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Applied and Environmental Microbiology, June 2009, p. 4053-4057, Vol. 75, No. 12
0099-2240/09/$08.00+0     doi:10.1128/AEM.00231-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Possible Environmental Origin of Resistance of Aspergillus fumigatus to Medical Triazoles{triangledown}

Eveline Snelders,1,2 Robert A. G. Huis in 't Veld,1,2 Anthonius J. M. M. Rijs,1,2 Gert H. J. Kema,3 Willem J. G. Melchers,1,2 and Paul E. Verweij1,2*

Department of Medical Microbiology,1 Nijmegen Institute for Infection, Inflammation, and Immunity, Radboud University Nijmegen Medical Center, P.O. Box 9101, 6500 HB Nijmegen, The Netherlands,2 Plant Research International, Wageningen, The Netherlands3

Received 30 January 2009/ Accepted 11 April 2009

We reported the emergence of resistance to medical triazoles of Aspergillus fumigatus isolates from patients with invasive aspergillosis. A dominant resistance mechanism was found, and we hypothesized that azole resistance might develop through azole exposure in the environment rather than in azole-treated patients. We investigated if A. fumigatus isolates resistant to medical triazoles are present in our environment by sampling the hospital indoor environment and soil from the outdoor environment. Antifungal susceptibility, resistance mechanisms, and genetic relatedness were compared with those of azole-resistant clinical isolates collected in a previous study. Itraconazole-resistant A. fumigatus (five isolates) was cultured from the indoor hospital environment as well as from soil obtained from flower beds in proximity to the hospital (six isolates) but never from natural soil. Additional samples of commercial compost, leaves, and seeds obtained from a garden center and a plant nursery were also positive (four isolates). Cross-resistance was observed for voriconazole, posaconazole, and the azole fungicides metconazole and tebuconazole. Molecular analysis showed the presence of the dominant resistance mechanism, which was identical to that found in clinical isolates, in 13 of 15 environmental isolates, and it showed that environmental and clinical isolates were genetically clustered apart from nonresistant isolates. Patients with azole-resistant aspergillosis might have been colonized with azole-resistant isolates from the environment.

* Corresponding author. Mailing address: Department of Medical Microbiology, Radboud University Nijmegen Medical Center, P.O. Box 9101, 6500 HB Nijmegen, The Netherlands. Phone: 31-24-3614356. Fax: 31-24-3540216. E-mail: p.verweij{at}mmb.umcn.nl

{triangledown} Published ahead of print on 17 April 2009.

Applied and Environmental Microbiology, June 2009, p. 4053-4057, Vol. 75, No. 12
0099-2240/09/$08.00+0     doi:10.1128/AEM.00231-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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