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Vibrio vulnificus  is autochthonous to estuaries and warm coastal waters. Infection occurs via open wounds or ingestion, where its asymptomatic colonization of seafood, most infamously oysters, provides a gateway into the human food chain. Colonization begins with initial surface contact, which is often mediated by bacterial surface appendages called pili. Type IV Tad pili are widely distributed in the Vibrionaceae, but evidence for a physiological role for these structures is scant. The  V. vulnificus  genome codes for three distinct  tad  loci. Recently, a positive correlation was demonstrated between the expression of  tad-3  and the phenotypes of a  V. vulnificus  descendent (NT) that exhibited increased biofilm formation, auto-aggregation, and oyster colonization relative to its parent. However, the mechanism by which  tad  pilus expression promoted these phenotypes was not determined. Here, we show that deletion of the  tad  pilin gene ( flp ) altered the near-surface motility profile of NT cells from high curvature, orbital retracing patterns characteristic of cells actively probing the surface to low curvature traces indicative of wandering and diminished bacteria–surface interactions. The NT  flp  pilin mutant also exhibited decreased initial surface attachment, attenuated auto-aggregation and formed fragile biofilms that disintegrated under hydrodynamic flow. Thus, the  tad-3  locus, designated  iam , promoted  i nitial surface attachment,  a uto-aggregation and resistance to  m echanical clearance of  V. vulnificus  biofilms. The prevalence of  tad  loci in the Vibrionaceae suggests that they may play equally important roles in other family members.

A Tad pilus promotes the establishment and resistance of Vibrio vulnificus biofilms to mechanical clearance