Extended-spectrum beta-lactamase- and carbapenemase-producing isolates causing hospital- and community-acquired infections in Tunisia (2001-2019): expansion of CTX-M-15-C2 and CTX-M-27-C1 ST131 subclades.

UNLABELLED

The prevalence of infections caused by extended-spectrum beta-lactamase (ESBL)-producing (ESBL-EC) and carbapenemase-producing (CP-EC) is increasing worldwide. We investigated the epidemiology of ESBL-EC and CP-EC causing hospital-acquired (HA) infections in a large teaching hospital in Tunisia over the last two decades and compared it with a collection of 107 community-acquired (CA) ESBL-EC isolates. Between 2001 and 2019, the incidence of HA ESBL-EC increased significantly from 0.08 to 0.32 cases per 1,000 patient days, due entirely to the rapid emergence and expansion of ST131, which accounted for 42.3% (157/371) of HA ESBL-EC. Most ESBL-EC harbored the CTX-M type (92%) with a predominance of blaCTX-M-15. The C2/H30-Rx subclone ( = 103, 65.6%) accounted for 90% of ST131 isolates between 2003 and 2012 and was exclusively associated with CTX-M-15, whereas cluster C1-M27, which was associated with CTX-M-27, emerged in 2013 and expanded gradually to 55% of ST131 in 2019. ST131 prevalence was higher among CA ESBL-EC than HA ESBL-EC (63.6% vs. 42.3%, = 0.002). CA C2 subclone and non-ST131 isolates showed higher virulence scores than HA isolates. The incidence of CP-EC remained stable over the study period with a mean of 0.08 cases per 1,000 patient days. Among the 38 identified CP-EC isolates, only 16.2% belonged to the ST131 clone and 81.5% produced OXA-48-like carbapenemases. ST131 is the major driver of ESBL-EC spread in both hospital and community settings in Tunisia, mainly linked to the expansion of the CTX-M-15-C2 and CTX-M-27-C1 subclades. The emergence of CP-EC requires ongoing genomic surveillance.

IMPORTANCE

We aimed to investigate the microbiological features of extended-spectrum beta-lactamase (ESBL)-producing (ESBL-EC) and carbapenemase-producing (CP-EC) causing hospital- and community-acquired infections in Tunisia over the last two decades. The study captured the emergence and expansion of the CTX-M-15-C2 ST131 subclade and successively the CTX-M-27-C1 ST131 subclade, which were responsible for the steady increase in the prevalence of ESBL-EC. However, the incidence of CP-EC remained stable over the study period with a highly diverse content in carbapenemase genes dominated by blaOXA-48-like. This is the first study to provide comprehensive data on the epidemiology of ESBL-EC and CP-EC in a North African country.