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In bacterial pathogens, strain-specific chromosomal segments often contain genes encoding strain-specific traits, and because these genes often appear to be dedicated to pathogenic interactions with eucaryotic hosts, the segments containing them may be considered so-called pathogenicity islands (G. Blum, M. Ott, A. Lischewski, A. Ritter, H. Imrich, H. Tschape, and J. Hacker, Infect. Immun. 62:606-614, 1994). We evaluated the contribution to pathogenesis of a recently identified strain-specific chromosomal segment from an Escherichia coli K1 mammalian-newborn sepsis strain: transfer of E. coli K-12 DNA sequences near 64 min, by P1 transduction, into K1 strain RS218 resulted in an RS218-K-12 chimera that (i) contained a shortened NotIotl restriction fragment (relative to wild-type RS218) encompassing the 64-min region; (ii) lacked invasiveness in newborn rats; and (iii) grew in vitro, in both rich and minimal laboratory media, indistinguishably from strain RS218. In addition, genomic DNA from the chimera failed to hybridize with sequences of the K1 capsule genes from strain RS218, suggesting that the chromosomal segment near 64 min which was lost contained these sequences and indeed contained K1-specific virulence genes. Transfer of K-12 sequences resulting in deletion of E. coli pathogen-specific chromosomal segments may afford a general method of detecting genes encoding virulence and/or other distinguishing traits.

Pathogenicity island evaluation in Escherichia coli K1 by crossing with laboratory strain K-12