Clinical infectious diseases : an official publication of the Infectious Diseases Society of America
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Review
Insights into the epidemiology and control of infection with vancomycin-resistant enterococci.
Despite control efforts, the incidence of nosocomial infections due to vancomycin-resistant enterococci (VRE) continues to increase in the United States. VRE are thought to spread primarily by cross-contamination. Recent molecular epidemiologic studies have refined our understanding of this phenomenon. ⋯ Although eradication of endemic VRE may not be possible, aggressive, multifaceted programs have been successful in diminishing the problem. A mathematical model of transmission of VRE and the effect of infection control measures in settings where they are endemic has been reported. The use of such a model may allow more precise determination of the impact of control strategies in the future.
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Randomized Controlled Trial Multicenter Study Comparative Study Clinical Trial
Prospective randomized trial of 10% povidone-iodine versus 0.5% tincture of chlorhexidine as cutaneous antisepsis for prevention of central venous catheter infection.
A multicenter prospective, randomized, controlled trial, with 0.5% tincture of chlorhexidene versus 10% povidone-iodine as cutaneous antisepsis for central venous catheter (CVC) insertion, was conducted for patients in intensive care units. Of 374 patients, 242 had a CVC inserted for >3 days and were used for the primary analysis. Outcomes included catheter-related bacteremia, significant catheter colonization (> or = 15 colony-forming units [cfu]), exit-site infection, serial quantitative exit-site culture (every 72 h), and molecular subtyping of all isolates. ⋯ There was a trend toward fewer exit-site infections in the chlorhexidine group (0 of 125 patients) versus those in the povidone-iodine group (4 of 117 patients; P=.053). Results of an intention-to-treat analysis were unchanged from the primary analysis. No difference was demonstrable between 0.5% tincture of chlorhexidine and 10% povidone-iodine when used for cutaneous antisepsis for CVC insertion in patients in the intensive care unit.
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Acetaminophen, also known as paracetamol, is a nonsteroidal anti-inflammatory drug with potent antipyretic and analgesic actions but with very weak anti-inflammatory activity. When administered to humans, it reduces levels of prostaglandin metabolites in urine but does not reduce synthesis of prostaglandins by blood platelets or by the stomach mucosa. Because acetaminophen is a weak inhibitor in vitro of both cyclooxygenase (COX)-1 and COX-2, the possibility exists that it inhibits a so far unidentified form of COX, perhaps COX-3. ⋯ This may be evidence that there are >2 isoforms of the enzyme. Recently, a variant of COX-2 induced with high concentrations of nonsteroidal anti-inflammatory drugs was shown to be highly sensitive to inhibition by acetaminophen. Therefore COX-3 may be a product of the same gene that encodes COX-2, but have different molecular characteristics.
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Case Reports
Report of 2 fatal cases of adult necrotizing fasciitis and toxic shock syndrome caused by Streptococcus agalactiae.
We describe 2 cases of fatal necrotizing fasciitis and toxic shock syndrome caused by Streptococcus agalactiae-a rare entity that has been reported in only 9 patients-in 2 nonpregnant adults.