A centrally coordinated intervention succeeded in containing a nationwide CRE outbreak after local measures failed. The intervention demonstrates the importance of strategic planning and national oversight in combating antimicrobial resistance.

The use of active surveillance and contact precautions, as part of a multifactorial intervention, may be an effective strategy to decrease rates of nosocomial transmission of carbapenem-resistant K. pneumoniae colonization or infection.

We found a large reservoir of CRKP in PACFs. Infection-control policies and antibiotic exposure were associated with patient colonization.

Carbapenem-resistant Klebsiella pneumoniae (CRKP) has emerged during recent years in several intensive care units. The objective of our study was to determine the incidence of CRKP and the risk factors associated with acquisition during intensive care unit (ICU) stay. This prospective cohort study was conducted between May 2007 and April 2008 in a medical-surgical ICU at a tertiary medical center. Rectal surveillance cultures were obtained from patients on admission and twice weekly. Of screened patients, 7.0% (21/299) were CRKP colonized on admission to the ICU. One hundred eighty (81%) patients were screened at least twice. Of these, 48 (27%) patients acquired CRKP during ICU stay. Of the 69 CRKP colonized patients (both imported and ICU acquired), 29% (20/69) were first identified by microbiologic cultures, while screening cultures identified 49 patients (71%). Of these, 23 (47%) subsequently developed clinical microbiological cultures. Independent risk factors for CRKP acquisition included recent surgery (OR 7.74; CI 3.42-17.45) and SOFA score on admission (OR 1.17; CI 1-1.22). In conclusion, active surveillance cultures detected a sizable proportion of CRKP colonized patients that were not identified by clinical cultures. Recent surgical procedures and patient severity were independently associated with CRKP acquisition.

Hashomer, Israel, were assessed for hVISA by using the Etest macromethod. A total of 16 patients (6%) were positive for hVISA. Resistance to teicoplanin alone and to vancomycin alone using the Etest macromethod was found in 14 and 10 patients, respectively. Standard MICs to vancomycin were between 1 to 4 mg/ml. Most of these isolates (12 of 16 [75%]) would have been missed without specific testing. The median number of bacteremic days was 4. Seven patients had positive blood cultures for more than 5 days. Twelve patients died, and for eight of these the deaths were directly related to hVISA sepsis. We found that hVISA bacteremia was prevalent in our institution, and we suggest seeking hVISA in patients with persistent S. aureus bacteremia.Infections due to methicillin-resistant Staphylococcus aureus (MRSA) are responsible for 50% of hospital acquired S. aureus infections with increasing morbidity and mortality (13). A recent meta-analysis demonstrated increased mortality in bacteremia associated with MRSA compared to methicillin-susceptible S. aureus (MSSA) (5). Glycopeptides are considered the drug of choice for treating MRSA bacteremia and sepsis. S. aureus strains with reduced vancomycin susceptibility were first reported in 1997 (9). S. aureus strains with reduced vancomycin susceptibility include vancomycin-resistant S. aureus strains (VRSA; MIC Ն 16 g/ml) and vancomycin-intermediate S. aureus strains (VISA; MIC ϭ 4 to 8 g/ml). Until 2006, the MIC for VISA was defined as 8 to 16 g/ml by the Clinical and Laboratory Standards Institute (CLSI; formerly the National Committee for Clinical Laboratory Standards), and these guidelines are still the ones approved by the U.S. Food and Drug Administration for vancomycin; the MIC for heterogeneous VISA (hVISA) strains was defined by the presence of subpopulations of VISA at a rate of 1 organism per 10 5 to 10 6 organisms (14,15,20,23). Up till April 2006 only four cases with infections due to VRSA have been reported, which exhibit the vanA gene complex found in vancomycin-resistant enterococci (2, 3, 12). A few dozen VISA strains have been reported in recent years, which have slower growth rates, thickened cell walls, and reduced levels of PBP4. The underlying genetic and biochemical mechanism by which this occurred is not known. The majority of these cases with VISA have occurred in patients who were treated with vancomycin for prolonged periods of time (7,11,19). hVISA seems to be the stage that precedes the development of VISA, and it is believed that vancomycin creates a selective pressure for these resistant strains (21).The best method for detecting hVISA is controversial. Methods are not standardized, and no clear guidelines have been issued. Population analysis profiling (PAP) is considered the gold standard, but this approach is labor-intensive and expensive. Thus, it is not realistic to use such a method for a routine service in a busy hospital setup. Various other methods used to detect hVISA were described and compared by Walsh et al. (22). Of the numerou...