Erik Torell

The first major extended-spectrum β-lactamase outbreak in Scandinavia was caused by clonal spread of a multiresistant Klebsiella pneumoniae producing CTX-M-15†

Between May and December 2005, 64 multidrug‐resistant isolates of Klebsiella pneumoniae were detected from patients admitted to Uppsala University Hospital. This represented a dramatic increase in ESBL‐producing K. pneumoniae compared to previous years. To investigate the epidemiology and to characterize the resistance mechanisms of the isolates, a study was initiated. Antibiotic susceptibility was determined by means of the Etest and the disc diffusion method. Extended‐spectrum beta‐lactamase (ESBL) production was identified by clavulanic acid synergy test and confirmed with PCR amplification followed by DNA sequencing. DNA profiles of the isolates were examined with pulsed‐field gel electrophoresis (PFGE). All isolates were resistant or exhibited reduced susceptibility to cefadroxil, cefuroxime, cefotaxime, ceftazidime, aztreonam, piperacillin/tazobactam, ciprofloxacin, tobramycin, and trimethoprim‐sulfamethoxazole. They produced ESBL of the CTX‐M‐15 type, and the involvement of a single K. pneumoniae clone was shown. This is the first major clonal outbreak of multiresistant ESBL‐producing K. pneumoniae in Scandinavia. The outbreak demonstrates the epidemic potential of enterobacteria containing ESBLs of the CTX‐M type, even in a country with a relatively low selective pressure and a low prevalence of multiresistant bacteria.

Intrahospital spread of Vancomycin-resistant Enterococcus faecium in Sweden

During a 17-week period vancomycin-resistant Enterococcus faecium (VRE) was found in clinical specimens from 4 in-patients. All bacterial isolates were phenotypically VanA, showing high-level resistance to vancomycin (MIC 256 micrograms/ml) and teicoplanin (MIC 24-256 micrograms/ml). The corresponding gene (vanA) was detected with PCR in strains from 3 of the patients. Three patients had been hospitalized at the renal unit at Orebro Medical Centre Hospital (OMCH). The fourth patient, diagnosed in another hospital, had received treatment in the oncology unit at OMCH. All patients recovered without treatment specific for VRE. Isolates from 2 patients were indistinguishable by pulsed-field gel electrophoresis of genomic DNA. Genetically, these strains were related to the VRE isolates from the 2 other patients. Screening of hospital staff and other in-patients for gastrointestinal carriage of VRE was negative. Glycopeptide-resistant enterococci have not previously been found in OMCH. No new cases were identified during a 10-month follow-up period. Our cases represent the first nosocomial outbreak of VRE in Sweden.

Community-acquired pneumonia and bacteraemia in a healthy young woman caused by methicillin-resistant Staphylococcus aureus (MRSA) carrying the genes encoding Panton-Valentine leukocidin (PVL).

Community-acquired pneumonia and bacteraemia in a healthy young woman caused by methicillin-resistant Staphylococcus aureus (MRSA) carrying the genes encoding Panton-Valentine leukocidin (PVL).

Ampicillin-resistant Enterococci in a Swedish University Hospital: Nosocomial Spread and Risk Factors for Infection

Ampicillin-resistant enterococci (ARE) have recently emerged as clinical pathogens in Sweden. Between 1991 and 1995 the incidence of ARE among enterococcal isolates at Uppsala University Hospital increased from 0.5% to 8.1%. Shedding of ARE from infected cases and risk factors for infection with ARE were studied during a period of 7 months for 38 ARE cases and 38 controls with ampicillin-susceptible enterococci. ARE cases had longer mean duration of hospitalization than controls (29 d vs. 15 d; p = 0.002). In univariate analysis other risk factors for infection with ARE were found to be prior therapy with > 2 antimicrobials (odds ratio [OR] 3.3; 95% confidence interval [CI] 1.2-9.5), > 4 weeks of antimicrobial therapy (OR 6.9; CI 1.8-28.3) and cephalosporin therapy (OR 9.1; CI 2.6-33.7). Fourteen of 26 skin carriers of ARE were found to be shedding ARE to the environment, compared to 2 of 12 non-skin carriers (p = 0.03). Pulsed-field gel electrophoresis suggested multifocal origin of the majority of the infecting ARE strains. Non-recognized fecal colonization and silent spread of ARE among many patients and over a prolonged time period is suggested to be the main explanation for the increase of ARE infections in our hospital. Infection control measures focusing on protecting patients at high risk for ARE infections and further efforts to optimize antimicrobial use are proposed.Ampicillin-resistant enterococci (ARE) have recently emerged as clinical pathogens in Sweden. Between 1991 and 1995 the incidence of ARE among enterococcal isolates at Uppsala University Hospital increased from 0.5% to 8.1%. Shedding of ARE from infected cases and risk factors for infection with ARE were studied during a period of 7 months for 38 ARE cases and 38 controls with ampicillin-susceptible enterococci. ARE cases had longer mean duration of hospitalization than controls (29 d vs. 15 d; p = 0.002). In univariate analysis other risk factors for infection with ARE were found to be prior therapy with > 2 antimicrobials (odds ratio [OR] 3.3; 95% confidence interval [CI] 1.2-9.5), > 4 weeks of antimicrobial therapy (OR 6.9; CI 1.8-28.3) and cephalosporin therapy (OR 9.1; CI 2.6-33.7). Fourteen of 26 skin carriers of ARE were found to be shedding ARE to the environment, compared to 2 of 12 non-skin carriers (p = 0.03). Pulsed-field gel electrophoresis suggested multifocal origin of the majority of the infecting ARE strains. Non-recognized fecal colonization and silent spread of ARE among many patients and over a prolonged time period is suggested to be the main explanation for the increase of ARE infections in our hospital. Infection control measures focusing on protecting patients at high risk for ARE infections and further efforts to optimize antimicrobial use are proposed.

A case-control study of risk factors for urinary acquisition of Klebsiella pneumoniae producing CTX-M-15 in an outbreak situation in Sweden.

Abstract A retrospective case–control study was initiated at Uppsala University Hospital in 2006 during a major outbreak caused by a Klebsiella pneumoniae strain producing CTX-M-15. To identify risk factors associated with acquisition of the outbreak strain in the urinary tract, 52 case patients with a urine culture positive for the outbreak strain between 1 May and 31 December 2005 were enrolled. Case patients were matched 1:2 with concurrently hospitalized control patients with significant growth of susceptible Escherichia coli in a urine sample. Conditional logistic regression analyses identified hospital stay ≥9 days (odds ratio (OR) 18.8, 95% confidence interval (CI) 5.74–61.2), nasogastric feeding tube (OR 18.0, 95% CI 2.28–142) and diarrhoea (OR 9.62, 95% CI 3.30–28.1) as risk factors with high ORs. The odds of previous use of cephalosporins were 7.58 (95% CI 3.13–18.4) times higher in case patients compared with the controls. Several multivariable models were evaluated to reduce bias from confounding. These models identified prolonged period of hospitalization, diarrhoea, malignancy and antibiotic use as the most important risk factors for acquisition of the outbreak strain, factors that are often found in elderly patients with a poor functional status.