Short-sighted evolution of bacterial opportunistic pathogens with an environmental origin
- Departamento de Biotecnología Microbiana, Centro Nacional de Biotecnología, Consejo Superior de Investigaciones Científicas, Madrid, Spain
...The evolution of non-pathogenic bacteria towards virulence has been deciphered in occasions. Many “professional” pathogens harbor different sets of genes, dubbed as pathogenicity islands, which have been acquired by horizontal gene transfer, and allow such pathogens to infect the human host (Groisman and Ochman, 1996; Morschhauser et al., 2000; Gal-Mor and Finlay, 2006). The best studied among these evolution processes is that of Yersinia pestis, the causal agent of plague (Achtman et al., 2004; Zhou and Yang, 2009). The genus Yersinia is formed by 15 different species among which only Y. pestis, Yersinia pseudotuberculosis, and Yersinia enterocolitica are human pathogens. Phylogenetic reconstruction of the evolution of this genus indicates that Y. pseudotuberculosis and Y. enterocolitica diverged more than 40 million years ago, while Y. pestisdiverged from Y. pseudotuberculosis less than 20,000 years ago (Achtman et al., 1999). The ancestor of these pathogenic Yersiniae evolved towards virulence, from a non-pathogenic environmental Yersiniae, by acquiring a virulence plasmid named pCD1 (Wren, 2003). This plasmid contains genes coding for a Type III secretion system, which activity allows subversion of the immune system, and is required for the virulence of this pathogen. It is worth mentioning that the acquisition of this plasmid occurred before the divergence between Y. pseudotuberculosis and Y. enterocolitica, hence more than 40 million years ago; long before the origin of the genus Homo(Wood, 1992; McHenry, 1994). This means that the evolution of human pathogens is not exclusively driven by the infection of humans (Martinez, 2013). As stated before, the speciation of Y. pestis fromY. pseudotuberculosis is a much more recent process that involves both the acquisition of some genes and the loss of other ones. The loss of genes has been frequently associated to genome reduction evolution mostly in the case of endosymbionts (Perez-Brocal et al., 2006). For these microorganisms, several metabolic functions can be covered by the host and un-needed genes are lost just by gene drift. The situation concerning Yersinia is not the same. In its process of evolution Y. pestis had lost a set of genes encoding insect toxins. Consequently, the evolved organism does not kill insects, a property that allowed its improved transmission by beats of colonized insects (Chouikha and Hinnebusch, 2012). Since this may mean that Y. pestis is in the process of evolution toward commensalism in insects, we may conclude that a relevant element for the success of Y. pestis as a human pathogen comes from its adaptation to a completely different host, in this case the insects...
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