JAC Advance Access originally published online on May 4, 2005
Journal of Antimicrobial Chemotherapy 2005 55(6):846-852; doi:10.1093/jac/dki116
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Increasing ceftriaxone resistance in Salmonella isolates from a university hospital in Taiwan
1 Department of Clinical Pathology, Lin-Kou Medical Center, Chang Gung Memorial Hospital, 5 Fu-Hsin Street, Kweishan 333, Taoyuan, Taiwan; 2 Department of Applied Microbiology, National Chiayi University, 300 University Road, Chiayi 600, Taiwan; 3 Department of Pediatrics, Chang Gung Children's Hospital, 5 Fu-Hsin Street, Kweishan, Taoyuan 333, Taiwan
* Corresponding author: Tel: +886-3-3281200 ext. 8896; Fax: +886-3-3288957; Email: chchiu{at}adm.cgmh.org.tw
Objectives: Salmonella infection is a distressing health problem worldwide. This study reports the changing epidemiology of Salmonella infections in Taiwan during 1999–2003, with emphasis on increasing ceftriaxone resistance.
Methods: Records of Salmonella clinical isolates in Chang Gung Memorial Hospital during 1999–2003 were reviewed. All isolates were identified and antimicrobial susceptibility determined by standard methods. A total of 22 ceftriaxone-resistant isolates were investigated by PCR sequencing of the blaTEM, blaSHV, blaCTX-M and ampC genes. Southern-blot hybridization was used to localize the ampC gene. Infrequent-restriction-site PCR was used to genotype these isolates.
Results: A total of 3635 Salmonella isolates, including 3592 (98.8%) non-typhoid Salmonella, were identified. Serogroup B (55.6%) remained the most predominant, but the prevalence has been decreasing. In contrast, serogroup D infections have increased significantly from 13.6 to 22.8%. Overall resistance to ampicillin and chloramphenicol remained high, with the highest rate (91% to both drugs) observed in Salmonella enterica serotype Choleraesuis in 2003. A sudden upsurge of ciprofloxacin resistance from zero to 69% was found in S. Choleraesuis. Ceftriaxone resistance increased in several serogroups (0.8–2.1%; average, 1.5%). The resistance was associated with plasmid-mediated blaCMY-2 in 14 cases and extended-spectrum ß-lactamases (ESBLs), including CTX-M-3 (n=6), SHV-2a (n=1) and SHV-12 (n=1), in others. Diverse serotypes and genotypes were found among the ceftriaxone-resistant isolates.
Conclusions: Increasing ceftriaxone resistance in non-typhoid Salmonella appears to link to the spread of plasmid-mediated ampC or ESBL genes. Effective measures should be taken to prevent the problem worsening.
Keywords: antimicrobial resistance , ampC , extended-spectrum ß-lactamases
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