It is well accepted that stress can negatively affect healing. Restraint-stressed mice exhibit delayed wound closure and have greater bacterial loads than controls, suggesting that bacterial clearance is impaired in this model. Interestingly, wound healing in isolated mice is delayed to a similar magnitude, yet these wounds have low bacterial loads. This finding challenges the notion that stress-impaired healing requires impaired bacterial clearance; here we explore its role (and necessity). Bacteria samples were collected from the skin of group-housed mice and cultured. Three housing conditions were established: group-housed, isolated 3 weeks before wounding, and isolated at wounding. Mice received two 3.5mm dorsal punch biopsies. 25μL of vehicle or bacteria solution was placed topically on each wound. Daily photographs monitored wound closure. Regardless of bacterial burden, group-housed mice exhibited faster wound closure than isolated mice. Artificially increasing bacterial load to that of control animals resulted in higher bacterial counts in isolates. The addition of bacteria did not affect healing rates in isolates, whereas it accelerated healing in group-housed controls. Surprisingly, similar healing delays were seen in mice that were isolated immediately or at 3 weeks prior to wounding. These data indicate that isolation-stress immediately alters tissue repair. In this model, bacterial burden did not appear to affect wound closure rates. These results indicate that social stressors negatively impact tissue repair comparably to other stressors, but through disparate mechanisms.