| Literature DB >> 26344335 |
D Nurjadi1, J Schäfer2, B Friedrich-Jänicke3, A Mueller4, A Neumayr5, A Calvo-Cano6, A Goorhuis7, N Molhoek8, H Lagler9, A Kantele10, P J J Van Genderen8, J Gascon6, M P Grobusch7, E Caumes11, C Hatz12, R Fleck2, F P Mockenhaupt3, P Zanger13.
Abstract
To investigate the global occurrence of trimethoprim-sulfamethoxazole resistance and the genetic mechanisms of trimethoprim resistance, we analysed Staphylococcus aureus from travel-associated skin and soft-tissue infections treated at 13 travel clinics in Europe. Thirty-eight per cent (75/196) were trimethoprim-resistant and 21% (41/196) were resistant to trimethoprim-sulfamethoxazole. Among methicillin-resistant S. aureus, these proportions were 30% (7/23) and 17% (4/23), respectively. DfrG explained 92% (69/75) of all trimethoprim resistance in S. aureus. Travel to South Asia was associated with the highest risk of acquiring trimethoprim-sulfamethoxazole-resistant S. aureus. We conclude that globally dfrG is the predominant determinant of trimethoprim resistance in human S. aureus infection.Entities:
Keywords: Communicable diseases; Panton–Valentine leukocidin; emerging drug resistance; methicillin-resistant Staphylococcus aureus; molecular epidemiology; sentinel surveillance; staphylococcal skin infections; travel; trimethoprim–sulfamethoxazole combination
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Year: 2015 PMID： 26344335 DOI： 10.1016/j.cmi.2015.08.021
Source DB: PubMed Journal: Clin Microbiol Infect ISSN： 1198-743X Impact factor: 8.067