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Molecular basis of bacterial resistance to chloramphenicol and florfenicol

Stefan Schwarz1, Corinna Kehrenberg, Benoît Doublet

  • 1Institut für Tierzucht, Bundesforschungsanstalt für Landwirtschaft (FAL), Höltystrasse 10, 31535 Neustadt-Mariensee, Germany. stefan.schwarz@fal.de

FEMS Microbiology Reviews
|November 13, 2004
PubMed

Insights

Chloramphenicol (Cm) and florfenicol (Ff) are potent protein synthesis inhibitors. This review details resistance mechanisms, including acetyltransferases and transporters, and their spread via mobile genetic elements.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Genetics

Background:

  • Chloramphenicol (Cm) and florfenicol (Ff) are critical antibiotics inhibiting bacterial protein biosynthesis.
  • Widespread use of Cm has led to significant bacterial resistance.
  • Florfenicol (Ff), a derivative, is used in veterinary medicine, with fewer known cross-resistance mechanisms.

Purpose of the Study:

  • To provide a comprehensive overview of resistance mechanisms against Cm and Ff.
  • To focus on chloramphenicol acetyltransferases (CATs), efflux pumps, and multidrug transporters.
  • To analyze the genetic basis and spread of resistance genes.

Main Methods:

  • Review of existing literature on Cm and Ff resistance.
  • Construction of phylogenetic trees for CAT and exporter proteins using multisequence alignment.
  • Analysis of mobile genetic elements associated with resistance genes.

Main Results:

  • Identified key resistance mechanisms including enzymatic inactivation (CATs) and active efflux (transporters).
  • Demonstrated that only a subset of Cm resistance genes confer Ff resistance.
  • Highlighted the role of mobile genetic elements in the dissemination of both Cm and Cm/Ff resistance.

Conclusions:

  • Understanding resistance mechanisms is crucial for effective antibiotic use.
  • Phylogenetic analysis provides insights into the evolution of resistance proteins.
  • Mobile genetic elements facilitate the spread of resistance, even without direct antibiotic pressure.

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