Histopathological analysis of Salmonella chronic carriage in the mouse hepatopancreatobiliary system.

Salmonella Typhi asymptomatic chronic carriage represents a challenge for the diagnosis and prevention of typhoid fever in endemic areas. Such carriers are thought to be reservoirs for further spread of the disease. Gallbladder carriage has been demonstrated to be mediated by biofilm formation on gallstones and by intracellular persistence in the gallbladder epithelium of mice. In addition, both gallstones and chronic carriage have been associated with chronic inflammation and the development of gallbladder carcinoma. However, the pathogenic relationship between typhoid carriage and the development of pre-malignant and/or malignant lesions in the hepatopancreatobiliary system as well as the host-pathogen interactions occurring during chronic carriage remains unclear. In this study, we monitored the histopathological features of chronic carriage up to 1 year post-infection. Chronic cholecystitis and hepatitis ranging from mild to severe were present in infected mice regardless of the presence of gallstones. Biliary epithelial hyperplasia was observed more commonly in the gallbladder of mice with gallstones (uninfected or infected). However, pre-malignant lesions, atypical hyperplasia and metaplasia of the gallbladder and exocrine pancreas, respectively, were only associated with chronic Salmonella carriage. This study has implications regarding the role of Salmonella chronic infection and inflammation in the development of pre-malignant lesions in the epithelium of the gallbladder and pancreas that could lead to oncogenesis.

Histopathological examination of the pancreas of the Koala (Phascolarctos cinereus).

This retrospective study, which was based on koala pancreatic specimens taken 2, 24, 48 and 72h after death, showed that the degree of autolysis did not necessarily exclude histopathological examination. Disorders not previously reported in the pancreas of koalas included the following: inflammation and necrosis; atrophy and fibrosis of exocrine pancreatic tissue; lymphosarcoma; pancreatic heterotopy; and ductal adenocarcinoma.

Exocrine pancreatic involvement in critically ill patients.

PURPOSE OF REVIEW: To learn about the prevalence, pathophysiology, and treatment of exocrine pancreatic involvement in critically ill patients. RECENT FINDINGS: Elevations in the levels of pancreatic enzymes are observed in up to 80% of intensive care patients. Most of these patients do not develop clinically relevant pancreatitis. However, elevations in enzyme levels do represent pancreatic damage with a risk of complications. Different factors have been discussed, which may contribute to pancreatic damage in critically ill patients. These include splanchnic hypoperfusion during shock or major surgery, bacterial translocation, elevated triglyceride levels, development of biliary sluge, and biliary pancreatitis, as well as several drugs. Imaging procedures and inflammatory markers help to identify relevant disease. Several therapeutic options have been discussed recently with a focus on early enteral nutrition. SUMMARY: Pancreatic damage is frequently observed in critically ill patients. Although in most of these patients, this is without major clinical consequences, some patients develop relevant pancreatitis, which contributes to morbidity and mortality. Risk factors have been identified and therapeutic strategies have been changed.

Spontaneous exocrine pancreas hypoplasia in specific pathogen-free C3HeB/FeJ and 101/H mouse pups causes steatorrhea and runting.

Under specific pathogen-free conditions, 1.3% to 1.8% of litters born in our inbred 101/H and C3HeB/FeJ mouse colonies had pups with steatorrhea and runting. Clinically affected male and female pups were first identified when they were from 14 to 25 d old. Unaffected littermates were healthy and were weaned successfully. Postmortem findings in 8 clinically affected mice included a small, poorly differentiated exocrine pancreas comprising cytokeratin-negative duct-like structures but lacking recognizable acinar cells with their normal carboxypeptidase B-positive zymogen granules. Endocrine pancreas islets were unremarkable and contained insulin-positive beta cells and glucagon-positive alpha cells. There was mild inflammation of the hindgut but no evidence of intestinal pathogens or marked inflammation or necrosis of pancreas, either alone or as part of a multisystemic inflammatory condition. Sera from pups in 4 affected litters did not contain antibodies to reovirus 3, mouse coronavirus, rotavirus, or mouse adenovirus 2. Furthermore, 4 sets of parental mice and sentinel mice from the facility were negative for 13 viruses, bacteria, and parasites. C3HeB/FeJ and 101/H inbred strains may be genetically predisposed because the steatorrhea and runting was absent in 13 other mouse strains and subspecies bred in the specific pathogen-free facility. This condition resembles exocrine pancreas hypoplasia, but the inheritance is complex. A wider implication is that runting coupled with steatorrhea are phenotypic criteria to suspect pancreatic disease that could be used in the context of a mouse N-ethyl-N-nitrosourea-mutagenesis program to identify potential mutants with defects in pancreas development.