Large drug resistance virulence plasmids of clinical isolates of Salmonella enterica serovar Choleraesuis

Salmonella enterica serovar Choleraesuis generally causes systemic human sa lmonellosis without diarrhea, and therefore, antimicrobial treatment is ess ential for such patients, The drug resistance information on this organism is thus of high value. Serovar Choleraesuis usually harbors a virulence pla smid (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 carr ied a pSCV of more than 125 kb in size. A pSCV was defined as a plasmid car rying spvC and characteristic deletions detected by PCR and by DNA-DNA hybr idization (for the former criterion), The results of PCR, restriction fragm ent profiles, and Southern DNA-DNA hybridizations of the profiles all indic ated that such larger pSCVs were derived from the 50-kb plasmid recombined, vith 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 sul fonamides (SUL), and its resistance gene, sulII, checked with PCR and DNA-D NA 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 sum gene, but not bla(TEM -1), was carried only on the 6-kb non-pSCV, Of the remaining six large plas mids, 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 bla(TEM-1) gene. The s ix strains mere also resistant to trimethoprim-sulfamethoxazole. None of th e 50-kb pSCVs carried resistance genes. These drug resistance genes on the large pSCVs were apparently also acquired through recombination.