|Authors: ||G.C. McGhee, L. Bellomo, S.E. Blumer, G.W. Sundin|
|Keywords: ||Tn5393, strA-strB genes, pEA29, transposon|
Streptomycin-resistant (SmR) 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 SmR 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, SmR strains contained both pEa34 and the ubiquitous virulence plasmid pEA29. More recently, we have observed SmR 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 SmR strains between discrete growing regions of the state or for the observation of new SmR strains arising in these new areas.
Our current data suggests that a small number of SmR strains are responsible for the dissemination of streptomycin resistance in Michigan.
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