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Antifungal Resistance in Pulmonary Aspergillosis

Paul E Verweij1,2,3, Yinggai Song1,4,5,6, Jochem B Buil1,2

  • 1Department of Medical Microbiology, Radboud University Medical Center, Nijmegen, the Netherlands.

Seminars in Respiratory and Critical Care Medicine
|January 10, 2024
PubMed

Insights

Aspergillus fumigatus resistance mutations emerge through genetic variation and selection. Understanding these mechanisms in pulmonary diseases like ABPA, CPA, and IPA can improve antifungal treatments.

Area of Science:

  • Medical Mycology
  • Antimicrobial Resistance
  • Pulmonary Medicine

Background:

  • Aspergilli cause significant human pulmonary diseases, including allergic bronchopulmonary aspergillosis (ABPA), chronic pulmonary aspergillosis (CPA), and acute invasive pulmonary aspergillosis (IPA).
  • Aspergillus fumigatus is a primary pathogen, utilizing various morphotypes (conidia, hyphae, sporulation) that influence adaptation and resistance.
  • Antifungal drug exposure drives resistance mutations in A. fumigatus through genetic variation and selection.

Purpose of the Study:

  • To explore the mechanisms of antifungal resistance in Aspergillus species causing pulmonary diseases.
  • To differentiate resistance mutation types (TR-mediated vs. single-point) based on their origin (environmental vs. in-host).
  • To correlate resistance genotypes with specific Aspergillus-related lung conditions.

Main Methods:

  • Literature review of reported cases and resistance mechanisms.
  • Analysis of mutation types (tandem repeat-mediated and single-point) in different Aspergillus disease contexts.
  • Comparison of resistance emergence in environmental versus in-host settings.

Main Results:

  • Environmental resistance is often TR-mediated, while in-host resistance typically involves single-point mutations.
  • Environmental resistance mutations are rarely found in invasive aspergillosis (IA), suggesting low in-host selection risk.
  • Aspergilloma shows dominant single-point mutations, whereas ABPA, CPA, and CF exhibit both TR-mediated and single-resistance mutations.

Conclusions:

  • Resistance mechanisms in Aspergillus vary depending on the disease and the site of selection (environment vs. host).
  • Distinct mutation patterns are observed in different chronic and invasive pulmonary aspergillosis forms.
  • Understanding these resistance pathways is crucial for developing improved diagnostic and therapeutic strategies against Aspergillus infections.

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