Abstract
IntroductionShiga toxin-producing Escherichia coli (STEC) can cause severe to fatal disease in humans. Antimicrobial treatment is sometimes necessary, but contraindicated due to undesirable clinical outcome. However, recent studies have shown promising outcomes following antimicrobial treatment. Before the establishment of a possible antimicrobial treatment strategy for STEC infections, the prevalence of antimicrobial resistance in STEC needs to be determined.Gap statementThe resistance status of Norwegian clinical STEC is not known and should be assessed.AimWe aim to characterize genotypic antimicrobial resistance determinants in clinical STEC in Norway, and determine the prevalence of genotypic resistance in order to inform possible antimicrobial treatment options for STEC infections.MethodologyWe included all clinical STEC submitted to the Norwegian Reference Laboratory from March 2018 to April 2020. All samples were whole-genome sequenced and screened for genotypic antimicrobial resistance,virulence determinants and plasmid incompatibility groups. We performed phylogenetic clustering of STEC by core-genome multi-locus sequence typing, and statistical association analyses between isolate characteristics and genotypic resistance.ResultsA total of 459 STEC were analysed. For 385 (83.9 %) STEC we did not identify any antimicrobial resistance determinants. Seventy-four STEC (16.1 %) harboured antimicrobial resistance determinants against one or more antimicrobial classes. The most frequent genotypic resistance was identified against aminoglycosides (10.5 %). Thirty-nine STEC (8.5 %) had a multi-drug resistance (MDR) genotype. Genotypic resistance was more prevalent in non-O157 than O157 STEC (P=0.02). A positive association was seen between genotypic resistance and the low-virulent STEC O117:H7 phylogenetic cluster (no. 14) (P<0.001). Genotypic resistance was not significantly associated to high-virulent STEC. STEC O146:H28 and isolates harbouring the plasmid replicon type IncQ1 were positively associated with MDR.ConclusionThe overall prevalence of genotypic resistance in clinical STEC in Norway is low (16.1 %). Genotypic resistance is more prevalent in non-O157 strains compared to O157 strains, and not significantly associated to high-virulent STEC. Resistance to antimicrobials suggested for treatment, especially azithromycin is low and may present an empiric treatment alternative for severe STEC infections.
Highlights
Shiga toxin-producing Escherichia coli (STEC) can cause severe to fatal disease in humans
Genotypic resistance is more prevalent in non-O157 strains compared to O157 strains, and not significantly associated to high-virulent STEC
Resistance to antimicrobials suggested for treatment, especially azithromycin is low and may present an empiric treatment alternative for severe STEC infections
Summary
Shiga toxin-producing Escherichia coli (STEC) can cause severe to fatal disease in humans. Antimicrobials are presently contraindicated in the treatment of STEC infections, as there are indications that treatment could increase the risk of developing HUS, associated with increase in the Shiga toxin (Stx) production [6, 7]. Recent studies have shown that it is possible to treat some STEC infections with certain classes of antimicrobials with a successful outcome [8,9,10]. Azithromycin, ciprofloxacin and fosfomycin (alone or in combination) are among the antimicrobials that have shown promising results in the treatment of severe STEC infections [8, 9, 11,12,13]. Several in vitro studies investigating antimicrobials and their effects on Stx production have demonstrated that azithromycin, gentamicin and meropenem are potential candidates for treatment [14,15,16]
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