A recent, frequently quoted study has suggested that for bloodstream infections (BSIs) due to extended-spectrum β-lactamase-producing Enterobacteriaceae (ESBL) Escherichia coli, treatment with β-lactam/β-lactamase inhibitors (BLBLIs) might be equivalent to treatment with carbapenems. However, the majority of BSIs originate from the urinary tract. A multicenter, multinational efficacy analysis was conducted from 2010 to 2012 to compare outcomes of patients with non-urinary ESBL BSIs who received a carbapenem (69 patients) vs those treated with piperacillin-tazobactam (10 patients). In multivariate analysis, therapy with piperacillin-tazobactam was associated with increased 90-day mortality (adjusted odds ratio, 7.9, P=.03). For ESBL BSIs of a non-urinary origin, carbapenems should be considered a superior treatment to BLBLIs.

e Carbapenems are considered the treatment of choice for Acinetobacter baumannii infections. Many facilities implement preventive measures toward only carbapenem-resistant A. baumannii (CRAB). However, the independent role of the carbapenem resistance determinant on patient outcomes remains controversial. In a 6-year analysis of adults with A. baumannii bloodstream infection (BSI), the outcomes of 149 CRAB isolates were compared to those of 91 patients with carbapenem-susceptible A. baumannii. In bivariable analyses, CRAB BSIs were significantly associated with worse outcomes and with a delay in the initiation of appropriate antimicrobial therapy (DAAT). However, in multivariable analyses, carbapenem resistance status was no longer associated with poor outcomes, while DAAT remained an independent predictor. The epidemiological significance of A. baumannii should not be determined by its resistance to carbapenems. Acinetobacter baumannii is one of the ESKAPE (Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, A. baumannii, Pseudomonas aeruginosa, and Enterobacter species) pathogens (1), which result in a variety of serious infectious clinical syndromes (2-4). Apart from a continuous increment in incidence, offending human strains have also become more resistant (5). The prevalence of the extensively drug-resistant (XDR) A. baumannii phenotype (6) has increased exponentially worldwide (5,7,8).Carbapenems are considered the agents of choice for treating A. baumannii infections, as long as the isolates are susceptible (4, 9, 10). Therefore, resistance to carbapenems frequently determines the epidemiological significance of the pathogen (2, 10). Many hospitals utilize infection control preventive measures (isolation precautions, cohorting, and screening for asymptomatic carriage), targeting only patients with carbapenem-resistant A. baumannii (CRAB) strains (11). However, both molecular epidemiology and clinical epidemiology investigations do not support these practices. Many of the mechanisms of resistance to carbapenems are chromosomally encoded (12). Therefore, it might be appropriate to target the prevention of patient-to-patient transmission of all A. baumannii isolates, since even susceptible organisms might become resistant after they are acquired by a new host. Moreover, controlled clinical data correlating resistance to carbapenems with worse patient outcomes were subjected to several biases, i.e., the majority of studies had low sample size, infection was not appropriately differentiated from colonization, and most studies did not control for time to initiation of appropriate antimicrobial therapy (13)(14)(15)(16)(17)(18)(19)(20)(21)(22). Delay in initiating appropriate antimicrobial therapy (DAAT) is the strongest modifiable predictor of worse outcomes among septic patients (23,24), and DAAT has frequently been reported in A. baumannii infections (25). Therefore, the aim of this study was to explore the independent role of the carbapenem resistance phenotype on the clinical outcomes of pat...

In this study conducted at 2 distinct CRE endemic regions, there were unique epidemiologic features to CREn: (i) polyclonality, (ii) neonates accounting for more than 7% of cohort, and (iii) high rate of colonization (almost one-half of all cases represented colonization). Since false-positive Modified Hodge Tests in Enterobacter spp. are common, close monitoring of carbapenem resistance mechanisms (particularly carbapenemase production) among Enterobacter spp. is important.

BackgroundEpidemiological characteristics of patients with bloodstream infections (BSI) due to extended-spectrum β-lactamase producing (ESBL) and carbapenem-resistant (CRE) strains are often similar. Mortality rates for CRE BSI are 70 %, and mean time to initiation of appropriate therapy is ~5 days. A bedside score was developed to differentiate CRE-BSIs from ESBL-BSIs, in order to help decrease the time to initiation of appropriate therapy for CRE and mortality rates.FindingsScore was developed based of data (2007–2010) abstracted from charts of adult patients from Assaf Harofeh Medical Center (AHMC, Zeriffin, Israel), and validated on a cohort of patients from Detroit Medical Center (DMC, MI, USA). A multivariate model for presence of CRE was generated. A clinical prediction score and ROC curve was derived. 451 patients with ESBL BSIs (285 from AHMC and 166 from DMC) and 74 patients with CRE BSIs (58 from AHMC and 16 from DMC) were included. The prediction score included chemotherapy in the past 3 months (19 points), presence of foreign invasive devices (10 points), no peripheral vascular disease (10 points), reduced consciousness or cognition at time of acute illness (9 points), time in hospital prior to BSI ≥ 3 days (7 points), and age younger than 65 years (6 points). A score of ≥32 to define “high CRE risk” had sensitivity of 59 %, specificity of 76 %, PPV of 34 % and NPV of 90 %.ConclusionsThe score’s 90 % NPV implies it could reduce un-necessary (and toxic) empiric use of anti-CRE therapeutics, but this should be studied prospectively and on broader populations in order to test its potential role in reducing mortality.

A “high risk” clone of carbapenem-resistant Klebsiella pneumoniae (CRKP) identified by multilocus sequence typing (MLST) as sequence type (ST) 258 has disseminated worldwide. As the molecular epidemiology of the CRE pandemic continues to evolve, the clinical impact of non-ST258 strains is less well defined. We conducted an epidemiological investigation of CRKP based on strains MLST. Among 68 CRKP patients, 61 were ST258 and 7 belonged to non-ST258. Klebsiella pneumoniae ST258 strains were significantly associated with blaKPC production and with resistance to an increased number of antimicrobials. Clinical outcomes were not different. Based on this analysis, one cannot rely solely on the presence of blaKPC in order to diagnose CRKP.