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Vibrio parahaemolyticus

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Through Gram-negative bacteria, Sea and Motility

Pathogenesis

While infection can occur by the fecal-oral route, ingestion of bacteria in raw or undercooked seafood, usually oysters, is the predominant cause of the acute gastroenteritis caused by V. parahaemolyticus. Wound infections also occur, but are less common than seafood-borne disease. The disease mechanism of V. parahaemolyticus infections has not been fully elucidated.

Clinical isolates usually possess a pathogenicity island (PAI) on the second chromosome. The PAI can be acquired by horizontal gene transfer and contains genes for several virulence factors. Two fully sequenced variants exist of the V. parahaemolyticus PAI with distinctly different lineages. Each PAI variant contains a genetically distinct Type III Secretion System (T3SS), which is capable of injecting virulence proteins into host cells to disrupt host cell functions or cause cell death by apoptosis. The two known T3SS variants on V. parahaemolyticus chromosome 2 are known as T3SS2α and T3SS2β. These variants correspond to the two known PAI variants. Aside from the T3SS, two genes encoding well-characterized virulence proteins are typically found on the PAI, the thermostable direct hemolysin gene (tdh) and/or the tdh-related hemolysin gene (trh). Strains possessing one or both of these hemolysins exhibit beta-hemolysis on blood agar plates. A distinct correlation seems to exist between presence of tdh, trh, and the two known T3SS variants: observations have shown T3SS2α correlating with tdh+/trh- strains, while T3SS2β correlates with tdh-/trh+ strains.

GefA, a GGEEF domain containing diguanylate cyclase, has recently been characterized from the V. parahaemolyticus genome. GefA plays a significant role in pathogenesis. By inhibiting swarming motility and promoting biofilm formation, it helps the bacteria to colonize within a host. Additionally, GefA influences the expression of virulence factors like the T3SS1, which directly contributes to the injection of the effector molecules into the host cell.

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