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Related Concept Videos

Antifungal Agents01:15

Antifungal Agents

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Amphotericin B is a broad-spectrum antifungal agent that exploits structural differences between fungal and mammalian cell membranes. Its amphipathic structure—featuring a hydrophobic polyene-lactone ring and a hydrophilic region containing mycosamine and carboxylic acid groups—enables selective binding to ergosterol, a sterol predominantly found in fungal plasma membranes. This selective interaction underlies the drug’s antifungal activity, although weak binding to...
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Antibiotic resistance is a major public health concern that arises when bacteria evolve mechanisms to withstand the effects of antibiotic treatments. This resistance can be intrinsic, acquired through genetic mutations, or transferred between bacteria via horizontal gene transfer. The development of antibiotic resistance poses significant challenges in treating bacterial infections and necessitates ongoing research to develop new therapeutic strategies.Intrinsic resistance occurs when bacterial...
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Antibiotic resistance in bacteria arises when microorganisms evolve the ability to withstand drugs designed to kill them or inhibit their growth, rendering once-effective treatments useless. This phenomenon, driven by genetic change and selection under antibiotic exposure, poses a profound threat to modern medicine. Mechanisms include drug-inactivating enzymes (e.g., β-lactamases), efflux pumps that eject antibiotics, mutations altering antibiotic targets, decreased drug uptake, and...
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Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
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Calcineurin-Dependent Stress Adaptation Enables Caspofungin Heteroresistance Leading to Stable Resistance in Candida Glabrata.

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Multidimensional assessment of in-host fitness costs of echinocandin resistance in the opportunistic fungal pathogen <i>Candida glabrata</i> reveals the niche-specific requirement for <i>FKS1</i> and <i>FKS2</i> during infection and gut colonization.

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Updated: Mar 30, 2026

Whole Genome Sequencing of Candida glabrata for Detection of Markers of Antifungal Drug Resistance
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Echinocandin Resistance in Candida.

David S Perlin1

  • 1Public Health Research Institute, New Jersey Medical School-Rutgers Biomedical and Health Sciences, Newark.

Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America
|November 15, 2015
PubMed
Summary

Echinocandin antifungal resistance, particularly in Candida glabrata, poses a significant challenge due to FKS mutations. Understanding resistance mechanisms is crucial for developing new antifungal therapies.

Keywords:
CandidaFKScaspofunginechinocandinmicafungin

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Area of Science:

  • Mycology
  • Infectious Diseases
  • Pharmacology

Background:

  • Invasive fungal infections are a major concern in immunocompromised patients.
  • Limited antifungal drug classes and emerging resistance, especially in Candida species, complicate treatment.
  • Echinocandins are key antifungals targeting fungal cell wall synthesis.

Purpose of the Study:

  • To review the mechanisms and clinical factors contributing to echinocandin resistance.
  • To highlight the challenges posed by multidrug-resistant Candida glabrata strains.
  • To emphasize the need for improved diagnostics and therapeutics.

Main Methods:

  • Review of literature on echinocandin resistance mechanisms.
  • Discussion of molecular mechanisms involving FKS mutations in glucan synthase.
  • Analysis of clinical factors promoting resistance development.

Main Results:

  • Echinocandin resistance is primarily mediated by FKS mutations in glucan synthase.
  • Candida glabrata exhibits higher-level resistance and is often multidrug-resistant.
  • Complex cellular stress responses contribute to the emergence of resistant strains.
  • Clinical factors like prophylaxis and biofilms promote resistance.

Conclusions:

  • Understanding echinocandin resistance is vital for combating invasive fungal infections.
  • Development of novel diagnostic tools and therapeutic strategies is essential.
  • Addressing resistance in Candida glabrata is a priority for effective patient care.