Abstract
The aim of this lecture is to integrate microbial evolutionary biology and the molecular and cellular analysis of pathogenicity in order to establish, in certain " textbook cases ", a continuum between the propensity to generate chronic infection, the genetic, molecular and cellular basis of this chronic pathogenicity, genomic reduction and progression to full parasitism. To this end, we have chosen two examples, one, Staphylococcus aureus, dealt with in the lecture, and the other, Chlamydia, dealt with in the seminar. In the case of S. aureus, we have placed particular emphasis on the description and functional integration of innate and adaptive immunity manipulation mechanisms, whose combined effectors generate the process of chronicity and recurrence. We have defined the following parameters in detail : evasion, deposition and activation of the complement system ; inhibition of antibody-mediated opsono-phagocytosis ; deletion of B and T lymphocytes by secretion of superantigen-functioning toxins ; inhibition of phagocytic cell recruitment/activation ; resistance to host antimicrobial peptides produced by skin keratinocytes and phagocytic cells ; resistance to reactive oxygen species (ROS) ; escape from NETs (neutrophil extracellular traps) ; causes phagocytic cell death through secretion of cytolysins (leukocidins) forming membrane pores. Not to mention the protection afforded by biofilm formation, so characteristic of staphylococci (S. aureus and S. epidermidis).
