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Bio-energetics Investigation of Candida albicans Using Real-time Extracellular Flux Analysis
08:48

Bio-energetics Investigation of Candida albicans Using Real-time Extracellular Flux Analysis

Published on: March 19, 2019

Pathogenicity and drug resistance in Candida albicans and other yeast species. A review

Nagendra Nath Mishra1, Tulika Prasad, Neeraj Sharma

  • 1Department of Biotechnology, Seth J. M. Institute of Engineering and Technology, Radaur-135133, Yamuna Nagar, India. nagendranathmishra@yahoo.co.in

Acta Microbiologica Et Immunologica Hungarica
|September 28, 2007
PubMed

Insights

Candida yeast infections are increasingly resistant to antifungal drugs due to mechanisms like impaired uptake, target alterations, and drug efflux. Biofilm formation exacerbates this resistance, complicating treatment for immunocompromised patients.

Area of Science:

  • Mycology
  • Infectious Diseases
  • Pharmacology

Background:

  • Pathogenic *Candida* yeasts cause serious infections, especially in immunocompromised individuals, and are significant causes of hospital-acquired infections.
  • Increasing treatment failures in candidiasis underscore a growing problem with long-term antifungal therapy.
  • Candida cells develop multidrug resistance (MDR) during treatment, posing a significant challenge to chemotherapy.

Purpose of the Study:

  • To elucidate the mechanisms of drug resistance in *Candida* species, particularly against azole antifungal agents.
  • To understand how *Candida* biofilms contribute to antifungal drug resistance.
  • To identify key resistance mechanisms involved in clinical isolates of *Candida* species.

Main Methods:

  • Review and categorization of known resistance mechanisms against azole antifungal agents.
  • Investigation of cell wall and plasma membrane changes affecting drug uptake.
  • Analysis of alterations in the drug target Erg11p (lanosterol 14alpha-demethylase) and gene expression.
  • Examination of drug efflux mediated by ATP-binding cassette (ABC) transporters and major facilitator superfamily (MFS) transporters.
  • Assessment of resistance in *Candida* biofilms, including those on medical devices.

Main Results:

  • Mechanisms of azole resistance include impaired drug uptake, altered drug target affinity or expression (Erg11p mutations/overexpression), and increased drug efflux via ABC (CDR1, CDR2) and MFS (CaMDR1) transporters.
  • Formation of *Candida* biofilms is strongly associated with multidrug resistance.
  • Biofilm-associated *Candida* exhibits uniform resistance to a broad range of antifungal drugs.

Conclusions:

  • A combination of resistance mechanisms contributes to the development of drug resistance in clinical *Candida* isolates.
  • Understanding these mechanisms is crucial for developing effective therapeutic strategies against candidiasis.
  • The prevalence of biofilm-associated resistance highlights the need for strategies targeting biofilm formation and associated resistance phenotypes.

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