Pseudomonas aeruginosa, a gram-negative bacterium, is often the root cause behind hospital-acquired infections. Predominantly affecting delicate and immunocompromised patients in intensive care units (ICUs), it’s frequently isolated in moist hospital environments, surviving through biofilm formation. According to a report by the European Centre for Disease Prevention and Control, P. aeruginosa was isolated as the primary microorganism in ICU-acquired pneumonia cases and the fifth most prevalent bacterium in acquired bloodstream infections.
From January 2018 to June 2024, we’ve observed a rise in cases of Verona Integron-encoded Metallo-beta-lactamase (VIM) producing P. aeruginosa (PA-VIM) among patients in our surgical intensive care unit (SICU). Unchecked use of carbapenems, a last-resort drug used to treat multidrug-resistant P. aeruginosa, has led to the development of resistance mechanisms, namely decreased permeability, overexpression of intrinsic efflux systems, and production of carbapenemases. The emergence of resistance is a growing concern, resulting in VIM, the most widespread metallo-beta-lactamase in P. Aeruginosa, leading to limited therapeutic solutions.
To understand this phenomenon better, we conducted a study to investigate PA-VIM in the SICU, focusing on the long-term outbreaks involving a persistent environmental reservoir. The approach taken included active case finding, identifying and analyzing factors influencing PA-VIM acquisition, discovering environmental reservoirs, executing a whole-genome sequencing analysis of patient and environmental strains, and implementing control measures.
Over the course of these outbreaks, 32 patients were found to have a minimum of one PA-VIM positive clinical sample during their stay in the SICU. The factors significantly associated with PA-VIM acquisition included exposure to antibiotics and antifungals, use of a nasogastric tube, and enteral nutrition. Out of 342 environmental samples from the SICU that included sink drains and other items used for enteral nutrition, almost 20% tested positive for PA-VIM. Two significant clones consisting of both patient and environmental strains were identified.
Despite the trials, it was found that attempts to eradicate the PA-VIM reservoir (disinfection, descaling, or replacement of sink drains) failed or achieved only a fleeting effect. In a given moist hospital setting, P. aeruginosa spreads via contaminated equipment or surfaces, a pattern that necessitated a more thoughtful approach to containment.
Source: https://aricjournal.biomedcentral.com/articles/10.1186/s13756-025-01599-2