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Invasive candidiasis

Nature Reviews Disease Primers volume 4, Article number: 18026 (2018) | Download Citation

Abstract

Invasive candidiasis is an important health-care-associated fungal infection that can be caused by several Candida spp.; the most common species is Candida albicans, but the prevalence of these organisms varies considerably depending on geographical location. The spectrum of disease of invasive candidiasis ranges from minimally symptomatic candidaemia to fulminant sepsis with an associated mortality exceeding 70%. Candida spp. are common commensal organisms in the skin and gut microbiota, and disruptions in the cutaneous and gastrointestinal barriers (for example, owing to gastrointestinal perforation) promote invasive disease. A deeper understanding of specific Candida spp. virulence factors, host immune response and host susceptibility at the genetic level has led to key insights into the development of early intervention strategies and vaccine candidates. The early diagnosis of invasive candidiasis is challenging but key to the effective management, and the development of rapid molecular diagnostics could improve the ability to intervene rapidly and potentially reduce mortality. First-line drugs, including echinocandins and azoles, are effective, but the emergence of antifungal resistance, especially among Candida glabrata, is a matter of concern and underscores the need to administer antifungal medications in a judicious manner, avoiding overuse when possible. A newly described pathogen, Candida auris, is an emerging multidrug-resistant organism that poses a global threat.

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Acknowledgements

This work was supported in part by the Division of Intramural Research, National Institute of Allergy and Infectious Diseases, US National Institutes of Health.

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Affiliations

  1. Division of Infectious Diseases, University of Alabama at Birmingham, Birmingham, AL, USA.

    • Peter G. Pappas
  2. Fungal Pathogenesis Section, Laboratory of Clinical Immunology & Microbiology, National Institutes of Allergy and Infectious Diseases, NIH, Bethesda, MD, USA.

    • Michail S. Lionakis
  3. Unit for Mycology, Statens Serum Institute, Copenhagen, Denmark.

    • Maiken Cavling Arendrup
  4. Department of Clinical Microbiology, Rigshospitalet, Copenhagen, Denmark.

    • Maiken Cavling Arendrup
  5. Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark.

    • Maiken Cavling Arendrup
  6. Division of Infectious Diseases, University of Texas Health Science Center, Houston, TX, USA.

    • Luis Ostrosky-Zeichner
  7. Department of Medicine and Radboud Center for Infectious Diseases, Radboud University Medical Center, Nijmegen, Netherlands.

    • Bart Jan Kullberg

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Contributions

Introduction (P.G.P.); Epidemiology (M.C.A. and L.O.-Z.); Mechanisms/pathophysiology (M.S.L. and M.C.A.); Diagnosis, screening and prevention (M.C.A.); Management (P.G.P. and B.J.K.); Quality of life (P.G.P.); Outlook (B.J.K.); Overview of Primer (P.G.P.).

Competing interests

P.G.P. has received research grants from Merck, Gilead, Astellas, Cidara, IMMY Diagnostics, T2 Biosystems and Mayne Pharma and is a scientific adviser for Cidara, IMMY, Matinas, Amplyx and Mayne Pharma. He is not affiliated with any speakers’ bureau and owns no equities in pharmaceutical companies. M.C.A. has received research grants, payment for contract work on minimum inhibitory concentrations and/or lecture honoraria from the following companies: Merck, Astellas, Basilea, Pfizer, Gilead, Cidara, Amplyx, F2G, Novabiotics and T2Biosystems. She is not affiliated with any speakers’ bureau and owns no equities in pharmaceutical companies. L.O.-Z. has received research grants, consulting honoraria and/or lecture honoraria from the following companies: Merck, Astellas, Pfizer, Gilead, Scynexis, Cidara, Amplyx and Vical. B.J.K. is a scientific adviser for Amplyx, Astellas, Basilea, Cidara and Scynexis. He is not affiliated with any speakers’ bureau and owns no equities in pharmaceutical companies. M.S.L. declares no competing interests.

Corresponding author

Correspondence to Peter G. Pappas.

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DOI

https://doi.org/10.1038/nrdp.2018.26