Search

The aim of this study was to describe the molecular epidemiology and the mechanisms of resistance to beta-lactams of emerging extensive-drug-resistant Pseudomonas aeruginosa (XDRPA) in a tertiary-care university hospital over a three-year period. Analysis included antimicrobial susceptibility profiling and pulsed-field gel electrophoresis (PFGE). Resistance mechanisms to beta-lactams were identified: production of naturally occurring and acquired beta-lactamases, overproduction of MexAB-OprM and MexXY efflux systems and loss of porin OprD were assessed. Eighteen patients were colonised or infected with XDRPA which remained susceptible to colistin and, to a lesser extent, to rifampicin. beta-lactam resistance was, in most cases, due to the overproduction of AmpC, overproduction of the MexXY efflux system and loss of porin OprD. One isolate produced the class D extended-spectrum oxacillinase (OXA-ESBL) Oxa-28, but none produced metallo-beta-lactamase (MBL) or class A extended-spectrum beta-lactamase (ESBL). The XDRPA clustered in eight PFGE patterns and both the acquisition and loss of resistance determinants was observed within a single clone during its spread. The emergence of XDRPA isolates in our university hospital has been characterised by genotypic heterogeneity, variation of mechanisms of resistance to beta-lactams in a single clone and the predominance of chromosomally encoded resistance mechanisms.

Through numerous reports of Pseudomonas aeruginosa outbreaks linked to transmission from environmental reservoirs, infection control practitionners have a univocal picture of its epidemiology: it is an opportunistic pathogen responsible of major outbreaks in intensive care units (ICU) with a major role played by the water network. The objective of this review was to answer to three questions: what is the part of hospital acquisition of P. aeruginosa? What is the part of outbreaks on incidence of hospital-acquired infections? What is the part of environment as a reservoir for transmission? Genotyping of hospital-acquired P. aeruginosa isolates allows us to define the endogenous or exogenous source of the infection and replace the concept of imported/acquired infection. If 80% of infections could be considered as acquired in ICU, the proportion of infections from exogenous source could be estimated at 50%. Even in a context of major outbreak, the epidemic clone represents 20% of the patients colonized and among these patients, only 50% are recognized with clinical samples. Some studies show that water fittings are a major source of P. aeruginosa in ICU. Other reports demonstrate a weak epidemiological link between environmental and clinical strains. Finally, despite the fact that the relative contributions of endogenous and exogenous sources to P. aeruginosa acquisition are not well established, we can assume that the epidemiological pattern of P. aeruginosa infection and colonization is not univocal and may vary both between ICU and within ICU depending on the period considered.

Objective: To assess the role of the water environment in the Pseudomonas aeruginosa colonization of patients in intensive care units in the absence of a recognized outbreak., Design and Setting: Prospective, single-centre study over an 8-week period in two adult ICUs at a university hospital. Environmental samples were taken from the water fittings of rooms once per week, during a 8-week period. Patients were screened weekly for P. aeruginosa carriage. Environmental and humans isolates were genotyped by using pulsed-field gel electrophoresis., Results: P. aeruginosa was detected in 193 (86.2%) of the 224 U-bend samples and 10 of the 224 samples taken from the tap (4.5%). Seventeen of the 123 patients admitted were colonized with P. aeruginosa. Only one of the 14 patients we were able to evaluate was colonized by a clone present in the water environment of his room before the patient's first positive sample was obtained., Conclusion: The role of the water environment in the acquisition of P. aeruginosa by intensive care patients remains unclear, but water fittings seem to play a smaller role in non-epidemic situations than expected by many operational hospital hygiene teams.

Abstract: Through numerous reports of Pseudomonas aeruginosa outbreaks linked to transmission from environmental reservoirs, infection control practitionners have a univocal picture of its epidemiology: it is an opportunistic pathogen responsible of major outbreaks in intensive care units (ICU) with a major role played by the water network. The objective of this review was to answer to three questions: what is the part of hospital acquisition of P. aeruginosa? What is the part of outbreaks on incidence of hospital-acquired infections? What is the part of environment as a reservoir for transmission? Genotyping of hospital-acquired P. aeruginosa isolates allows us to define the endogenous or exogenous source of the infection and replace the concept of imported/acquired infection. If 80% of infections could be considered as acquired in ICU, the proportion of infections from exogenous source could be estimated at 50%. Even in a context of major outbreak, the epidemic clone represents 20% of the patients colonized and among these patients, only 50% are recognized with clinical samples. Some studies show that water fittings are a major source of P. aeruginosa in ICU. Other reports demonstrate a weak epidemiological link between environmental and clinical strains. Finally, despite the fact that the relative contributions of endogenous and exogenous sources to P. aeruginosa acquisition are not well established, we can assume that the epidemiological pattern of P. aeruginosa infection and colonization is not univocal and may vary both between ICU and within ICU depending on the period considered. [Copyright &y& Elsevier]