AI Article Synopsis

  • The study utilizes Hain GenoType MTBDR assays to uncover that certain mutations can lead to incorrect resistance results for fluoroquinolones, impacting both wild-type and mutant probe binding.
  • These mutations, while rare worldwide, are present in about 7% of multidrug-resistant tuberculosis strains in specific areas.
  • This finding highlights the need for careful interpretation of assay results in TB treatment to ensure accurate resistance detection.

Article Abstract

In this study, using the Hain GenoType MTBDR assays (versions 1 and 2), we found that some nonsynonymous and synonymous mutations in in result in systematic false-resistance results to fluoroquinolones by preventing the binding of wild-type probes. Moreover, such mutations can prevent the binding of mutant probes designed for the identification of specific resistance mutations. Although these mutations are likely rare globally, they occur in approximately 7% of multidrug-resistant tuberculosis strains in some settings.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5365657PMC
http://dx.doi.org/10.1128/AAC.02169-16DOI Listing

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Article Synopsis
  • - The study investigates the prevalence of stomach infections and their antibiotic resistance, particularly to fluoroquinolones and clarithromycin, highlighting high resistance rates and treatment failures in symptomatic patients.
  • - Molecular testing using the GenoType Helico DR kit revealed that 42.4% of patients tested positive for infections, with significant resistance rates at 53.9% for fluoroquinolones and 58.5% for clarithromycin, alongside specific genetic mutations linked to resistance.
  • - The findings emphasize the urgent need for antibiotic susceptibility testing and tailored therapy based on the Maastricht VI Consensus recommendations to address the rising rates of resistance and improve treatment outcomes.
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