Stress is known to be one of the risk factors of stroke but only a few experimental studies have examined the possible mechanisms by which prior stress may affect stroke outcome. In stroke patients, infections impede neurological recovery and increase morbidity as well as mortality. We previously reported that stress induces a bacterial translocation and that prior immobilization stress worsens experimental stroke outcome through mechanisms that involve inflammatory mediators such as release of pro-inflammatory cytokines and enzyme activation. We now investigate whether bacterial translocation from the intestinal flora of rats with stress prior to experimental ischemia is involved in stroke outcome. We used an experimental paradigm consisting of exposure of Fischer rats to repeated immobilization sessions before permanent middle cerebral artery occlusion (MCAO). The presence of bacteria and the levels and expression of different mediators involved in the bacterial translocation were analyzed. Our results indicate that stress prior to stroke is related to the presence of bacteria in different organs (mesenteric nodes, spleen, liver and lung) after MCAO and increases inflammatory colonic parameters (such as COX-2, iNOS and MPO), but decreases colonic immunoglobulin A (IgA), and these results are related with colonic inflammation and bacterial translocation. Understanding the implication of bacterial translocation during stress-induced stroke worsening is of great potential clinical relevance, given the high incidence of infections after severe stroke and their main role in mortality and morbidity in stroke patients.