Photobacterium damselae subsp. damselae, a generalist pathogen with unique virulence factors and high genetic diversity

Abstract

Photobacterium damselae subsp. damselae causes vibriosis in a variety of marine animals, including fish species of importance in aquaculture. It also may cause wound infections in humans that can progress to a fatal outcome. Two major virulence factors are encoded within the large conjugative plasmid pPHDD1, the phospholipase D damselysin (Dly) and the pore-forming toxin phobalysin P (PhlyP). The two toxins exert hemolytic and cytolytic activities in a synergistic manner. Even though PhlyP has close homologues in many Vibrio species, it has unique features that differentiate it from related toxins. Dly phospholipase constitutes a singular trait of P. damselae subsp. damselae among the Vibrionaceae, although related toxins are found in members of the Aeromonadaceae. Fish farm outbreaks can also be caused by plasmidless strains. Such observations led to the characterization of two ubiquitous chromosome-encoded toxins with lesser cytolytic activity, the pore formingtoxin phobalysin C (PhlyC) and the phospholipase-hemolysin PlpV. The high genetic diversity of this pathogen deserves special attention, as it has a number of strainspecific features, including the cell envelope polysaccharide synthesis clusters. Fish outbreaks are likely caused by multiclonal populations which contain both plasmidless and pPHDD1-harboring isolates and not by well-adapted clonal complexes. Still, among such genetic heterogeneity, it is feasible to identify conserved weak points in the biology of this bacterium: the two-component regulatory system RstAB (CarSR) was found to be necessary for the maximal production of virulence factors, and its inactivation severely impaired virulence.