Affiliation:
1. Unit for Enteropathogenic Bacteria and Legionella and National Reference Centre for Salmonella and other Bacterial Enterics, Robert Koch Institute, Wernigerode, Germany
2. Unit for Gastrointestinal Infections, Zoonoses and Tropical Infections, Robert Koch Institute, Berlin, Germany
3. Unit for Nosocomial Pathogens and Antibiotic Resistances, Robert Koch Institute, Wernigerode, Germany
Abstract
Non-typhoidal
Salmonella enterica
is an important gastrointestinal pathogen causing a considerable burden of disease. Resistance to third generation cephalosporins poses a serious threat for treatment of severe infections. In this study occurrence, phylogenetic relationship, and mechanisms of third generation cephalosporin resistance were investigated for clinical non-typhoidal
S. enterica
isolates in Germany. From 2017 to 2019, we detected 168 unique clinical
S. enterica
isolates with phenotypic resistance to third generation cephalosporins in a nation-wide surveillance. Compared to previous years, we observed a significant (P=0.0002) and consistent increase in resistant isolates from 0.41 % in 2005 to 1.71 % in 2019. In total, 34 different serovars were identified, most often S. Infantis (n=41; 24.4 %), S. Typhimurium (n=27; 16.1 %), S. Kentucky (n=21; 12.5 %), and S. Derby (n=17; 10.1 %). Whole genome analyses revealed extended-spectrum β-lactamase (ESBL) genes as main cause for third generation cephalosporin resistance, and most prevalent were bla
CTX-M-1 (n=55), bla
CTX-M-14 (n=25), and bla
CTX-M-65 (n=23). There was no strict correlation between serovar, phylogenetic lineage, and ESBL type but some serovar/ESBL gene combinations were detected frequently, such as bla
CTX-M-1 and bla
CTX-M-65 in S. Infantis or bla
CTX-M-14b in S. Kentucky. The ESBL genes were mainly located on plasmids, including IncI, IncA/C variants, emerging pESI variants, and a novel bla
CTX-M-1harbouring plasmid. We conclude that third generation cephalosporin resistance is on the rise among clinical
S. enterica
isolates in Germany, and occurrence in various
S. enterica
serovars is most probably due to multiple acquisition events of plasmids.
Funder
Bundesministerium für Gesundheit
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