Bacterial translocation in experimental stroke: what happens to the gut barrier?

The reasons of post-stroke infections are still incompletely understood. Bacterial translocation (BT), the passage of viable microbes across an even anatomically intact intestinal barrier, has been described in many critical illnesses. To date, it has not been studied as a source of infection in an animal stroke model. To address this, a permanent left middle cerebral artery occlusion (MCAO) model in rats was used. After 24, 48, and 72 hours (h), sham and experimental groups were sacrificed and samples were taken for BT. Similarity between bacteria detected in tissues (blood, mesenteric lymph node, liver, spleen, and lung) and intestinal microflora was shown with phenotypic methods and antibiotyping. Possible ileum tissue injuries were shown by histopathologic examination (including morphometric analysis). Although there was no bacterial proliferation in the sham groups, 55.5%, 45.4%, and 30% bacterial proliferation was detected in MCAO groups at postoperative hour 24, 48, and 72, respectively. In MCAO groups the bacterial proliferation in tissues and ileum tissue injury scores were higher over time compared to sham groups (p < 0.05). Our findings support the view that stroke, itself leads to mucosal damage and bacterial translocation (Tab. 5, Fig. 2, Ref. 27).