Dissemination of the strA-strB streptomycin-resistance genes among commensal and pathogenic bacteria from humans, animals, and plants


  • G. W. SUNDIN,

    Corresponding author
    1. Department of Microbiology and Immunology, University of Illinois-Chicago, 835 S. Wolcott Ave., Chicago, IL 60612
      Fax: +1 (312) 996 6415. E-mail Sundin@uic.edu
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  • C. L. BENDER

    1. *Department of Plant Pathology, 110 Noble Research Centre, Oklahoma State University, Stillwater, OK 74078, USA
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  • The research in Carol Bender's laboratory leading to this review was inspired by our initial discovery that streptomycin resistance in Pseudomonas syringae was mediated by the strA-strB genes. Carol Bender's research centres on the genetics of bactericide resistance and phytotoxin biosynthesis in P. syringae. George Sundin received his PhD under the direction of Carol Bender working on the genetics and ecology of copper and streptomycin resistance and plasmid diversity in P. syringae.

Fax: +1 (312) 996 6415. E-mail Sundin@uic.edu


Gene transfer within bacterial communities has been recognized as a major contributor in the recent evolution of antibiotic resistance on a global scale. The linked strA-strB genes, which encode streptomycin-inactivating enzymes, are distributed worldwide and confer streptomycin resistance in at least 17 genera of gram-negative bacteria. Nucleotide sequence analyses suggest that strA-strB have been recently disseminated. In bacterial isolates from humans and animals, strA-strB are often linked with the sulII sulfonamide-resistance gene and are encoded on broad-host-range nonconjugative plasmids. In bacterial isolates from plants, strA-strB are encoded on the Tn3-type transposon Tn5393 which is generally borne on conjugative plasmids. The wide distribution of the strA-strB genes in the environment suggests that gene transfer events between human, animal, and plant-associated bacteria have occurred. Although the usage of streptomycin in clinical medicine and animal husbandry has diminished, the persistence of strA-strB in bacterial populations implies that factors other than direct antibiotic selection are involved in maintenance of these genes.