Molecular epidemiology and antimicrobial resistance of extended-spectrum beta-lactamases-producing Enterobacter cloacae complex among mothers, neonates, healthcare workers and hospital environments in Tanga, Tanzania

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Abstract Background The Enterobacter cloacae complex (ECC) is an emerging healthcare-associated pathogen and an increasing cause of infections in neonatal intensive care units. Its clinical relevance is driven by the rapid acquisition of multidrug resistance (MDR), particularly to extended-spectrum β-lactams (ESBLs) and carbapenems. This study investigated the distribution patterns and genomic diversity of MDR ECC in two hospitals in Tanzania. Methods Between April 2022 and March 2023, samples from neonates, mothers, healthcare workers and hospital environments were analysed. ECC isolates underwent European Committee on Antimicrobial Susceptibility Testing–guided antimicrobial susceptibility testing and whole-genome sequencing to determine sequence types (STs), resistance determinants, plasmids and phylogenetic relationships. Results A total of 132 ESBL-producing ECC isolates were recovered, with the majority originating from environmental sources (65.9%, n/N = 87/132). Neonatal colonization after ≥48 h of hospitalization was 10.2% (n/N = 18/176). Overall, 74.2% (n/N = 98/132) of isolates were MDR, while 10.6% (n/N = 14/132) showed resistance to carbapenems. Whole-genome sequencing of 120 isolates revealed predominance of Enterobacter hormaechei (93.3%, n/N = 112/120) and widespread ESBL genes, mainly blaCTX-M-15 (87.5%, n/N = 105/120). Carbapenemase genes blaNDM-1 and blaNDM-5 were identified in 10% (n/N = 12/120), frequently associated with IncX3 plasmids, while the colistin resistance gene mcr-10.1 was chromosomal. Forty-one distinct STs were detected, including 12 novel STs. ST346 was the most prevalent lineage. Repeated temporal clusters of identical STs, including ST346, were detected across environmental and human isolates. Conclusions These findings demonstrate substantial MDR ECC colonization in neonatal wards, suggesting hospital environments as reservoirs for resistant ECC. Temporally clustered isolates across environmental and patient samples underscore the need for strengthened infection prevention and genomic surveillance.

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