Changing molecular epidemiology and resistance patterns of carbapenem-resistant Klebsiella pneumoniae in California long-term acute care hospitals
Kyle J Gontjes, Brendan J Kelly, Leigh Cressman, Anne Jaskowiak-Barr, Laurel Glaser, Laura L Cowden, Alexa Patel, Jennifer Han, Ellie J C Goldstein, Warren B Bilker, Evan S Snitkin, Ebbing LautenbachAbstract
Background
The epidemiology of carbapenem-resistant Klebsiella pneumoniae (CRKP) must be monitored over time to understand resistance dynamics to existing and novel antibiotics.
Methods
Antibiotic susceptibility testing and whole-genome sequencing were performed on clinical CRKP isolates collected from the same California long-term acute care hospital network across two time periods: 2014-15 (period 1) and 2021-23 (period 2). Differences in sequence type (ST) diversity, carbapenem resistance-associated genotypes, and resistance to clinically important antibiotics were evaluated.
Results
Eight hundred eighty-one isolates were collected (period 1, 374; period 2, 507). Study period 1’s population was dominated by ST258 (94.1%). ST diversity markedly increased in period 2, with a reduced prevalence of ST258 (41.6%) and an increased abundance of other epidemic lineages: ST14 (27.4%), ST307 (6.9%), and ST17 (6.5%). Changes to circulating resistance genotypes and plasmids reflected the increased ST diversity. Increases in blaKPC-3-harboring isolates (66.0% vs. 76.1%) and non-carbapenemase-containing isolates (2.7% vs 12.6%) aligned with decreases in blaKPC-2-harboring isolates (30.5% vs. 6.3%). Statistically significant differences in resistance patterns were also observed between study periods, including colistin (35.0% vs. 20.2%), fosfomycin (27.0% vs. 13.4%), meropenem-vaborbactam (9.4% vs. 2.0%), and ceftazidime-avibactam (1.1% vs. 9.1%). Differential patterns of resistance emergence and spread across circulating STs largely drove resistance patterns in study period 2.
Conclusions
The comparison of clinical CRKP isolates collected from the same healthcare network and separated by nearly a decade revealed increasing ST diversity, mainly due to the introduction of numerous epidemic lineages, which coincided with differing patterns of circulating resistance-associated genotypes and antibiotic resistance.