The pathogenicity islands (PAIs) of the uropathogenic Escherichia coli strain 536: island probing of PAI II536.

Pathogenicity islands (PAIs) represent distinct pieces of DNA that are present in the genomes of pathogenic bacteria but absent from the genomes of related nonpathogenic strains. They carry (often more than one) virulence genes and are linked to transfer RNA (tRNA) loci. In addition, they carry mobility genes and direct repeats at their ends and are often unstable [1]. The first PAIs have been identified in the genomes of uropathogenic Escherichia coli (UPEC) [2–4], and PAIs of 120 species of pathogens have been described [5]. UPECs can produce various virulence factors, such as specific adhesins (P, S, type I, F1C), toxins (a-hemolysin, cytotoxic necrotizing factor I), capsules (K1, K5, K12), specific O antigens (O1, O2, O4, O6, O18), iron-uptake systems (aerobactin, yersiniabactin), and factors contributing to serum resistance. Most genes, coding for these factors are located on PAIs [3, 4]. The uropathogenic strain E. coli 536, which was isolated from a patient with pyelonephritis, represents a model organism for the analysis of the genetic basis of urovirulence [2, 6]. The strain exhibits the serotype O6:K15:H31 and carries four PAIs in its chromosome. PAI I536 and PAI II536, which are 70 and 120 kb in size, carry the genes for hemolysin and, in the case of PAI II536, P fimbriae. PAI III536 carries the S fimbrial gene cluster, and PAI IV536 is almost identical to the functional core region of the “high pathogenicity island” (HPI) of pathogenic Yersinia species, encoding the yersiniabactin iron-uptake system [4, 7]. In addition, the genes responsible for the capsule synthesis seem also to be located on another PAI (Janke B, et al., unpublished data). As shown recently, PAI I536 and PAI II536, which are located next to the tRNA genes selC and leuX at map positions 82 and 97 in the E. coli chromosome, respectively, are unstable [2]. With relatively high frequencies, these PAIs can be deleted from the chromosome of strain 536. In previous studies [2], the deletion processes of PAI I536 and PAI II536 have been analyzed on the basis of the loss of hemolysin production. In this report, however, we use the new method of “island probing,” as described by Rajakumar et al. [8], for the first time