Bacterial overgrowth and translocation in an experimental pancreatitis model

Abstract

Abstract Background A combination of secretory hyperstimulation and transduodenal intraductal bile acid exposure results in homogeneous pancreatitis with graded severity in a rat model. The model was modified by using an exteriorized common bile duct (CBD) as ductal infusion port while keeping the integrity of the gut intact. The objective was to determine whether bacterial translocation (BT) is present and relates to small bowel bacterial overgrowth (SBBO). Methods Fifty rats were divided into four groups: group 1, mild pancreatitis (intravenous caerulein); group 2, control (intravenous saline); group 3, necrotic pancreatitis (intravenous caerulein, intraductal glycodeoxycholic acid); and group 4, control (intravenous and intraductal saline). During infusion the CBD was clamped just above the papilla of Vater. Three days later samples from peripheral blood, peritoneal fluid and abdominal organs were harvested for quantitative microbial culturing. The splenic portion of the pancreas was removed for histopathological analysis. Results Histological examination showed minimal oedema in groups 2 and 4; group 1 was characterized by acinar vacuolization and group 3 had a combination of acinar necrosis with inflammation. BT to one or more abdominal organs took place. The difference in incidence of translocation between group 1 (six of 14) and group 2 (none of eight) was significant (P < 0·05). Furthermore, there was a significant difference in translocation between group 3 (six of eight) and group 4 (one of six) (P < 0·05), and in duodenal total bacterial counts between groups 3 and 4 (P < 0·05). Gram-negative rods and anaerobic bacterial counts were different between group 3 (mean(s.d.) 2·46(0·88)) and group 4 (0) (P < 0·05). However, total bacterial growth in the ileum did not differ significantly between groups. Conclusion In this pancreatitis model, without biliary obstruction, bacterial overgrowth of the duodenum occurred, accompanied by BT. Colonic bacteria were predominantly involved. This model offers the possibility of studying the relationship between SBBO, BT and the pathogenesis of necrotic (infected) pancreatitis.