Emerging broad-spectrum b-lactamases in Escherichia coli: latest ESBLs and carbapenemases
Abstract number: 1732_199
Increasing b-lactam resistance in E. coli has become a worrying threat worldwide. In that species, most of the mechanisms involved in the b-lactam resistance are linked to the production of b-lactamases, including clavulanic-acid inhibited expanded-spectrum b-lactamases (ESBLs) and carbapenemases which are the most powerful enzymes able to degradate most b-lactams. Besides the most common ESBLs circulating in Enterobacteriaceae (TEM-, SHV, and CTX-M-types), there are other emerging enzymes which are mostly plasmid-encoded and are distributed in a large variety of species. The ESBL VEB-1 is known to be largerly distributed in South-East Asia, PER-1 in Turkey, Italy, Korea, and also South America, and GES/IBC-type enzymes in Greece and Japan mostly. All these ESBLs are known to efficiently hydrolyze expanded-spectrum b-lactams, and some variants of the GES family are also hydrolysing imipenem at a low level. Other enzymes of the KPC family have been also reported in E. coli. KPC-2 has been shown to be prevalent in E. coli in Israel and KPC-3 has been reportyed sporadically in the USA. These latter enzymes are considered as ESBLs since they are inhibited by clavulanic acid and their hydrolytic efficiencies toward imipenem are very high, thus giving rise to high level resistance to carbapenems in those E. coli isolates.
In addition to these ESBL determinants, metallo-b-lactamases (MBL) have been identified in E. coli. These enzymes which are not inhibited by clavulanic acid and hydrolyse carbapenems very efficiently are of the IMP and VIM groups. In E. coli, IMP-1 has been identified in Japan and VIM-2 in Greece, but the most worrying observation is that related to the spread of VIM-1 in Greece. Indeed, this determinant has been identified in clinical isolates also harbouring ESBL encoding genes, thus leading to panresistance in those strains.
Noteworthy, most of the ESBL and MBL encoding genes encountered in E. coli are vehiculed by plasmids and located into class 1 integron structures, thus facilitating the occurrence of multidrug resistance via the co-localisation of other antibiotic resistance genes.
A particular attention will be needed in the next future to trace the isolates harbouring these worrying determinants, and also to trace the corresponding plasmids which are powerful tools for such dissemination.
|Session name:||European Society of Clinical Microbiology and Infectious Diseases|
|Location:||ICC, Munich, Germany|
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