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Carbapenemase-producing Enterobacteriaceae (CPE) outbreaks are mostly attributed to patient-to-patient transmission via healthcare workers.
Objective
We describe successful containment of a prolonged OXA-48–producing S. marcescens outbreak after recognizing the sink traps as the source of transmission.
Methods
The Sheba Medical Center intensive care unit (ICU), contains 16 single-bed, semi-closed rooms. Active CPE surveillance includes twice-weekly rectal screening of all patients. A case was defined as a patient detected with OXA-48 CPE >72 hours after admission. A root-cause analysis was used to investigate the outbreak. All samples were inoculated on chrom-agar CRE, and carbapenemase genes were detected using commercial molecular Xpert-Carba-R. Environmental and patient S. marcescens isolates were characterized using PFGE.
Results
From January 2016 to May 2017, 32 OXA-48 CPE cases were detected, and 81% of these were S. marcescens. A single clone was the cause of all but the first 2 cases. The common factor in all cases was the use of relatively large amounts of tap water. The outbreak clone was detected in 2 sink outlets and 16 sink traps. In addition to routine strict infection control measures, measures taken to contain the outbreak included (1) various sink decontamination efforts, which eliminated the bacteria from the sink drains only temporarily and (2) educational intervention that engaged the ICU team and lead to high adherence to ‘sink-contamination prevention guidelines.’ No additional cases were detected for 12 months.
Conclusions
Despite persistence of the outbreak clones in the environmental reservoir for 1 year, the outbreak was rapidly and successfully contained. Addressing sink traps as hidden reservoirs played a major role in the intervention.
To assess the prevalence of and risk factors for carbapenem-resistant Klebsiella pneumoniae (CRKP) carriage among patients in post-acute-care facilities (PACFs) in Israel.
Design, Setting, and Patients.
A cross-sectional prevalence survey was conducted in 12 PACFs. Rectal swab samples were obtained from 1,144 patients in 33 wards. Risk factors for CRKP carriage were assessed among the cohort. Next, a nested, matched case-control study was conducted to define individual risk factors for colonization. Finally, the cohort of patients with a history of CRKP carriage was characterized to determine risk factors for continuous carriage.
Results.
The prevalence of rectal carriage of CRKP among 1,004 patients without a history of CRKP carriage was 12.0%. Independent risk factors for CRKP carriage were prolonged length of stay (odds ratio [OR], 1.001; P < .001), sharing a room with a known carrier (OR, 3.09; P = .02), and increased prevalence of known carriers on the ward (OR, 1.02; P = .013). A policy of screening for carriage on admission was protective (OR, 0.41; P = .03). Risk factors identified in the nested case-control study were antibiotic exposure during the prior 3 months (OR, 1.66; P = .03) and colonization with other resistant pathogens (OR, 1.64; P = .03). Among 140 patients with a history of CRKP carriage, 47% were colonized. Independent risk factors for continued CRKP carriage were antibiotic exposure during the prior 3 months (OR, 3.05; P = .04), receipt of amoxicillin-clavulanate (OR, 4.18; P = .007), and screening within 90 days of the first culture growing CRKP (OR, 2.9; P = .012).
Conclusions.
We found a large reservoir of CRKP in PACFs. Infection-control polices and antibiotic exposure were associated with patient colonization.
The recent emergence of carbapenem resistance among Enterobacteriaceae is a major threat for hospitalized patients, and effective strategies are needed.
Objective.
To assess the effect of an intensified intervention, which included active surveillance, on the incidence of infection with carbapenem-resistant Klebsiella pneumoniae.
Setting.
Sheba Medical Center, a 1,600-bed tertiary care teaching hospital in Tel Hashomer, Israel.
Design.
Quasi-experimental study.
Methods.
The medical records of all the patients who acquired a carbapenem-resistant K. pneumoniae infection during 2006 were reviewed. An intensified intervention was initiated in May 2007. In addition to contact precautions, active surveillance was initiated in high-risk units. The incidence of clinical carbapenem-resistant K. pneumoniae infection over time was measured, and interrupted time-series analysis was performed.
Results.
The incidence of clinical carbapenem-resistant K. pneumoniae infection increased 6.42-fold from the first quarter of 2006 up to the initiation of the intervention. In 2006, of the 120 patients whose clinical microbiologic culture results were positive for carbapenem-resistant K. pneumoniae, 67 (56%) developed a nosocomial infection. During the intervention period, the rate of carbapenem-resistant K. pneumoniae rectal colonization was 9%. Of the 390 patients with carbapenem-resistant K. pneumoniae colonization or infection, 204 (52%) were identified by screening cultures. There were a total of 12,391 days of contact precautions, and of these, 4,713 (38%) were added as a result of active surveillance. After initiation of infection control measures, we observed a significant decrease in the incidence of carbapenem-resistant K. pneumoniae infection.
Conclusions.
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.
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