Faecal carriage of multidrug-resistant bacteria and associated risk factors: results from a point prevalence study

Abstract

Objectives Since 2003, incidences of carbapenemase-producing Gram-negative bacilli (CP-GNB) and vancomycin-resistant Enterococcus faecium (VRE) have steadily increased in France. We therefore conducted a point prevalence study to estimate carriage rates of CP-GNB, VRE and ESBL-producing Enterobacterales (ESBL-PE) and associated risk factors. Methods Between September 2019 and January 2020, all inpatients hospitalized on a given day in 11 teaching hospitals in the Paris urban area were eligible. Patient interviews and rectal swab screening results were recorded by dedicated nurses. The swabs were plated onto selective chromogenic media and processed using the GeneXpert® system. Results Of 2396 patients, 364 (15.2%) yielded at least one multiresistant bacterial isolate, including 29 CP-GNB carriers (1.2%), 13 VRE carriers (0.5%) and 338 ESBL-PE carriers (14%). In 15 patients (4.4% of ESBL-PE carriers and 36.6% of CP-GNB/VRE carriers), concomitant CP-GNB/VRE and ESBL-PE carriage was observed. In 7/29 CP-GNB and 7/13 VRE carriers, carbapenemase production and vanA in the screening samples was only detected with Xpert® tests. The OXA-48 gene was predominant in 13/34 CP-GNB isolates from 29 carriers. From the 338 ESBL-PE carriers, 372 isolates were recovered, mainly Escherichia coli (61.2%). Among 379 children, 1.1% carried a CP-GNB/VRE strain, and 12.4% carried an ESBL strain. Previous hospitalization outside mainland France, previous antimicrobial treatment and previous ESBL-PE carriage were the main risk factors associated with CP-GNB and/or VRE carriage. Conclusions The low CP-GNB and VRE prevalence likely reflects the French policy to limit intrahospital spread of CP-GNB and VRE strains.

The place of new antibiotics for Gram-negative bacterial infections in intensive care: report of a consensus conference

“…In France, ertapenem-resistant Enterobacterale isolates vary between 0.02 and 0.2% [ 23 ]. A 2019 study in 11 Parisian hospitals found that only 1.2% of patients were colonized with carbapenemase-producing Enterobacteriales [ 4 ]. In an intensive care setting, REA-REZO 2018 data showed that 14.4% of health care-associated infections were attributed to Pseudomonas aeruginosa , with 23.3% of carbapenem-resistant strains, without specifying the mechanism of resistance [ 24 ].…”

Rationale and evidence for the use of new beta-lactam/beta-lactamase inhibitor combinations and cefiderocol in critically ill patients

“…In 2017, in the 37 European countries contributing to the eCDC surveillance program, the prevalence of carbapenem resistance among invasive isolates of K. pneumoniae and E. coli ranged from 0 to 65% and from 0% to 1.6%, respectively; 16 (43%) countries reported regional or interregional spread of CPE while four countries (Greece, Italy, Turkey and Malta) declared an endemic situation [ 25 ]. In France, CPE infections remain infrequent, with less than 1000 cases reported annually [ 26 ], in line with a low prevalence of colonization—indeed, in a recent study including 2396 hospitalized patients, the rate of intestinal carriage of CPE was still 1.2% [ 27 ].…”

“…From references [31-35, 38, 40, 42-45, 50, 51, 54, 56-60, 63, 64, 66, 68, 69, 74, 75] Susceptibility profiles are indicated for carbapenem-resistant isolates only KPC: Klebsiella pneumoniae carbapenemase; MBL: metallo-β-lactamase; NDM: New-Delhi MBL; MIC: minimal inhibitory concentration a OXA-48 and derivatives (e.g., OXA-181 and OXA-232)-note that these β-lactamases hydrolyze penicillins and carbapenems but not broad-spectrum cephalosporins; b NDM is the main MBL type in Enterobacterales (other types such as VIM are less common); c main efflux pump systems implicated in carbapenem resistance in P. aeruginosa are MexAB-OprM and MexEF-OprN; d various MBL types (VIM, IMP, NDM, SPM)-other carbapenemase types are occasionally documented in P. aeruginosa, including class A (KPC and GES) and C (OXA-48-like) carbapenemases; e mainly OXA-23-, OXA-24/40-, and OXA-58-like enzymes; f ceftolozane-tazobactam is not active against carbapenemase-producing isolates of P. aeruginosa; g intrinsic resistance or limited susceptibility (species); h activity resting on the combination of aztreonam and avibactam (see the text for explanations); i no defined EUCAST breakpoint (insufficient data) remain infrequent, with less than 1000 cases reported annually [26], in line with a low prevalence of colonization-indeed, in a recent study including 2396 hospitalized patients, the rate of intestinal carriage of CPE was still 1.2% [27].…”