Background: In healthcare environments, sinks are being increasingly recognized as reservoirs for multidrug-resistant Gram-negative bacteria. In our hospital, carbapenemase-producing, Verona Integron-encoded Metallo-beta-lactamase (VIM)-positive Pseudomonas aeruginosa (VIM-PA) was detected at low endemicity in patients, and environmental culturing revealed that sink drains were primary reservoirs. Therefore, an intervention was initiated in several wards to install sink drain plugs as physical barriers against splashing to prevent transmission of VIM-PA from drain reservoirs to the surrounding sink environment.
View Article and Find Full Text PDFIn hospitals, sinks act as reservoirs for bacterial pathogens. To assess the extent of splashing, fluorescein dye was added to four hospital sinks previously involved in pathogen dispersal to the environment and/or transmission to patients, and one sink that was not. Applying dye to the p-trap or tailpiece did not result in any fluorescent droplets outside of the drain.
View Article and Find Full Text PDFVerona Integron-encoded Metallo-beta-lactamase (VIM) is the most frequently-encountered carbapenemase in the healthcare-related pathogen Pseudomonas aeruginosa. In the Netherlands, a low-endemic country for antibiotic-resistant bacteria, no national surveillance data on the prevalence of carbapenemase-producing P. aeruginosa (CPPA) was available.
View Article and Find Full Text PDFIn hospitals, Verona Integron-encoded Metallo-beta-lactamase (VIM)-positive Pseudomonas aeruginosa may colonize sink drains, and from there, be transmitted to patients. These hidden reservoirs are difficult to eradicate since P. aeruginosa forms biofilms that resist disinfection.
View Article and Find Full Text PDFVerona-Integron-encoded-Metallo-β-lactamase-positive Pseudomonas aeruginosa (VIM-PA) is a cause of hard-to-treat nosocomial infections, and can colonize hospital water networks alongside Acanthamoeba. We developed an in-vitro disinfection model to examine whether Acanthamoeba castellanii can harbour VIM-PA intracellularly, allowing VIM-PA to evade being killed by currently used hospital disinfectants. We observed that A.
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