Integroncontaining IncU plasmids pRAS1 and pAr-32 from the fish pathogen Aeromonas salmonicida. Antimicrob. Agents Chemother

• Main Authors: Henning Sørum, Trine M. L’abée-lund, Asta Solberg, Anette Wold
• Other Authors: The Pennsylvania State University CiteSeerX Archives
• Format: Text
• Language: English
• Published: 2003
• Subjects: Norway; Atlantic salmon; Salmo salar
• Online Access: http://citeseerx.ist.psu.edu/viewdoc/summary?doi=10.1.1.689.64; http://www.ncbi.nlm.nih.gov/pmc/articles/PMC152485/pdf/0249.pdf

A 45-kb R plasmid, pRAS1, that confers resistance to tetracyclines, trimethoprim, and sulfonamides was isolated in 1989 from an atypical strain of the fish pathogen Aeromonas salmonicida. This plasmid could be transferred by conjugation to Escherichia coli with a high degree of efficiency (frequency, 0.48). The following year pRAS1 was isolated from A. salmonicida subsp. salmonicida in the same area. Incompatibility group U plasmid pRAS1 contained a drug resistance-determining region of 12 kb consisting of a class 1 integron similar to In4 of Tn1696 but with a dfrA16 gene cassette inserted. Close to IS6100 at the right end of Tn4 was a truncated Tn1721. Restriction enzyme analysis showed that R plasmid pAr-32, isolated from A. salmonicida in Japan in 1970, had the same backbone structure as pRAS1, while the drug resistance-determining region contained a complex class 1 integron with an aadA2 cassette; the chloramphenicol resistance gene catA2, as in In6 of pSa; and a duplicate of the 3 conserved segment of the integron. The intensity of farming of Atlantic salmon (Salmo salar L.) has increased rapidly since the 1970s in Norway (31). Aeromo-nas salmonicida subsp. salmonicida, the etiological agent of the salmonid disease furunculosis, was introduced into Norwegian salmon farms through smolts imported into mid-Norway from