Mission & Objectives


The aim of ESGAI is to:

  • improve knowledge about the role of anaerobic bacteria in a wide range of human infections including less frequently studied ones: such as one-sided tonsillitis of adults, the infections of the oral cavity or their role in therapy resistant chronic prostatitis.
  • initiate studies to improve identification and typing of anaerobic bacteria by the protein-based method MALDI-TOF MS.
  • investigate the antimicrobial resistance patterns in anaerobic bacteria in Europe.
  • investigate the antibiotic resistance mechanisms and their genetic background in anaerobic bacteria.
  • develop standardised methods for testing antimicrobial agents against anaerobic bacteria and cooperate with EUCAST to set break points for anaerobes.
  • organise a symposium or workshop at each ECCMID
  • organise scientific meetings and postgraduate educational courses or technical workshops to improve knowledge about isolation identification and resistance determination of anaerobic bacteria.


Clinical usage of antimicrobial agents has been accompanied by the isolation of antimicrobial-resistant bacteria. During the last years there have been reports showing increasing numbers of anaerobic bacteria resistant to different antimicrobial agents. Resistance in anaerobic bacteria has a significant impact on the selection of antimicrobial agents for empirical therapy. The development of antibiotic resistance in anaerobic bacteria has been documented for beta-lactam drugs, clindamycin, macrolides, tetracyclines and nitroimidazoles. The Bacteroides fragilis group is more resistant to antimicrobial agents than most other anaerobic bacteria. The Bacteroides genus and new genera Prevotella and Porphyromonas have become increasingly resistant to many anti-anaerobic agents. Fusobacterium strains resistant to beta-lactam drugs are relatively frequent. Resistant clostridia and Propionibacterium acnes have also been reported.

The resistance mechanisms in anaerobic bacteria are:

  • hydrolysis of the antimicrobial drug by several enzymes before reaching the site of action (most common, sometimes plasmid mediated).
  • decreased permeability of the organisms.
  • modification at the site of action of the antimicrobial agent.
  • efflux mechanisms which eliminate the antimicrobial drug from the bacterial cell.