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Home / Publications / Efflux Pumps in Mycobacteria: Antimicrobial Resistance, Physiological Functions, and Role in Pathogenicity

Efflux Pumps in Mycobacteria: Antimicrobial Resistance, Physiological Functions, and Role in Pathogenicity

  • Authors: Almeida da Silva PE, Couto I, Machado D, Ramos D, Viveiros M, von Groll A
  • Publication Year: 2016
  • Journal: Efflux-Mediated Antimicrobial Resistance in Bacteria
  • Link: https://link.springer.com/chapter/10.1007/978-3-319-39658-3_21%20

The emergence of multidrug and extensively drug-resistant tuberculosis represents a major threat to the control of the disease. Antimicrobial drug resistance in Mycobacterium tuberculosis is not merely a consequence of the occurrence of gene mutations in the drug targets but a balance between the acquisition of mutations and drug efflux. The low permeability of the mycobacterial cell wall acts synergistically with active drug efflux pumps, and this combined mechanism may particularly constitute the first step for the development of drug resistance. Besides drug efflux, efflux pumps also have physiological functions in the bacteria, and their expression is subjected to tight regulation in response to multiple environmental and physiological signals. Understanding the mechanisms underlying drug efflux, efflux pump regulation and their contribution for pathogenicity not only enables the development of more rapid and accurate tools for the guidance of antituberculosis therapy but also provides knowledge for the development of new therapeutic strategies.

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About GHTM

GHTM is a R&D Unit that brings together researchers with a track record in Tropical Medicine and International & Global Health. It aims at strengthening Portugal's role as a leading partner in the development and implementation of a global health research agenda. Our evidence-based interventions contribute to the promotion of equity in health and to improve the health of populations.

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UID/PRR/04413/2025 - DOI: 10.54499/UID/PRR/04413/2025

UID/PRR2/04413/2025 - DOI: 10.54499/UID/PRR2/04413/2025

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