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Genetic features of BEL-1-producing and KPC-2-producing E. coli from hospital wastewater: human source or sewages adaptation

Laura Romero-Oraá; Marina R. Pulido; Fatima Galán; María Victoria García Palacios; Alvaro Pascual; Lorena López-Cerero
Environmental Science and Pollution Research · Vol. 31, Issue 31 · pp. 43896-43902 · 2024

Abstract

Hospital sewage is an ecosystem that facilitates the transfer of antibiotic and heavy metal resistance genes and the interaction of human and environmental bacteria. In this environment, we have detected the presence of 7 KPC-2 and BEL-1 co-producing E. coli isolates of two different clones over a 10-month period in the same hospital. All isolates carried bla KPC-2 and the operon mer on the same Inc P plasmid of similar size and an Inc N plasmid of different size each clone carrying bla BEL-1 . Both IncN-blaBEL-1 plasmids shared a 77 kb region containing bla BEL-1 alongside with fosE , bla OXA-10 and aac(6’)-1b genes in a class 3 integron within a Tn 3 transposon. The major Inc N plasmid contained in addition a region homolog to P1-like bacteriophage RCS47, including the lytic RepL and lysogenic proteins, but other phage regions were incomplete. The characters such as the temporal persistence in sewage, the absence of colonized patients in the hospital or in the region, the presence of a p1 phage-plasmid fusion and the infrequent class 3 integron as genetic platform would indicate that BEL-1-producing isolates could have been generated in situ by adaptation to human sewage. Part of the microbiota in these discharges could be explained by the interactions of sewage ecosystems and not derive directly from the hospital.

Bibliographic Information

JournalEnvironmental Science and Pollution Research
PublisherSpringer
Publication Date2024-06-24
Publication Year2024
Volume31
Issue31
Pages43896-43902
Document TypeJournal Article
eISSN1614-7499
DOI10.1007/s11356-024-33875-w

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NARA Access Coverage1994-01-01~Current
Journal Homepagehttps://www.springer.com/journal/11356
Publisher PageOpen Publisher Page
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