Evolution of Bacterial Pathogens Within the Human Host.

Selective pressures within the human host, including interactions with innate and adaptive immune responses, exposure to medical interventions such as antibiotics, and competition with commensal microbiota all facilitate the evolution of bacterial pathogens. In this chapter, we present examples of pathogen strategies that emerged as a result of selective pressures within the human host niche and discuss the resulting coevolutionary "arms race" between these organisms. In bacterial pathogens, many of the genes responsible for these strategies are encoded on mobile pathogenicity islands or plasmids, underscoring the importance of horizontal gene transfer in the emergence of virulent microbial species.

Antivirulence genes: insights into pathogen evolution through gene loss.

The emergence of new pathogens and the exploitation of novel pathogenic niches by bacteria typically require the horizontal transfer of virulence factors and subsequent adaptation--a "fine-tuning" process--for the successful incorporation of these factors into the microbe's genome. The function of newly acquired virulence factors may be hindered by the expression of genes already present in the bacterium. Occasionally, certain genes must be inactivated or deleted for full expression of the pathogen phenotype to occur.

Characterization of the activity and expression of arginine decarboxylase in human and animal Chlamydia pathogens.

Chlamydia pneumoniae encodes a functional arginine decarboxylase (ArgDC), AaxB, that activates upon self-cleavage and converts l-arginine to agmatine. In contrast, most Chlamydia trachomatis serovars carry a missense or nonsense mutation in aaxB abrogating activity. The G115R missense mutation was not predicted to impact AaxB functionality, making it unclear whether AaxB variations in other Chlamydia species also result in enzyme inactivation.