Further Characterization of Three <i>Yersinia enterocolitica</i> Strains with a Nalidixic Acid–Resistant Phenotype Isolated from Humans with Diarrhea

Drummond, Niall; Stephan, Roger; Haughton, Pippa; Murphy, Brenda; Fanning, Séamus

doi:10.1089/fpd.2012.1468

Cited by 4 publications

(2 citation statements)

References 17 publications

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“… 28 Y. enterocolitica is a zoonotic pathogen that causes gastrointestinal disease and porcine animal seems to be the main carrier of this bacterial species. 29 Likewise, the food chain could boost Y. enterocolitica antimicrobial resistance.…”

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confidence: 99%

Antimicrobial resistance and plasmid replicons in Yersinia enterocolitica strains isolated in Brazil in 30 years

Frazão

Andrade

Darini

et al. 2017

The Brazilian Journal of Infectious Diseases

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Some studies evaluated the resistance profile of the Y. enterocolitica strains isolated in diverse countries. However, in Brazil the isolation and the study of Y. enterocolitica are not common and therefore information about the antimicrobial resistance profile of this species in this country is scarce. Therefore, the aim of this study was to evaluate the antimicrobial resistance of Y. enterocolitica of biotypes 1A, 2 and 4 isolated from clinical and non-clinical sources between 1979 and 2012, in Brazil. This study showed that some Yersinia enterocolitica of different biotypes remain susceptible to antimicrobials used for gastroenteritis treatment. Moreover, neither acquired resistance genes nor diversity of plasmids replicons were found; however, variation in the in vitro intrinsic resistant pattern was detected, except the non-resistance to cefoxitin in all strains. Notwithstanding, due to epidemiological link between Y. enterocolitica and the pork production chain, monitoring plasmid acquired resistance in Y. enterocolitica could also be considered for antimicrobial resistance control purposes and food safety measures.

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confidence: 99%

Antimicrobial resistance and plasmid replicons in Yersinia enterocolitica strains isolated in Brazil in 30 years

Frazão

Andrade

Darini

et al. 2017

The Brazilian Journal of Infectious Diseases

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“…This is the first report of a chronic Ye infection case due to a strain evolving in the same patient. Between December 1999 and October 2013, antibiotics were apparently successful in the treatment of five independent Ye bacteremia episodes; however, discontinuation of antibiotics was change of aspartic acid 87 into a tyrosine, asparagine, or glycine [14][15][16][17] . In Ye.3 and Ye.4, we observed a previously undescribed deletion of 3 nucleotides in the gyrA QRDR, leading to substitution of aspartic acid 82 and serine 83 by a unique glycine.…”

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confidence: 99%

In-host evolution ofYersinia enterocoliticaduring a chronic human infection

Cyril,

Pierre,

Julien

et al. 2024

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Following a pacemaker implantation, a 75-years-old patient suffered from five successive bacteremia episodes between in 1999 and 2013 despite long-term antibiotic treatment, with intermittent vegetation apparition on the device atrial lead. Four blood isolates, identified asYersinia enterocoliticabioserotype 4/O:3, were further genetically and phenotypically characterized. Phylogenetic reconstruction showed that the patient was chronically infected by the same strain, which evolved within the host for 14 years. Single-nucleotide polymorphism (SNP) analysis indicates that the last two isolates evolved in parallel and formed two independent lineages within the host. Pan-genome analysis and genome comparison showed that their common evolution was characterized by 41 small insertion/deletion events, loss of three large DNA fragments and mutations in 140 genes. A phylogenetic analysis by maximum likelihood identified two genes presenting a positive selection signal, suggesting that these mutations provided a survival advantage to bacteria during chronic infection. Quinolone resistance in the last two isolates was acquired through a so far undescribed deletion in thegyrAgene.Mass-spectrometry analysis revealed a strong proteome remodeling in the last two isolates which was correlated with a truncation in the stringent response regulator DksA. A reduced carbon, energy and purine metabolism supports their severe growth defectsin vitro. 3rd-generation cephalosporin resistance of the last isolate was correlated with a truncation of OmpF, the main porin translocating antibiotics through the outer-membrane, as well as an increased production of BlaA and AmpC β-lactamases.This is the first report of genetic and phenotypic changes associated to within-host adaptation of a pathogenicYersiniaspecies under antibiotic pressure.

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