Surgery was required by 37% (n = 739) of patients. Failure of initial therapy was more common in patients with co-morbidities vs those without (49.3% n = 767 vs 37.1% n = 163), in university vs non-university hospitals (49.7% n = 573 vs 42.4% n = 357) and in patients with nosocomial vs non-nosocomial cSSTI (53.3% n = 106 vs 45.9% n = 824). Treatment failure (defined as a need for antibiotic change) was reported in 46.6% (n = 930) of patients (mortality rate 3.4%). The most common antibiotic agent used, alone or in combination, was amoxicillin–clavulanate (29.9% n = 596) followed by piperacillin–tazobactam (18.2% n = 364). Once hospitalised, patients were usually treated on Day 1 (81.6% empirically and 17.3% with a specific therapy). aureus) and Gramnegative bacilli in 33.6% (n = 343) of patients. Microbiological diagnosis was available for 51.1% (n = 1020) of patients, revealing Gram-positive cocci in 68.9% (n = 703) (9.9% methicillin-resistant Staphylococcus aureus, 26.9% methicillin-sensitive S. One-quarter of infections (25.6% n = 510) were recurrences and 10% (n = 199) were nosocomial. Based on information in the patient records, 78.0% (n = 1557) of patients reported ≥1 co-morbidity or receiving relevant medications in the 3 months prior to hospitalisation (64.3% n = 1284) 29.9% (n = 596) had received antibacterials/antivirals. Results: The total population included 1996 patients mean age 60.6 years 57.8% male, 1154 from university hospitals, 842 from non-university hospitals. There was a slight decline in 30-day post-discharge mortality from 7.1% in the reference period 1995–1997 to 6.0% in 2004–2006. The mean length of hospital stay with community-acquired bacteremia decreased from 18.5 days in 1995 to 15.5 days in 2006, corresponding to a 16% relative reduction over this period. Results: Of the 4492 patients who were hospitalized with community-acquired bacteremia between 19, 597 (13.3%) died during hospitalization and 3895 (86.7%) were discharged alive. Here we compare the use of a cefotaxime (CTX) screen against current methods for the detection of strains with altered PBP3. Given that strains with altered PBP3 have reduced susceptibility to AMP, amoxicillin-clavulanate (AMC) and cephalosporins, a paradigm shift away from AMP MIC as a basis for detection is warranted. Many of these problems are compounded in strains with both altered PBP3 and B-lactamase. CLSI DD uses a 10 μg disc even though Karpanoja (2004) showed poor correlation of zones sizes and MIC near the BP with these discs and recommended using a 2 μg disc with better correlation, which is the disc strength used by EUCAST.
By strict CLSI criteria, BLNAR strains have AMP MICs ≥4 mg/L although most use the non-susceptible BP of ≥2, consistent with the EUCAST resistant BP of >1. Their detection is problematic because MICs cluster near the breakpoints (BPs), there is no consensus on BPs and there is poor correlation between MIC and disc diffusion (DD) zones. influenzae (BLNAR) have an N526K substitution in penicillin binding protein 3 (PBP3). Objectives: Most B-lactamase negative ampicillin (AMP) resistant H.
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