Evolution and host-specific adaptation of .

The major human bacterial pathogen causes multidrug-resistant infections in people with underlying immunodeficiencies or structural lung diseases such as cystic fibrosis (CF). We show that a few environmental isolates, driven by horizontal gene acquisition, have become dominant epidemic clones that have sequentially emerged and spread through global transmission networks over the past 200 years. These clones demonstrate varying intrinsic propensities for infecting CF or non-CF individuals (linked to specific transcriptional changes enabling survival within macrophages); have undergone multiple rounds of convergent, host-specific adaptation; and have eventually lost their ability to transmit between different patient groups.

Genome-wide screen in human plasma identifies multifaceted complement evasion of Pseudomonas aeruginosa.

Pseudomonas aeruginosa, an opportunistic Gram-negative pathogen, is a leading cause of bacteremia with a high mortality rate. We recently reported that P. aeruginosa forms a persister-like sub-population of evaders in human plasma.

Molecular Mechanisms Involved in Pseudomonas aeruginosa Bacteremia.

Bloodstream infections (BSI) with Pseudomonas aeruginosa account for 8.5% of all BSIs, their mortality rate, at about 40%, is the highest among causative agents. For this reason and due to its intrinsic and acquired resistance to antibiotics, P.

Zebrafish Embryo Infection Model to Investigate Interaction With Innate Immunity and Validate New Therapeutics.

The opportunistic human pathogen is responsible for a variety of acute infections and is a major cause of mortality in chronically infected patients with cystic fibrosis (CF). Considering the intrinsic and acquired resistance of to currently used antibiotics, new therapeutic strategies against this pathogen are urgently needed. Whereas virulence factors of are well characterized, the interplay between and the innate immune response during infection remains unclear.

Inflammasome activation by Pseudomonas aeruginosa's ExlA pore-forming toxin is detrimental for the host.

During acute Pseudomonas aeruginosa infection, the inflammatory response is essential for bacterial clearance. Neutrophil recruitment can be initiated following the assembly of an inflammasome within sentinel macrophages, leading to activation of caspase-1, which in turn triggers macrophage pyroptosis and IL-1β/IL-18 maturation. Inflammasome formation can be induced by a number of bacterial determinants, including Type III secretion systems (T3SSs) or pore-forming toxins, or, alternatively, by lipopolysaccharide (LPS) via caspase-11 activation.

An unusual community-acquired invasive and multi systemic infection due to ExoU-harboring Pseudomonas aeruginosa strain: Clinical disease and microbiological characteristics.

Community-acquired Pseudomonas aeruginosa infections are rare. Most cases involve patients either with underlying immunosuppression or structural chronic lung diseases. We report here an atypical case of a severe community-acquired invasive infection due to a hypervirulent ExoU-producing strain, in an immunocompetent patient.