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Antimicrobial Agents and Chemotherapy, August 2001, p. 2299-2303, Vol. 45, No. 8
0066-4804/01/$04.00+0   DOI: 10.1128/AAC.45.8.2299-2303.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Large Drug Resistance Virulence Plasmids of Clinical Isolates of Salmonella enterica Serovar Choleraesuis

Chishih Chu,1 Cheng-Hsun Chiu,2 Wan-Yu Wu,1 Chi-Hong Chu,3 Tsui-Ping Liu,1 and Jonathan T. Ou1,*

Department of Microbiology and Immunology, Chang Gung University College of Medicine,1 and Department of Pediatrics, Chang Gung Children's Hospital,2 Kweishan 333, Taoyuan, and Department of Surgery, Tri-Service General Hospital, Taipei 100,3 Taiwan

Received 11 December 2000/Returned for modification 9 April 2001/Accepted 26 May 2001

Salmonella enterica serovar Choleraesuis generally causes systemic human salmonellosis without diarrhea, and therefore, antimicrobial treatment is essential for such patients. The drug resistance information on this organism is thus of high value. Serovar Choleraesuis usually harbors a virulence plasmid (pSCV) of 50 kb in size. Of the 16 clinical isolates identified to be serovar Choleraesuis, all except one harbored a pSCV and seven of them carried a pSCV of more than 125 kb in size. A pSCV was defined as a plasmid carrying spvC and characteristic deletions detected by PCR and by DNA-DNA hybridization (for the former criterion). The results of PCR, restriction fragment profiles, and Southern DNA-DNA hybridizations of the profiles all indicated that such larger pSCVs were derived from the 50-kb plasmid recombined with non-pSCVs found in some clinical isolates. Fifteen of the 17 strains, including a laboratory strain, were then tested for drug resistance against 16 antibiotics with E-test and the dilution method. The laboratory strain, which harbored a 50-kb pSCV and a 6-kb non-pSCV, was resistant only to sulfonamides (SUL), and its resistance gene, sulII, checked with PCR and DNA-DNA hybridization, was located on the 6-kb non-pSCV. All 14 clinical strains were resistant to multiple drugs. Of the 14, 7 were resistant to SUL, and the resistance gene was located on a plasmid. The sulII gene, but not blaTEM-1, was carried only on the 6-kb non-pSCV. Of the remaining six large plasmids, three of 90 kb, two of 136 kb, and one of 140 kb, the last three were pSCVs and carried the other SUL gene (sulI) and the blaTEM-1 gene. The six strains were also resistant to trimethoprim-sulfamethoxazole. None of the 50-kb pSCVs carried resistance genes. These drug resistance genes on the large pSCVs were apparently also acquired through recombination.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, Chang Gung University College of Medicine, 259 Wenhua 1 Rd., Kweishan 333, Taoyuan, Taiwan. Phone: 886-3-3286455. Fax: 886-3-3286455 and 886-3-3283031. E-mail: jontou{at}mail.cgu.edu.tw.

Antimicrobial Agents and Chemotherapy, August 2001, p. 2299-2303, Vol. 45, No. 8
0066-4804/01/$04.00+0   DOI: 10.1128/AAC.45.8.2299-2303.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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