Virulence traits of P Aeruginosa are not static

Pseudomonas aeruginosa is an opportunistic human pathogen that in most clinical situations is of low virulence. In the healthy host, inhaled bacteria are cleared rapidly by an arsenal of innate defence mechanisms including mucociliary clearance and immunological innate or acquired responses. In some clinical situations when the host defence fails, P aeruginosa can escape, multiply and cause severe lung infections such as in cystic fibrosis (CF). It has also become one of the three major causes of nosocomial infections worldwide. The presentation will focus on some strategies that the bacterium has developed to circumvent host defence at the airway mucosal interface when encountering the host. Complete sequencing of P aeruginosa genome has been realized since 2000 and with 6.3 Mb, this bacterium shows a unique highly genetic complexity with 5570 putative genes among which up to 50 % have unidentified functions. Genome analysis reveals that 468 genes corresponding to 8.4 % of the genes have characteristics of transcriptional regulators or of environmental sensors. The multiplicity and the redundancy of genes encoding various secretion apparatus, attachment factors, together with factors that control their expression highlight the unique adaptative capacity of this bacteria. The pathogenic capacity of P aeruginosa is associated with a wide range of virulence traits including capacity of biofilm formation, production of toxins and enzymes able to degrade tissues or to induce host cell toxicity or rearrangement through type I, II or III secretion pathways. All these virulence traits are under the control of regulatory systems such as the two-component systems and the quorum sensing that sense environmental stimuli or bacterial cell density, respectively. For biofilm initiation and formation, P aeruginosa possesses an arsenal of adhesions including the type IV pili responsible for a peculiar surface-associated motion named twitching motility described as a walking-like movement and responsible for cellular aggregation, the flagellum required for primary adhesion and other molecules either assembled into extracellular appendages such as the recently described Cup systems or lectins and many others that we are currently identifying in the genome. The type III secretion system has been recently identified as a key element in the pathogenic progression of the bacterium. This system encodes up to 20 proteins including asecretion apparatus, a translocation apparatus by which effectors are translocated into the host cell and four effectors which alter host cell functions. For the present presentation, we will illustrate mostly these virulent aspects of the bacterium and …