Summary.
This study was designed to determine the role of a new temperate DNA phage BcP15 in relation to drug resistance. The multidrug resistant Shigella flexneri NK1925 was isolated from a patient of Infectious Diseases Hospital, Kolkata, India. This strain contained five plasmids ranging in size from 3 to 212 kb. After curing of five plasmids, this strain became sensitive to antibiotics. A plasmidless multidrug-resistant strain Burkholderia cepacia DR11 was isolated during the survey of microorganisms from coastal waters of deltaic Sunderbans. This strain always released a temperate phage BcP15 into culture supernatant. Turbid plaque formation was observed on the lawn of a plasmidless version (Pl−35) of Shigella flexneri NK1925. A few distinct clones (Pl−35R) appeared within the region of each plaque after 18 h incubation. S. flexneri NK1925, Pl−35, and Pl−35R clones showed the same PFGE band pattern of XbaI-digested chromosomal DNA. However, Pl−35R clones were resistant to co-trimoxazole, trimethoprim, and eryth- romycin, to which B. cepacia DR11 was also resistant. Southern hybridization results indicated that these three antibiotic resistances in Pl−35R clones were due to a BcP15 phage lysogen in the Pl−35 version of S. flexneri NK1925.