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Chemical, Mechanical, and Heat Cleaning to Decontaminate Hospital Drains Harboring Carbapenemase-Producing Enterobacteriales
- Alainna Juliette Jamal, Rajni Pantelidis, Rachael Sawicki, Angel Li, Wayne Chiu, Deborah Morrison, John Marshman, Mahin Baqi, David Richardson, Allison McGeer, Sergio Borgia
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- Journal:
- Infection Control & Hospital Epidemiology / Volume 41 / Issue S1 / October 2020
- Published online by Cambridge University Press:
- 02 November 2020, pp. s466-s467
- Print publication:
- October 2020
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Background: Carbapenemase-producing Enterobacteriales (CPE) outbreaks have been linked to contaminated wastewater drainage systems in hospitals. The optimal strategy for CPE decontamination of drains is unknown. In this randomized controlled trial, we aimed to determine whether combining chemical, mechanical, and heat cleaning was superior to routine cleaning for drain decontamination. Methods: We enrolled CPE-contaminated hospital drains at 2 geographic locations. Eligible drains were those initially found to be culture positive in a 2017 study and that remained positive (by RT-PCR) when retested twice in August 2018. Drains were stratified by type (sink versus shower) and randomized with a 1:1 allocation ratio (as per computer-generated randomization) to standard-of-care cleaning (comparator) or combined chemical, mechanical, and heat cleaning (intervention) on day 0. Drain tail pieces were swabbed on days 0 (before administration of the intervention), 1, 2, 3, 7, and 14, and at months 1, 2, 3, 4, 5, and 6. Swabs were placed into brain heart infusion with 10% Dey-Engley neutralizing broth and incubated overnight. Direct RT-PCR was performed to detect KPC, VIM, NDM, OXA-48–like, IMP, GES, and SME genes. The primary outcome was drain decontamination, defined as no detectable carbapenemase gene in the drain from day 1 to 7 (inclusive). Results: Overall, 33 CPE-contaminated drains were enrolled (7 sink and 26 shower); 17 and 16 drains were randomized to the intervention and comparator, respectively. Moreover, 12 (36%) drains met the primary outcome of decontamination, 18 (55%) remained contaminated, and 3 (9%) could not be assessed. Among drains that could be assessed, 11 of 15 (74%) in the intervention group met the primary outcome of decontamination compared to 1 of 15 (7%) in the comparator group (P = .0005). Of the 11 drains in the intervention group that were decontaminated, the carbapenemase gene present at enrollment was subsequently detected in 10 (91%): 1 (10%) at day 14, 3 (30%) at month 1, 4 (40%) at month 3, 1 (10%) at month 4, and 1 (10%) at month 6. The median time to a swab yielding CPE was 1 day in the comparator group versus 14 days in the intervention group (Fig. 1). Overall, 24 drains (73%) had a carbapenemase gene (that was not detectable at enrollment) appear in the follow-up. Of patients identified as CPE colonized or infected during this study, none occupied rooms with these drains. Conclusions: Chemical, mechanical, and heat cleaning were superior to standard cleaning for CPE decontamination of hospital drains at 7 days, but these trends were not sustained. Such cleaning may be useful if applied repeatedly.
Funding: None
Disclosures: Allison McGeer reports funds to her institution for studies for which she is the principal investigator from Pfizer and Merck as well as consulting fees from Sanofi-Pasteur, Sunovion, GSK, Pfizer, and Cidara.
Genomic Epidemiology of Carbapenemase-Producing Enterobacterales (CPE) in Toronto, Canada
- Alainna Juliette Jamal, Victoria Williams, Jerome Leis, Nathalie Tijet, Sandra Zittermann, Roberto Melano, Laura Mataseje, Michael Mulvey, Allison McGeer
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- Journal:
- Infection Control & Hospital Epidemiology / Volume 41 / Issue S1 / October 2020
- Published online by Cambridge University Press:
- 02 November 2020, pp. s479-s480
- Print publication:
- October 2020
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- Article
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- You have access Access
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Objective: We investigated whether whole-genome sequencing (WGS) data altered interpretations of clonal transmission as determined by conventional epidemiology and pulsed-field gel electrophoresis (PFGE) at a tertiary-care hospital (hospital Z, HZ). Methods: We included all carbapenemase-producing Enterobacterales (CPE)–colonized or –infected patients identified via population-based surveillance from 2007 through 2018, who were admitted to HZ during and/or in the year prior to or following CPE detection. HZ reported clonal transmission clusters using epidemiology and PFGE for CPE identified at HZ or reported to HZ by other hospitals as potentially acquired at HZ. We assessed single-nucleotide polymorphism (SNP) phylogenies and case epidemiology. Results: Overall, 85 CPE-colonized or -infected patients were included: 50 were detected at HZ and 35 were detected at another local hospital but were admitted to HZ in the previous or following year. HZ reported 6 transmission clusters (Table 1). SNP analyses confirmed clusters B, C, E, and F. In cluster A, SNP analyses cast doubt on 2 of 9 cases (possibly representing plasmid transmission) but also identified 2 additional cases with isolates highly related (0–3 SNP differences) to other isolates. One case may be the index case: a travel-related case who stayed on the same unit as case 1, 4 months before case 1 detection. The second case stayed in a room previously occupied by 5 cluster A cases. In cluster D, SNP analyses found 1 additional case whose isolate was highly related (ie, 17–19 SNP differences) to other isolates. This case was identified a year before cluster D at another hospital that shares patients with HZ; however, the case’s admission to HZ was after all cluster D cases were detected and no direct epidemiologic link was identified. Conclusions: WGS data can identify cases belonging to transmission clusters that conventional epidemiologic methods missed.
Funding: None
Disclosures: Allison McGeer reports funds to her institution from Pfizer and Merck for projects for which she is the principal investigator. She also reports consulting fees from Sanofi-Pasteur, Sunovion, GSK, Pfizer, and Cidara