Screening for mutations related to atovaquone/proguanil resistance in treatment failures and other imported isolates of Plasmodium falciparum in Europe
Authors
Cuadros González, JuanIdentifiers
Permanent link (URI): http://hdl.handle.net/10017/60498DOI: 10.1086/424469
ISSN: 0022-1899
Date
2004-11-01Academic Departments
Universidad de Alcalá. Departamento de Biomedicina y Biotecnología
Teaching unit
Unidad Docente de Microbiología
Funders
Friedrich Baur Stiftung, Ludwig-Maximilians-University (to TropNetEurop)
Bibliographic citation
Journal of Infectious Diseases, 2004, v. , n. , p. 1541-1546
Keywords
Plasmodium falciparum
Atovaquone/proguanil
Antiparasitic resistance
Description / Notes
8 p.
Document type
info:eu-repo/semantics/article
Version
info:eu-repo/semantics/acceptedVersion
Rights
© 2004 by the Infectious Diseases Society of America
Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)
Access rights
info:eu-repo/semantics/openAccess
Abstract
Background: Two single-point mutations of the Plasmodium falciparum cytochrome b gene (Tyr268Asn and Tyr268Ser) were recently reported in cases of atovaquone/proguanil (Malarone) treatment failure. However, little is known about the prevalence of codon-268 mutations and their quantitative association with treatment failure. Methods: We set out to assess the prevalence of codon-268 mutations in P. falciparum isolates imported into Europe and to quantify their association with atovaquone/proguanil treatment failure. Isolates of P. falciparum collected by the European Network on Imported Infectious Disease Surveillance between April 2000 and August 2003 were analyzed for codon-268 mutations, by use of polymerase chain reaction-restriction fragment-length polymorphism. Results: We successfully screened 504 samples for the presence of either Tyr268Ser or Tyr268Asn. One case of Ser268 and no cases of Asn268 were detected. Therefore, we can be 95% confident that the prevalence of Ser268 in the European patient pool does not exceed 0.96% and that Asn268 is less frequent than 0.77%. In 58 patients treated with atovaquone/proguanil, Tyr268Ser was present in 1 of 5 patients with treatment failure but in 0 of 53 successfully treated patients. Conclusions: Tyr268Ser seems to be a sufficient, but not a necessary, cause for atovaquone/proguanil treatment failure. The prevalence of both codon-268 mutations is currently unlikely to be >1% in the European patient pool.
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