Virulence determinants are clustered in many bacterial pathogens in pathogenicity islands (PAI) scattered along the chromosome. Many such islands have been described to date and new similar genomic structures will certainly be detected in the near future. Genomic structures similar to pathogenicity islands have also been identified in non-pathogenic bacteria. The products of their genes participate in symbiosis, xenobiotic degradation, determine antibiotic resistance and supply many other metabolic functions for bacteria. Pathogenicity islands may be defined by the following criteria: G+C content, codon usage patterns, dinucleotide frequency different from that of the core genome, the presence of IS elements, transposase and integrase genes that determine mobility islands, the presence of direct repetitions at their boundaries, integration into tRNA genes and/or IS elements. Such DNA regions from non-pathogenic organisms are called genomic islands. It seems that pathogenicity islands are members of genomic islands. The integration of islands into chromosome occurs with HGT through transduction, transfection, and conjugation, but phages are recognized as being the main force of gene transfer. Pathogenicity islands as well as other islands remain in bacterial genome since they provide selective advantages to their recipient within given, specific conditions thus enhancing their survival within an ecological niche and adaptation capacity to eukaryotic hosts.
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