Pseudomonas aeruginosa can manipulate eukaryotic host cells using secreted effectors delivered by the type III or the
type VI Secretion Systems (T3SS and T6SS). The T3SS allows the injection of bacterial effectors (Exo toxins) into eukaryotic cell. P. aeruginosa, encodes three T6SSs, H1-, H2- and H3-T6SS. The H1-T6SS is mainly involved in delivering toxins to kill bacterial competitors. Recently, two T6SS-secreted
phospholipases D, PldA (H2-T6SS) and PldB (H3-T6SS), were identified as trans-kingdom virulence effectors, triggering both killing of bacterial competitors and internalization into non-phagocytic cells. We deciphered the prevalence of T3SS and T6SS effectors encoding genes in 185 clinical isolates responsible for
infections (septicaemia, pulmonary
infections, urinary tract infections, and
chronic infections in CF patients), 47 environmental strains, and on 33
carbapenemase-producers. We included 107 complete genomes of P. aeruginosa available in public databases. The prevalence of pldA is increased in clinical isolates responsible for severe acute
infection and particularly in multi-drug resistant strains. In contrast, the pldB prevalence was high (96.8%) in all isolates. Regarding T3SS effectors, exoT and exoY are present in nearly all isolates while exoS and exoU were found to be exclusive with a higher prevalence of exoU + strains in severe acute
infections. The hypervirulent exoU + isolates are more prone to be pldA +, suggesting a role of PldA in virulence. Finally, we observed that extremely drug resistant isolates producing an
IMP-type
carbapenemase were all pldA +. Our results suggest that PldA might have a role during pulmonary
infections and have been co-selected in multidrug resistant strains particularly
IMP-producers.