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Mussel culture in Europe is currently suffering from mass mortality events with mortality rates up to 100%. Vibrios belonging to the Splendidus clade have recently been implicated in these events. In this study, we demonstrate that V. tasmaniensis LGP32 and V. crassostreae J2–9, two model pathogens of oysters, are also pathogenic to blue mussel larvae in an immersion challenge test. After five days, LGP32 and J2–9 had killed 93 and 73% of challenged mussel larvae, respectively. Because quorum sensing, bacterial cell-to-cell communication with small signal molecules, has been demonstrated to control the virulence of various vibrios, we further investigated whether it had an impact on the virulence of V. tasmaniensis and V. crassostreae. We identified the components of a multichannel quorum sensing system (as also found in many other vibrios) in the genomes of both species. Knock out of selected components of this pathway revealed that in general quorum sensing in V. tasmaniensis LGP32 and V. crassostreae J2–9 has no impact on motility, protease activity, biofilm formation and virulence towards mussel larvae. Finally, the quorum sensing inhibitor cinnamaldehyde did not protect mussel larvae from these pathogens. Together, these data indicate that the multichannel quorum sensing systems of V. tasmaniensis LGP32 and V. crassostreae J2–9 have no impact on virulence of the bacteria towards blue mussel larvae. Hence, quorum sensing controlling virulence is not a general feature in vibrios as it has different outcomes on virulence in different species.