive bacteria are the predominant cause of skin infections. Antimicrobial peptides (AMPs) are believed to be of major importance in skin's innate defense against these pathogens. This study aimed at providing clinical evidence for the contribution of AMP inducibility to determining the severity of Grampositive skin infection. Using real-time PCR, we determined the induction of human ␤-defensin 2 (HBD-2), HBD-3, and RNase 7 by comparing healthy and lesional mRNA levels in 32 patients with Gram-positive skin infection. We then examined whether AMP induction differed by disease severity, as measured by number of recurrences and need for surgical drainage in patients with Staphylococcus aureus-positive lesions. We found that HBD-2 and -3, but not RNase 7, mRNA expression was highly induced by Gram-positive bacterial infection in otherwise healthy skin. Less induction of HBD-3, but not HBD-2, was associated with more-severe S. aureus skin infection: HBD-3 mRNA levels were 11.4 times lower in patients with more than 6 recurrences (P ‫؍‬ 0.01) and 8.8 times lower in patients reporting surgical drainage (P ‫؍‬ 0.01) than in the respective baseline groups. This suggests that inducibility of HBD-3 influences the severity of Gram-positive skin infection in vivo. The physiological function of HBD-2 induction in this context remains unclear.

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Section: Discussionmentioning

confidence: 99%

Severity of Staphylococcus aureus Infection of the Skin Is Associated with Inducibility of Human β-Defensin 3 but Not Human β-Defensin 2

et al. 2010

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“…In addition to impetigo (pyoderma), GAS infection of the skin may penetrate the epidermis to cause cellulitis or erysipelas. Cellulitis is an infection of the subcutaneous tissues and is characterized by redness and inflammation of the skin with associated pain and swelling, while a wellcircumscribed infection that does not extend beyond the superficial layers is termed erysipelas (6,281). Bacteremia is the presence of GAS in the bloodstream and is often characterized by high fever, nausea, and vomiting as a result of a robust proinflammatory cytokine response.…”

Section: Types Of Invasive Infections Caused By Gasmentioning

confidence: 99%

Disease Manifestations and Pathogenic Mechanisms of Group A Streptococcus

et al. 2014

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SUMMARY Streptococcus pyogenes , also known as group A Streptococcus (GAS), causes mild human infections such as pharyngitis and impetigo and serious infections such as necrotizing fasciitis and streptococcal toxic shock syndrome. Furthermore, repeated GAS infections may trigger autoimmune diseases, including acute poststreptococcal glomerulonephritis, acute rheumatic fever, and rheumatic heart disease. Combined, these diseases account for over half a million deaths per year globally. Genomic and molecular analyses have now characterized a large number of GAS virulence determinants, many of which exhibit overlap and redundancy in the processes of adhesion and colonization, innate immune resistance, and the capacity to facilitate tissue barrier degradation and spread within the human host. This improved understanding of the contribution of individual virulence determinants to the disease process has led to the formulation of models of GAS disease progression, which may lead to better treatment and intervention strategies. While GAS remains sensitive to all penicillins and cephalosporins, rising resistance to other antibiotics used in disease treatment is an increasing worldwide concern. Several GAS vaccine formulations that elicit protective immunity in animal models have shown promise in nonhuman primate and early-stage human trials. The development of a safe and efficacious commercial human vaccine for the prophylaxis of GAS disease remains a high priority.

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“…This leads to considerable treatment variation among physicians based on their assessment of the severity of the infection and their preferred antibiotic regimens. Despite several expert panel recommendations and cellulitis treatment guidelines, [2][3][4][5][6][7][8][9][10][11][12][13] there are currently no clinical decision aides to assist clinicians when deciding which ED patients should be treated with oral antibiotics and which patients require intravenous (IV) therapy at first presentation.…”

mentioning

confidence: 99%