Oseltamivir overuse at a Chicago hospital during the 2009 influenza pandemic and the poor predictive value of influenza-like illness criteria.

We report on the overuse of oseltamivir at Rush University Medical Center, Chicago during the 2009 H1N1 influenza pandemic. Of 210 patients with suspected influenza who underwent respiratory virus reverse transcription polymerase chain reaction (RT-PCR) testing, 113 (54%) received empiric oseltamivir therapy. However, only 50 treated patients (44%) had laboratory confirmed 2009 H1N1. Factors associated with oseltamivir use included a younger median age (including age < 5 y), subjective fever, cough, rhinorrhea, myalgias, higher median temperature, and fulfilment of the US Centers For Disease Control and Prevention (CDC) influenza-like illness (ILI) criteria. However, on multivariate analysis, only subjective fever (p = 0.006, odds ratio (OR) 3.1, 95% confidence interval (CI) 1.4-6.7) and fulfilment of CDC ILI criteria (p = 0.001, OR 3.6, 95% CI 1.7-7.5) were significantly associated with the receipt of oseltamivir. The CDC ILI criteria had a poor positive predictive value of 43% (95% CI 33.3-53.3) for 2009 H1N1. While the ILI criteria are a useful epidemiologic tool, it is too imprecise for direct patient care.

Genetic Mechanisms of Antimicrobial Resistance of Acinetobacter baumannii.

OBJECTIVE: To summarize published data identifying known genetic mechanisms of antibiotic resistance in Acinetobacter baumannii and the correlating phenotypic expression of antibiotic resistance. DATA SOURCES: MEDLINE databases (1966-July 15, 2010) were searched to identify original reports of genetic mechanisms of antibiotic resistance in A. baumannii. DATA SYNTHESIS: Numerous genetic mechanisms of resistance to multiple classes of antibiotics are known to exist in A. baumannii, a gram-negative bacterium increasingly implicated in nosocomial infections. Mechanisms may be constitutive or acquired via plasmids, integrons, and transposons. Methods of resistance include enzymatic modification of antibiotic molecules, modification of antibiotic target sites, expression of efflux pumps, and downregulation of cell membrane porin channel expression. Resistance to ß-lactams appears to be primarily caused by ß-lactamase production, including extended spectrum ß-lactamases (b/aTEM, blaSHV, b/aTX-M,b/aKPC), metallo-ß-lactamases (blaMP, blaVIM, bla, SIM), and most commonly, oxacillinases (blaOXA). Antibiotic target site alterations confer resistance to fluoroquinolones (gyrA, parC) and aminoglycosides (arm, rmt), and to a much lesser extent, ß-lactams. Efflux pumps (tet, ade, abe) contribute to resistance against ß-lactams, tetracyclines, fluoroquinolones, and aminoglycosides. Finally, porin channel deletion (carO, oprD) appears to contribute to ß-lactam resistance and may contribute to rarely seen polymyxin resistance. Of note, efflux pumps and porin deletions as solitary mechanisms may not render clinical resistance to A. baumannii. CONCLUSIONS: A. baumannii possesses copious genetic resistance mechanisms. Knowledge of local genotypes and expressed phenotypes for A. baumannii may aid clinicians more than phenotypic susceptibilities reported in large epidemiologic studies.