Phenotypic evidence for inducible multiple antimicrobial resistance in Salmonella choleraesuis

被引:10
|
作者
Tibbetts, RJ
Lin, TL
Wu, CC [1 ]
机构
[1] Purdue Univ, Sch Vet Med, Dept Vet Pathobiol, W Lafayette, IN 47907 USA
[2] Purdue Univ, Anim Dis Diagnost Lab 1175, W Lafayette, IN 47907 USA
关键词
Salmonella choleraesuis; marA; multiple antimicrobial resistance;
D O I
10.1016/S0378-1097(02)01179-5
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Multiple antimicrobial resistance (MAR) in Salmonella choleraesuis is becoming a major concern. It has been demonstrated that a MAR phenotype can be induced in Escherichia coli and other members of the Enterobacteriaceae by exposing the isolates to salicylates, various antimicrobials, or organic solvents used to combat and control bacterial infection. Therefore the purpose of the present study was to determine whether this marA-associated MAR-phenotype is inducible in S. choleraesuis. Isolates used in the present study were able to withstand toxic effects of the organic solvent cyclohexane naturally, or following exposure to the inducing compounds salicylate, tetracycline, or chloramphenicol. All isolates possessed fragments of marA with the predicted size of 408 bp when amplified using marA-specific primers by PCR. The resulting PCR products that were sequenced revealed that amplified S. choleraesuis marA was 99% and 85% homologous to the published Salmonella typhimurium and E. coli marA sequences respectively. Minimum inhibitory concentrations of tetracycline (P < 0.08), chloramphenicol (P < 0.001), rifampin (P < 0.08), and nalidixic acid (P < 0.001) against cyclohexane-tolerant mutants were significantly increased when compared with wild-type S. choleraesuis. Northern hybridization signals for both marA and acrB were increased in the induced isolates when compared to uninduced controls while soxS expression did not change between induced and uninduced cultures. The results suggest that marA is present in S. choleraesuis and a MAR-phenotype is inducible in S. choleraesuis presumably due to the overexpression of marA and acrB and not to the overexpression of soxS. (C) 2002 Federation of European Microbiological Societies. Published by Elsevier Science B.V. All rights reserved.
引用
收藏
页码:333 / 338
页数:6
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