Pigment gallstone pathogenesis: slime production by biliary bacteria is more important than beta-glucuronidase production.

Pigment stones are thought to form as a result of deconjugation of bilirubin by bacterial beta-glucuronidase, which results in precipitation of calcium bilirubinate. Calcium bilirubinate is then aggregated into stones by an anionic glycoprotein. Slime (glycocalyx), an anionic glycoprotein produced by bacteria causing foreign body infections, has been implicated in the formation of the precipitate that blocks biliary stents. We previously showed that bacteria are present within the pigment portions of gallstones and postulated a bacterial role in pigment stone formation through beta-glucuronidase or slime production. Ninety-one biliary bacterial isolates from 61 patients and 12 control stool organisms were tested for their production of beta-glucuronidase and slime. The average slime production was 42 for biliary bacteria and 2.5 for stool bacteria (P <0.001). Overall, 73% of biliary bacteria and 8% of stool bacteria produced slime (optical density >3). In contrast, only 38% of biliary bacteria produced beta-glucuronidase. Eighty-two percent of all patients, 90% of patients with common bile duct (CBD) stones, 100% of patients with primary CBD stones, and 93% of patients with biliary tubes had one or more bacterial species in their stones that produced slime. By comparison, only 47% of all patients, 60% of patients with CBD stones, 62% of patients with primary CBD stones, and 50% of patients with biliary tubes had one or more bacteria that produced beta-glucuronidase. Most biliary bacteria produced slime, and slime production correlated better than beta-glucuronidase production did with stone formation and the presence of biliary tubes or stents. Patients with primary CBD stones and biliary tubes had the highest incidence of slime production. These findings suggest that bacterial slime is important in gallstone formation and the blockage of biliary tubes.

Intestinal immunisation with Escherichia coli protects rats against Escherichia coli induced cholangitis.

BACKGROUND: Cholangitis, an infection of the biliary tract, is most commonly caused by Gram negative bacteria, particularly Escherichia coli. Factors governing the severity of cholangitis, including the role of biliary IgA, are poorly understood. AIMS: The aim of this work was to find out if biliary IgA directed against E coli protects rats against hepatobiliary infection with E coli. SUBJECTS: Male Sprague-Dawley rats weighing 270-350 grams were used in all of the experiments. METHODS: At laparotomy, rats were immunised by injecting killed E coli or normal saline (controls) into Peyer's patches. With or without subsequent antigenic boosting (by oral administration of killed E coli), bile was collected at a second laparotomy, and rats were infected by introducing viable E coli into the bile duct. Production of IgA anti-E coli antibody was measured by enzyme linked immunosorbent assay of bile, and the presence of hepatobiliary infection was determined by quantitative culture of liver homogenates. RESULTS: Systemic infection was present in six of 12 control rats and in one of 24 immunised rats (p = 0.005) after death. There was an inverse correlation between immunisation and E coli colony counts in cultured liver homogenates (p = 0.024). CONCLUSION: The findings suggest that biliary IgA directed against E coli protected rats against hepatobiliary E coli infection and systemic sepsis.