CERULEIN-INDUCED ACUTE-PANCREATITIS IN RATS - DOES BACTERIAL TRANSLOCATION OCCUR VIA A TRANSPERITONEAL PATHWAY

Bacterial infectious complications are the most common cause of morbid ity and mortality associated with acute pancreatitis. Most pathogens a re common gastrointestinal flora, indicating that the gut is the sourc e of pancreatitis-related infections. However, the route whereby the m icroorganisms reach distant organs remains speculative. We tested the hypothesis that spread of bacteria occurs via a transperitoneal pathwa y. Acute interstitial pancreatitis (AIP) was induced in antibiotic (ge ntamicin, bacithracin, neomycin)-decontaminated rats by intravenous in fusion of cerulein. Effects of pancreatic necrosis CPN) were studied i n rats that received additional injections into the peritoneal cavity of pancreatic tissue obtained from donor rats. The rats were inoculate d with Escherichia coli (O-2:KN:H18) resistant to the antibiotics used for decontamination either orally (10(12) microorganisms; experiment I) or intraperitoneally (10(8) microorganisms; experiment II). More ov er, the rat peritoneal cavity wash was inoculated with 10(8) E. coli i n vitro (experiment III). In rats with AIP and PN, recovery of the bac teria from Liver, spleen, pancreas, lung, and blood following oral ino culation demonstrated that acute pancreatitis promotes bacterial trans location from the gut. The absence of E. coli in these organs followin g intraperitoneal inoculation showed that the bacteria do not spread f rom the peritoneal cavity. Rats with PN cleared E. coli from the perit oneal cavity in a shorter period than rats with AIP and controls (5 vs . 7 and 8 days; p < 0.05). The multiplication rate of E. coli in perit oneal cavity wash was lower in rats with PN than in rats with AIP and controls (p < 0.01). We conclude that (I) translocation of E. cell fro m the gut during cerulein-induced acute pancreatitis occurs via nonper itoneal pathways, (2) the peritoneal cavity acts as a trap for the bac teria rather than a source of bacterial seeding, and (3) PN impairs su rvival of E. coli in the peritoneal cavity via inhibition of the bacte rial multiplication in this model.