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Invasive Aspergillosis by Aspergillus flavus: Epidemiology, Diagnosis, Antifungal Resistance, and Management

1
Department of Medical Microbiology, Postgraduate Institute of Medical Education and Research, Research, Chandigarh 160012, India
2
Department of Medical Microbiology and Infectious Diseases, Erasmus MC, 3015GD Rotterdam, The Netherlands
3
Department of Medical Microbiology and Infectious Diseases, Canisius Wilhelmina Hospital (CWZ) and Center of Expertise, 6532SZ Nijmegen, The Netherlands
4
Center of Expertise in Mycology Radboudumc/CWZ, 6532SZ Nijmegen, The Netherlands
*
Author to whom correspondence should be addressed.
J. Fungi 2019, 5(3), 55; https://doi.org/10.3390/jof5030055
Received: 31 May 2019 / Revised: 28 June 2019 / Accepted: 29 June 2019 / Published: 1 July 2019
(This article belongs to the Special Issue Fungal Epidemiology)
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Abstract

Aspergillus flavus is the second most common etiological agent of invasive aspergillosis (IA) after A. fumigatus. However, most literature describes IA in relation to A. fumigatus or together with other Aspergillus species. Certain differences exist in IA caused by A. flavus and A. fumigatus and studies on A. flavus infections are increasing. Hence, we performed a comprehensive updated review on IA due to A. flavus. A. flavus is the cause of a broad spectrum of human diseases predominantly in Asia, the Middle East, and Africa possibly due to its ability to survive better in hot and arid climatic conditions compared to other Aspergillus spp. Worldwide, ~10% of cases of bronchopulmonary aspergillosis are caused by A. flavus. Outbreaks have usually been associated with construction activities as invasive pulmonary aspergillosis in immunocompromised patients and cutaneous, subcutaneous, and mucosal forms in immunocompetent individuals. Multilocus microsatellite typing is well standardized to differentiate A. flavus isolates into different clades. A. flavus is intrinsically resistant to polyenes. In contrast to A. fumigatus, triazole resistance infrequently occurs in A. flavus and is associated with mutations in the cyp51C gene. Overexpression of efflux pumps in non-wildtype strains lacking mutations in the cyp51 gene can also lead to high voriconazole minimum inhibitory concentrations. Voriconazole remains the drug of choice for treatment, and amphotericin B should be avoided. Primary therapy with echinocandins is not the first choice but the combination with voriconazole or as monotherapy may be used when the azoles and amphotericin B are contraindicated. View Full-Text
Keywords: invasive aspergillosis; Aspergillus flavus; epidemiology; molecular typing; azole resistance; amphotericin B resistance; treatment; epidemiological cut-off value invasive aspergillosis; Aspergillus flavus; epidemiology; molecular typing; azole resistance; amphotericin B resistance; treatment; epidemiological cut-off value
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Rudramurthy, S.M.; Paul, R.A.; Chakrabarti, A.; Mouton, J.W.; Meis, J.F. Invasive Aspergillosis by Aspergillus flavus: Epidemiology, Diagnosis, Antifungal Resistance, and Management. J. Fungi 2019, 5, 55.

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