314 A Modified Surveillance Protocol Identifies an Outbreak of Carbapenem Resistant Enterobacteriaceae (CRE) with Reduced Lactose Fermentation

Friday, March 19, 2010
Grand Hall (Hyatt Regency Atlanta)
Amy Mathers, MD , University of Virginia Health System, Charlottesville, VA
Heather Cox, PharmD , University of Virginia Health System, Charlottesville, VA
Joanne Carroll, BS , University of Virginia Health System, Charlottesville, VA
Kate Barowski , University of Virginia Health System, Charlottesville, VA
Megan Gosseling, MSN , University of Virginia Health System, Charlottesville, VA
Keri Hall, MD , Virginia Department of Health, Richmond, VA
Kevin Hazen, PhD , University of Virginia Health System, Charlottesville, VA
Costi D. Sifri, MD , University of Virginia Health System, Charlottesville, VA
Guidelines for surveillance and control of lactose-fermenting KPC-producing carbapenem resistant Enterobacteriaceae (CRE) have recently been published. A multispecies outbreak of KPC-positive CRE infections (n=41) at our institution was highly enriched for non- (9%) or weakly (20%) lactose-fermenting organisms.
To identify patients colonized with CRE regardless of lactose fermentation.
In April 2009, we performed targeted surveillance of CRE carriage in an intensive care unit with a patient (index case) with pneumonia due to KPC-producing Klebsiella oxytoca. Perirectal swabs of all patients in the ICU were inoculated in 5 mL tryptic soy broth with a 10 µg ertapenem disk. Following overnight incubation, 100 µL of broth was streaked on MacConkey agar. Unique colonies were classified as strongly, weakly or non-lactose fermenting. Pseudomonas spp. were eliminated by phenotypic appearance or oxidase testing. blaKPC and Tn4401 presence were confirmed by PCR analysis. Pulse field gel electrophoresis was performed to evaluated clonality. Species identification was performed by Vitek 2. Clinical data were gathered from the medical record.
Eight patients from a different unit with low risk for CRE colonization served as negative controls and the index patient served as a positive control. Point prevalence surveillance of the ICU demonstrated that 11 (85%) of 13 screened patients were colonized with CRE. Of the 12 CRE surveillance isolates, 3 (25%) were strongly lactose-fermenting K. oxytoca and 9 (75%) were weakly lactose-fermenting Enterobacter cloacae. The CRE isolates contained blaKPC and all other Tn4401 genes. Seven E. cloacae isolates were clonal by PFGE. K. oxytoca surveillance isolates were also clonal but not related to the index case isolate. Two types of KPC plasmids were identified: pUVA02 was associated with all K. oxytoca, including that of the index case, while pUVA01 was associated with 7 E. cloacae isolates. One E. cloacae isolate obtained from a patient co-colonized with K. oxytoca carried pUVA02. Lapses in proper infection control practices were observed during an audit of the unit. To address the outbreak, patients with CRE were placed on contact isolation and cohorted, the unit underwent enhanced environmental cleaning, and extensive staff education was performed. Biweekly perirectal surveillance of the unit over the following month revealed no new CRE colonization. Two patients expired from overwhelming septic shock; however, causative agent(s) were not identified, because antemortem cultures were not obtained.  
These results suggest that a screening protocol limited to lactose-fermenting organisms would have failed to identify most carriers of CRE in the study. Knowledge of local rates of CRE with reduced lactose fermentation is needed when developing a surveillance program.