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Query: UMLS:C0341503 (bacterial peritonitis)
 1,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with alcoholic liver disease and ascites had Haemophilus influenzae peritonitis and died in spite of vigorous antibiotic therapy. At autopsy, a phlegmonous gastritis was found as a likely cause of the peritonitis. Phlegmonous gastritis is an uncommon cause of unexplained gastrointestinal symptoms in alcoholics and in the elderly, and it may be pathogenetic in rare patients with bacterial peritonitis of unclear source.
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PMID:Phlegmonous gastritis and Hemophilus influenzae peritonitis in a patient with alcoholic liver disease. 353 62

The cytoprotective and acid-inhibitory effects of cimetidine and 16,16-dimethyl PGE2 were evaluated in a septic canine erosive gastritis model. In 21 dogs, total gastric fistulas were created, and after a 3-wk recovery period, basal, food-, and pentagastrin-stimulated acid output were measured. Then bacterial peritonitis was created by the intraperitoneal instillation of Pseudomonas, Bacteroides, Streptococcus Fecalis, Klebsiella and canine gallbladder bile. In 5 dogs no drug were given throughout the septic period while in 16 dogs either cimetidine, 6 or 12 mg/kg i.m. every 6 h, or 16,16-dimethyl PGE2, 0.2 or 0.4 microgram/kg i.m. every 6 h, was given 24 h before the induction of peritonitis and continued for 3 days. All 21 dogs had positive blood cultures on the 1st septic day. In the control animals, basal, food-, and pentagastrin-stimulated acid output significantly increased during the first 2 septic days, and gastroscopy demonstrated bleeding acute fundic erosions. Cimetidine decreased basal, food-, and pentagastrin-stimulated acid output in a dose-related manner, and only with the higher dose did it prevent gastric mucosal damage. 16,16-Dimethyl PGE2, 0.4 microgram/kg, significantly decreased acid output and prevented gastric mucosal damage. 16,16-Dimethyl PGE2 0.2 microgram/kg, although having no apparent effect on basal, food-, and pentagastrin-stimulated acid output, prevented the development of acute gastric erosions. Thus, in the canine septic model, acid output significantly increases during sepsis. Cimetidine prevents the development of sepsis-induced gastric erosions by inhibition of acid secretion and 16,16-dimethyl PGE2 by cytoprotection.
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PMID:Prevention of sepsis-induced gastric lesions in dogs by cimetidine via inhibition of gastric secretion and by prostaglandin via cytoprotection. 745 Apr 26

The normal indigenous intestinal microflora consists of about 10(15) bacteria that under physiological conditions reside mainly in the lower gastrointestinal tract. Bacterial overgrowth implies abnormal bacterial colonization of the upper gut, resulting from failure of specific defense mechanisms restricting colonization under physiological conditions. At present two types of bacterial overgrowth with defined pathogenesis can be distinguished: (1) gastric overgrowth with upper respiratory tract microflora resulting from selective failure of the gastric acid barrier, and (2) gastrointestinal overgrowth with Gram-negative bacilli (enteric bacteria) resulting from failure of intestinal clearance. Helicobacter pylori-induced gastritis of the oxyntic mucosa is the main cause of acquired failure of the gastric acid barrier, which is common among the healthy elderly. Intestinal clearance may fail as the result of impaired intestinal peristalsis or anatomical abnormalities that alter luminal flow. Impaired peristalsis is associated with conditions interfering with intestinal neuromuscular function including myopathic, neuropathic, autoimmune, infectious, inflammatory, metabolic, endocrine, and neoplastic diseases. Anatomical abnormalities are mainly the result of gastrointestinal surgery, intestinal diverticula or fistula. Combined failure of intestinal clearance and the gastric acid barrier results in more severe colonization with Gram-negative bacilli. Gram-negative bacilli are uncommon in the upper gut of otherwise healthy individuals with gastric hypochlorhydria, being acquired (H. pylori) or drug-induced. Significant bacterial overgrowth with Gram-negative bacilli is a rational in the search for an explanation to optimize clinical management. The clinical significance of colonization with upper respiratory tract microflora remains unclear. Translocation of live bacteria, their metabolic products, or antigens from a small bowel colonized by Gram-negative bacilli play a role in the pathogenesis of spontaneous bacterial peritonitis in hepatic disease and in certain types of sepsis, indicating that further studies can point to new patient populations with potential benefit from medical treatment.
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PMID:The pathogenesis of gastrointestinal bacterial overgrowth. 1585 46