Predominance of Non-carbapenemase Producing Carbapenem-Resistant Enterobacterales in South Texas

Abstract

BackgroundCarbapenem-resistant Enterobacterales (CRE) pose a significant global public health threat. Resistance among CRE is particularly complex, owing to numerous possible resistance mechanisms and broad definitions. We aimed to characterize the clinical and molecular profiles of CRE in the South Texas region.Materials and methodsWe compared the clinical, genotypic, and phenotypic profiles of carbapenemase producing Enterobacterales (CPE) with those of non-carbapenemase producers (NCPE) isolated from South Texas, United States between 2011 and 2019. Molecular characteristics and resistance mechanisms were analyzed using whole-genome sequences.ResultsThe majority (59%) of the CRE isolates were NCPE while 41% of isolates harbored carbapenemases, predmonantly blaKPC-type. The most common CPE was Klebsiella pneumoniae while majority of Enterobacter cloacae and Escherichia coli were NCPE Among K. pneumoniae, the clonal group 307 has emerged as a predmoninant group and was associated with as many CRE infections as the previous common clonal group 258. Patients with NCPE compared to CPE infections were associated with higher antimicrobial exposure prior to culture collection (days of therapy, 795 vs. 242; p < 0.001) and emergency department visits within past 90 days (22% vs. 4%; p = 0.011). The all cause 30-day mortality was 21%.ConclusionsThis study highlights the diversity of resistance mechanisms underlying CRE in South Texas, with 59% not harboring a carbapenemase. Individuals with NCPE infections were more likely to have had prior antimicrobial therapy and emergency department visits compared to those with CPE. Identification and distinction of these mechanisms by rapid identification of species and carbapenemase would allow for optimal treatment and infection control efforts.

Clinical epidemiology of carbapenem-resistant Enterobacterales in the Greater Houston region of Texas: a 6-year trend and surveillance analysis

“…Several studies have also reported that K. pneumoniae and KPC-producing CRE are pre-dominant in the U.S. [ 4 , 13 , 28 ]. These findings are contrary to a recent study, which reported that 43% of CRE cases were K. pneumoniae followed by 27% E. coli and 30.3% being KPC-producing CRE [ 29 ]. This contradictory finding may be due to the small sample size of that study, which included only 42 cases (43%) of K. pneumoniae .…”

Accessory Genomes Drive Independent Spread of Carbapenem-Resistant Klebsiella pneumoniae Clonal Groups 258 and 307 in Houston, TX

“…A more recent study assessing the clinical and genomic epidemiology of carbapenem-resistant Enterobacterales in the United States ( 3 ) showed that Houston was the first major city in the United States where carbapenem-resistant K. pneumoniae CG307 seemed to have established endemicity along with isolates belonging to CG258. Furthermore, a recent study suggests that CG307 may be spreading to other municipalities in South Texas and cocirculating with CG258 ( 31 ). The concomitant circulation of these major clones provided an opportunity to dissect their dynamics of dissemination, genetic relationships, and evolution using a pangenomic approach combined with clinical data.…”

Systematic Analysis of Mobile Genetic Elements Mediating β-lactamase Gene Amplification in Non-Carbapenemase-Producing Carbapenem Resistant Enterobacterales Bloodstream Infections

“…The reasons underlying the high prevalence of non-CP isolates in our bacteremia cohort are not currently known but may include relatively stringent infection control practices amongst our highly immunocompromised patients. Recently, Black et al noted a higher prevalence of non-CP-CRE (59%) in south Texas where non-CP-CRE patients were more likely to receive a longer duration of antibiotic treatment as well as more likely to have an emergency department visit compared to CPE albeit with low number of observations (39). This finding is consistent with our cancer patient population that receives a high level of antibiotic treatment (40) and coincides with the finding that previous antibiotic exposure has been identified as a risk factor for non-CP-CRE relative to CPE in other studies (7).…”