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Mechanisms of antimicrobial resistance in Gram-negative bacilli

Étienne Ruppé1, Paul-Louis Woerther, François Barbier

  • 1Department of Infectious Diseases, Genomic Research Laboratory, Geneva University Hospitals, Geneva, Switzerland, etienne.ruppe@gmail.com.

Annals of Intensive Care
|August 12, 2015
PubMed

Insights

Multidrug resistance in Gram-negative bacilli is a major challenge in intensive care units. Emerging carbapenemases and widespread resistance mechanisms threaten current antimicrobial therapies, necessitating urgent solutions.

Area of Science:

  • Infectious Diseases
  • Microbiology
  • Critical Care Medicine

Background:

  • Multidrug resistance (MDR) in Gram-negative bacilli (GNB) poses a significant challenge in intensive care units (ICUs).
  • The rise of extended-spectrum beta-lactamases (ESBLs), particularly CTX-M types, has increased resistance to third-generation cephalosporins in Enterobacteriaceae.
  • Emergence of carbapenemase-producing GNB (e.g., VIM, NDM, OXA-48, KPC) threatens the efficacy of carbapenems, a critical treatment option.

Purpose of the Study:

  • To review the current landscape of multidrug resistance in Gram-negative bacilli affecting critically ill patients.
  • To highlight the mechanisms driving resistance, including plasmid-borne ESBLs and carbapenemases, and chromosomal mutations.
  • To discuss the implications for antimicrobial therapy and the scarcity of treatment options for carbapenem-resistant GNB infections.

Main Methods:

  • Literature review and synthesis of current data on antimicrobial resistance in GNB within ICU settings.
  • Analysis of resistance mechanisms in both Enterobacteriaceae and non-fermenting GNB (Pseudomonas aeruginosa, Acinetobacter baumannii, Stenotrophomonas maltophilia).
  • Examination of the spread of resistance determinants on mobile genetic elements and their impact on MDR.

Main Results:

  • ESBLs and carbapenemases are major drivers of resistance in Enterobacteriaceae, often co-located with resistance genes for other antibiotic classes.
  • In non-fermenting GNB, resistance can arise from chromosomal mutations affecting beta-lactamases, efflux pumps, and permeability, as well as acquired carbapenemases.
  • Treatment options for infections caused by carbapenem-resistant GNB are limited, with growing concern over colistin resistance.

Conclusions:

  • The increasing prevalence of MDR GNB, particularly carbapenem-resistant strains, severely limits therapeutic options for ICU patients.
  • Co-resistance mediated by plasmids and mobile genetic elements accelerates the spread of multidrug resistance.
  • Urgent development of novel antimicrobial strategies and stringent infection control measures are crucial to combat this growing threat.

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