EMERGENCE AND PROGRESSION OF STREPTOMYCIN RESISTANCE IN ERWINIA AMYLOVORA IN MICHIGAN

Streptomycin-resistant (Sm^R) E. amylovora strains were first isolated in southwest Michigan in 1991. Since that time, resistant strains have gradually progressed northward to other apple and pear-producing regions. The large majority of Sm^R strains harbor the strA-strB genes on transposon Tn5393. strA and strB encode phosphotransferase enzymes that modify streptomycin to a nontoxic form. Mutational resistance to streptomycin, caused by a target-site alteration of the ribosomal rpsL gene, occurs in a small subset of E. amylovora strains from Michigan. Tn5393 was originally introduced to E. amylovora on the plasmid pEa34; thus, Sm^R strains contained both pEa34 and the ubiquitous virulence plasmid pEA29. More recently, we have observed Sm^R strains in which Tn5393 is encoded on pEA29, suggesting that the transposon has moved via transposition from pEa34 to pEA29. Because pEA29 is a non-conjugative plasmid, resistance is not thought to move horizontally through the bacterial population, and each insertion of Tn5393 into pEA29 is viewed as a separate event characterized by the unique location of the transposon on the plasmid. This unique insertion site allows for the tracking of specific Sm^R strains between discrete growing regions of the state or for the observation of new Sm^R strains arising in these new areas. Our current data suggests that a small number of Sm^R strains are responsible for the dissemination of streptomycin resistance in Michigan.