Genomic-based transmission analysis of carbapenem-resistant Pseudomonas aeruginosa at a tertiary care centre in Cologne (Germany) from 2015 to 2020

Abstract

Objectives To describe the propensity of carbapenem-resistant Pseudomonas aeruginosa to spread within a hospital critical care setting. Methods The study was conducted in a 700-bed tertiary centre in Cologne, Germany. P. aeruginosa resistant to piperacillin, ceftazidime, cefepime, imipenem, meropenem and ciprofloxacin, isolated from clinical and screening specimens from four critical care units from 2015 to 2020 were analysed. Genotyping was carried out by WGS (Illumina and MinION). MLST, core genome MLST (cgMLST) and resistome analysis was performed and merged with epidemiological data. Results Fifty-five out of 79 non-duplicate P. aeruginosa isolates were available, of which 20 were carbapenemase producers as follows: blaVIM-1 (n = 1), blaVIM-2 (n = 17), blaVIM-4 (n = 1), and blaNDM-1/blaGES-5 (n = 1). Forty-two of 55 isolates were hospital-acquired. cgMLST revealed three clusters: Cluster 1 (n = 15, ST111, blaVIM-2, recovered between 2015 and 2020); Cluster 2 (n = 4, ST970, carbapenemase negative); and Cluster 3 (n = 2, ST357, carbapenemase negative). The blaVIM-2 gene of Cluster 1 was integrated on the chromosome in a class 1 integron (type In59). Using conventional epidemiology, we were only able to confirm two patient-to-patient transmissions and one room-to-patient transmission on three different ICUs within Cluster 1. Isolates from Cluster 2 represented an outbreak occurring in 2019. Conclusions These data give insight into the epidemiology of carbapenem-resistant P. aeruginosa. Transmission dynamics differed between carbapenemase- and non-carbapenemase-producing isolates. A continuous acquisition of clonally related ST111 VIM-2 P. aeruginosa, being the main carbapenemase-producing strain, was observed over the whole study period, as well as an overall higher genomic diversity among non-carbapenemase-producing P. aeruginosa.

Molecular Analysis of Carbapenem and Aminoglycoside Resistance Genes in Carbapenem-Resistant Pseudomonas aeruginosa Clinical Strains: A Challenge for Tertiary Care Hospitals

“…Although non-carbapenemase-producing CRPA strains due to decreased outer membrane permeability, overexpression of efflux pump genes or increased chromosomal cephalosporinase AmpC production have been prevalent, carbapenemases have significantly contributed to the expansion of CRPA [18][19][20]. Carbapenemases identified among P. aeruginosa are bla NDM-1 , bla IMP , bla VIM , bla KPC-2 , bla KPC-90 and bla OXA-48 [21][22][23][24][25][26][27][28][29]. Coresistance of carbapenemases with other resistance-encoding genes in P. aeruginosa is usually linked with high levels of carbapenem resistance [17,30].…”

Infection Prevalence at a Tertiary Hospital in Hail, Saudi Arabia: A Single-Center Study to Identify Strategies to Improve Antibiotic Usage

“…The study concluded that ST111 VIM-2 P. aeruginosa was the main carbapenemase-producing strain that spread in the hospitals. 5 In Thailand, a study revealed that two N. gonorrhoeae isolates in heterosexual subjects had reduced susceptibility to ceftriaxone. The study isolated around 134 isolates of N. gonorrhoeae , and they found that two isolates NG-083 and NG-091 were not susceptible to ceftriaxone.…”