INTRODUCTION
The evolution of bacterial pathogens from non-pathogens or from avirulent strains is a major cause for concern in agriculture. As exemplified by the explosion of antibiotic resistance in human pathogens, bacteria can rapidly overcome control strategies and host resistance. As we are now discovering, the intrinsic plasticity of the bacterial genome combined with horizontal gene transfer is the major determinant influencing the expression of pathogenicity. Many of the disease symptoms caused by pathogens on plants, including blights, galls, chlorosis, scabs, leaf spots, and wilting, are attributable to genes that are often clustered together and, in some cases, acquired from distantly related bacteria. One mechanism that affects the virulence of plant pathogens is the loss or gain of DNA regions called genomic islands (GEI).
GEI were first described as pathogenicity islands (PAI) in human pathogenic Escherichia coli by Hacker et al. (1990), who discovered that a region of chromosomally located, virulence-associated genes of uropathogenic E. coli was absent from some E. coli isolates (Blum et al., 1994). The term GEI is now more appropriate given that the features of PAI are displayed by a number of regions of DNA with functions other than pathogenicity, for example, symbiosis, metabolic, or resistance islands (Hacker and Kaper, 2000; Hentschel and Hacker, 2001).