Streptococcus iniae is an aquatic zoonotic pathogen that causes hundreds of millions of dollars in losses annually to the world-wide aquaculture industry and poses a significant risk to humans who handle raw fish. In vivo screening of a randomly generated bacterial transposon mutant library created from the wlid-type S. iniae strain K288, led to the discovery of an attenuated transposon mutant with a disruption in a gene region near a putative polysaccharide deacetylase we named pdi. Here I describe a proposed role of the novel pdi gene in S. iniae virulence, and compare it to a paralogous virulence gene (pgdA) found in several other pathogenic species. Following the creation of the isogenic Δpdi mutant we observed its attenuation in an in vivo HSB virulence model, as well as decreased survival in whole fish blood. We also observed an impairment of the Δ pdi mutant in its ability to adhere and invade fish epithelial cells, a virulence mechanism that until now, has been speculated, but not yet associated with virulence in vivo or with a specific virulence gene.