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J-P Bru1, P Léophonte, C Carbon

  • 1Département de microbiologie clinique et maladies infectieuses, centre hospitalier d'Annecy, 1, avenue de Trésum, 74000 Annecy, France.

Medecine Et Maladies Infectieuses
|November 1, 2005
PubMed
Summary
This summary is machine-generated.

Antibiotic resistance mechanisms significantly impact treatment outcomes in respiratory infections. Not all resistance, particularly reduced target affinity, clearly predicts clinical failure, necessitating a nuanced approach to antibiotic selection.

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Area of Science:

  • Microbiology
  • Infectious Diseases
  • Clinical Pharmacology

Background:

  • Acquired antibiotic resistance is a major cause of treatment failure in community-acquired respiratory infections.
  • Understanding the link between phenotypic resistance and clinical outcomes is crucial for effective antimicrobial therapy.

Purpose of the Study:

  • To investigate the relationship between phenotypically defined acquired resistance and clinical failure in respiratory infections.
  • To determine the predictive value of critical antibiotic concentrations in relation to bacterial resistance mechanisms and clinical outcomes.

Main Methods:

  • Analysis of clinical data and bacterial resistance phenotypes in patients with community-acquired respiratory infections.
  • Evaluation of specific resistance mechanisms (e.g., betalactamase production, target modification/mutation) and their association with treatment outcomes.

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  • Assessment of the predictive accuracy of critical resistance concentrations for clinical failure.

    • Main Results:

    • Efficient resistance mechanisms (e.g., betalactamase secretion, macrolide target modification, fluoroquinolone target mutation) are clearly associated with clinical failure.
    • Resistance due to reduced target affinity (e.g., Streptococcus pneumoniae and betalactams) shows a less clear association with clinical failure.
    • Critical concentrations predict failure only when they identify bacteria with efficient resistance mechanisms, not when resistance is due to target affinity reduction or influenced by pharmacokinetics.

    Conclusions:

    • The choice of antibiotics must consider the presence, type, and efficiency of bacterial resistance mechanisms, as well as pharmacokinetic factors.
    • Phenotypic resistance, indicated by critical concentrations, is not universally predictive of clinical failure in respiratory infections.
    • A comprehensive approach integrating resistance mechanisms, clinical outcomes, and drug pharmacokinetics is essential for optimizing antibiotic selection.