This chapter outlines the evolutionary aspect of toxins, specially the ones produced by certain bacterias. Increasing evidence indicates that the evolution of toxin genes involves horizontal gene transfer and recombination events mediated through plasmids, phages, transposons, and other yet-undefined transmissible elements. In addition to the host environment, toxin evolution and transmission also can occur outside the human and animal host, including in soil and aquatic environments, in the phyllosphere, and in the guts of insects, parasites, and other vectors. The evolution of bacterial toxins involves HGT and recombination through exposure to a combination of both the host and external environments. New evidence suggests that acquisition of large DNA segments by horizontal gene transfer (HGT) may account for a much more rapid evolution of pathogens, particularly in terms of the origin of virulence factors such as toxins, than was previously thought. Most toxin genes are located on pathogenicity islands (PAIs) on plasmids or in the bacterial chromosome as prophages or transmissible elements. Possible mechanisms by which HGT contributes to bacterial pathogenesis include exchange and recombination of toxin and other virulence genes among different bacterial populations; one-step acquisition of toxin(s) and other virulence genes to increase survival against the host's immune system or to provide means for dissemination within the host or between hosts; and provision of mechanisms to enhance survival in the external environment when outside the host body.
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)