B. pseudomallei isolates are genetically quite diverse [4, 5], and this heterogeneity may be due at least in part to the highly variable distribution of bacteriophages among strains [6]. Such differences may provide certain strains

survival advantages in the environment and the host, as well as explain the variable clinical presentation of melioidosis. Also raising concern as a potential biological weapon is the very closely related B. mallei, causal agent of the primarily equine disease known as glanders [7]. In contrast to B. pseudomallei, B. mallei is a highly specialized pathogen, not found outside of a mammalian host in nature. B. mallei is a host-adapted clone of B. pseudomallei, and all of the BI 10773 ic50 B. mallei genome is nearly identical buy AG-881 to a set of genes within B. pseudomallei core genome. However, in addition to its core genome B. pseudomallei contains numerous contiguous gene clusters that were deleted from B. mallei during its evolution [8, 9]. B. thailandensis is another closely related organism often found in the same environmental samples (soil and water

of endemic melioidosis regions) as B. pseudomallei [10]. Unlike B. pseudomallei and B. mallei, B. thailandensis has very low virulence in most animal hosts, including humans. The ability to metabolize arabinose, and the corresponding loss of the arabinose assimilation operon from B. pseudomallei, phenotypically distinguishes B. thailandensis from B. pseudomallei [11]. The genes encoding arabinose assimilation may be considered as antivirulent, and their absence from B. pseudomallei (and B. mallei) may have allowed the development of the latter as pathogens [12]. Burkholderia

multivorans, a member of the Burkholderia cepacia complex, is an opportunistic pathogen associated with infection in cystic fibrosis patients that is also found in soil environments these [13]. The presence of prophages among bacterial isolates and their possible contribution to bacterial diversity is widespread. By carrying various elements contributing to virulence, prophages can contribute to the genetic individuality of a bacterial strain. This phenomenon has been reported in Salmonella spp [14] and Lactobacillus spp [15, 16], among others. Blasticidin S manufacturer Prophage-associated chromosomal rearrangements and deletions have been found to be largely responsible for strain-specific differences in Streptococcus pyogenes [17] and Xylella fastidiosa [18]. Thus, temperate phages carrying foreign DNA can play a role in the emergence of pathogenic variants. Lateral gene transfer between phage and host genomes, and phage lysogenic conversion genes, can alter host phenotype through production of phage-encoded toxins and disease-modifying factors that affect virulence of the bacterial strain.