Pathogenesis of pancreatic infection.
John Hunter studied comparative anatomy of the pancreas but was unaware of pancreatic infection which is now the leading cause of mortality in pancreatitis. This was investigated using a feline model of pancreatitis. Pathogens spread to the healthy and inflamed gland from many sources including colon, gallbladder, or a septic focus and by various routes including the circulation, reflux into the pancreatic duct or by transmural migration from the colon. Colonisation risk was proportional to necrosis and inflammation, confirming clinical observations. These studies showed that pathogens frequently colonised the pancreas, but infection developed only in animals with pancreatitis. In cats with pancreatitis, phagocytic function was reduced by 28%. This was probably owing to phagocytic capacity being overwhelmed by protease-antiprotease complexes because, in humans, granulocyte and lymphocyte function was normal. These experiments suggested that it would be difficult to prevent pancreatic colonisation, but indicated some types of therapy may have potential. These were investigated using this animal model of pancreatic infection. Treatment with either cefotaxime or levamisole (an immunostimulant) were effective. However, the anti-inflammatory drug dopamine, which reduced inflammation, did not eradicate all pathogens.
Widdison
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Bristol Royal Infirmary.
D000208:Acute Disease; D000818:Animals; D001424:Bacterial Infections / Q000188:drug therapy / Q000209:etiology* / Q000276:immunology; D002415:Cats; D004195:Disease Models, Animal; D004927:Escherichia coli Infections / Q000188:drug therapy / Q000209:etiology / Q000276:immunology; D009894:Opportunistic Infections / Q000188:drug therapy / Q000209:etiology* / Q000276:immunology; D010195:Pancreatitis / Q000188:drug therapy / Q000276:immunology / Q000382:microbiology*; D010587:Phagocytosis; D012307:Risk Factors