sábado, 30 de abril de 2011

Salmonella enterica Serotype Typhi with Nonclassical Quinolone Resistance Phenotype [EID CDC]

DOI: 10.3201/eid1706.101242
Suggested citation for this article: Accou-Demartin M, Gaborieau V, Song Y, Roumagnac P, Marchou B, Achtman M, et al. Salmonella enterica serotype Typhi with nonclassical quinolone resistance phenotype [expedited]. Emerg Infect Dis. 2011 Jun; [Epub ahead of print]

Salmonella enterica Serotype Typhi with Nonclassical Quinolone Resistance Phenotype

Marie Accou-Demartin, Valérie Gaborieau, Yajun Song, Philippe Roumagnac, Bruno Marchou, Mark Achtman, and François-Xavier Weill

Author affiliations: Institut Pasteur, Paris, France (M. Accou-Demartin, F.-X. Weill); Hôpital Purpan, Toulouse, France (V. Gaborieau, B. Marchou); University College Cork, Cork, Ireland (Y. Song, M. Achtman); and Centre de Coopération International en Recherche Agronomique pour le Développement, Montpellier, France (P. Roumagnac)

We report Salmonella enterica serotype Typhi strains with a nonclassical quinolone resistance phenotype (i.e., decreased susceptibility to ciprofloxacin but with susceptibility to nalidixic acid) associated with a nonsynonymous mutation at codon 464 of the gyrB gene. These strains, not detected by the nalidixic acid disk screening test, can result in fluoroquinolone treatment failure.

Typhoid fever caused by Salmonella enterica serotype Typhi (hereafter referred to as Salmonella Typhi) remains a major health problem in the developing world (1). Treatment with appropriate antimicrobial drugs has become hampered by gradual plasmid-mediated resistance to ampicillin, chloramphenicol, and cotrimoxazole, particularly in South and Southeast Asia (2). Consequently, since the early 1990s, fluoroquinolones (such as ofloxacin and ciprofloxacin [Cip]) have been widely used. However, multidrug-resistant Salmonella Typhi isolates that are also resistant to nalidixic acid (NalR) (MIC >256 μg/mL) and show decreased susceptibility to Cip (CipDS) (MIC range, 0.125 μg/mL–1 μg/mL) have emerged and become endemic on the Indian subcontinent and in Southeast Asia (3–5). This resistance to quinolones was caused by amino acid substitutions in the quinolone resistance–determining region (QRDR) of the DNA gyrase subunit gyrA, a key target of quinolones. Because these NalR–CipDS Salmonella Typhi


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