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Antimicrobial Agents and Chemotherapy, October 2004, p. 3934-3939, Vol. 48, No. 10
0066-4804/04/$08.00+0     DOI: 10.1128/AAC.48.10.3934-3939.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Mechanism of Resistance to Several Antimicrobial Agents in Salmonella Clinical Isolates Causing Traveler's Diarrhea

Roberto Cabrera,1,2,3 Joaquím Ruiz,3 Francesc Marco,1 Inés Oliveira,3 Margarita Arroyo,4 Ana Aladueña,4 Miguel A. Usera,4 M. Teresa Jiménez De Anta,1 Joaquím Gascón,3 and Jordi Vila1*

Servicio de Microbiología, IDIBAPS, Hospital Clínic,1 Centro de Salud Internacional, IDIBAPS, Universidad de Barcelona, Hospital Clínic Barcelona,3 Instituto de Salud Carlos III, Majadahonda, Madrid Spain,4 Instituto de Medicina Tropical "Pedro Kourí," Havana, Cuba2

Received 24 November 2003/ Returned for modification 1 March 2004/ Accepted 26 June 2004

The evolution of antimicrobial resistance in Salmonella isolates causing traveler's diarrhea (TD) and their mechanisms of resistance to several antimicrobial agents were analyzed. From 1995 to 2002, a total of 62 Salmonella strains were isolated from stools of patients with TD. The antimicrobial susceptibility to 12 antibiotics was determined, and the molecular mechanisms of resistance to several of them were detected as well. The highest levels of resistance were found against tetracycline and ampicillin (21 and 19%, respectively), followed by resistance to nalidixic acid (16%), which was mainly detected from 2000 onward. Molecular mechanisms of resistance were analyzed in 16 isolates. In these isolates, which were resistant to ampicillin, two genes encoding ß-lactamases were detected: oxa-1 (one isolate) and tem-like (seven isolates [in one strain concomitantly with a carb-2]). Resistance to tetracycline was mainly related to tetA (five cases) and to tetB and tetG (one case each). Resistance to chloramphenicol was related to the presence of the floR and cmlA genes and to chloramphenicol acetyltransferase activity in one case each. Different genes encoding dihydrofolate-reductases (dfrA1, dfrA12, dfrA14, and dfrA17) were detected in trimethoprim-resistant isolates. Resistance to nalidixic acid was related to the presence of mutations in the amino acid codons 83 or 87 of the gyrA gene. Further surveillance of the Salmonella spp. causing TD is needed to detect trends in their resistance to antimicrobial agents, as we have shown in our study with nalidixic acid. Moreover, such studies will lead to better treatment and strategies to prevent and limit their spread.

* Corresponding author. Mailing address: Servicio de Microbiología, Hospital Clínic de Barcelona, C/Villarroel 170, 08036 Barcelona, Spain. Phone: 34-93-2275522. Fax: 34-93-2279372. E-mail: vila{at}medicina.ub.es.

Antimicrobial Agents and Chemotherapy, October 2004, p. 3934-3939, Vol. 48, No. 10
0066-4804/04/$08.00+0     DOI: 10.1128/AAC.48.10.3934-3939.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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