Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0341503 (bacterial peritonitis)
 1,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Arizona hinshawii, a gram-negative enteric pathogen, causes serious infections in fowl, reptiles, and other animals. In humans, gastroenteritis, enteric fever, septicemia, and localized infections due to Arizona have occurred. There are no previous reports of spontaneous bacterial peritonitis secondary to Arizona, however. We report here a case of spontaneous bacterial peritonitis due to Arizona occurring in a patient with cirrhosis of the alcoholic type. The patient was treated with a 10-day course of gentamicin, and although she improved clinically, Arizona was cultured from the blood and bile postmortem.
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PMID:Spontaneous Arizona hinshawii peritonitis in cirrhosis with ascites. 723 42

Two patients on maintenance hemodialysis therapy developed fulminant spontaneous acute bacterial peritonitis (S.A.B.P.). Both had positive blood cultures and died within a few hours despite intensive antibiotic and supportive therapy. No intra-abdominal source of the peritonitis was found in either case. Though septicemia is an important cause of death in the hemodialyzed patient, this form of presentation (S.A.B.P.) has not been previously reported.
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PMID:Fulminant spontaneous acute bacterial peritonitis in maintenance hemodialysis. 726 84

The role of gastric mucus in the pathogenesis of septic erosions and as an explanation for prostaglandin cytoprotection is unclear. In a reproducible canine septic model bacterial peritonitis was induced in three groups of dogs. One group served as a control and each of the remaining groups received 16,16 dimethyl PGE2 either 0.2 microgram/kg. or 0.4 microgram/kg. I.M. q6h beginning 24 hours prior to peritonitis and continued during the septic period. Gastroscopy was performed and basal gastric juice collected prior to peritonitis and during the septic period. All animals in the control group developed acute gastric erosions and gastric juice protein significantly decreased while sialic acid and fucose significantly increased during the septic period. In the animals receiving 16,16 dimethyl PGE2 acute gastric erosions did not develop; sialic acid and fucose were significantly elevated compared to control dogs during sepsis. We conclude that prostaglandin cytoprotection may be related to increases in gastric glycoprotein secretion.
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PMID:The role of mucus glycoproteins in prostaglandin cytoprotection. 742 69

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

Postsplenectomy bacterial sepsis may be fatal, due to defects in both cellular and humoral immune responses. The objective of this study was to assess the efficacy of peritoneal macrophage antibacterial function in the early postsplenectomy period. Murine models of splenectomy and sham operation were characterized and peritoneal macrophages were harvested 24 h to 1 wk after surgery. Cells from splenectomized animals demonstrated a nonsignificant delay in phagocytosis of Escherichia coli at 24 h with, however, significantly impaired killing of intracellular organisms at 24 h and 1 wk compared to the sham group. Paradoxically, the production of the macrophage antibacterial product superoxide anion was not impaired at either time point in the splenectomy group compared with sham-operated and control mice. Nitric oxide release was significantly lower in the splenectomized group (p = 0.006), a possible explanation for reduced bacterial killing. Mortality from bacterial peritonitis was significantly higher with concomitant splenectomy than in the sham splenectomy group at 24 h (p < 0.02). The production of TNF from macrophages was up-regulated immediately following splenectomy, a cytokine which may contribute to mortality from bacteremic shock. Local defects in macrophage antimicrobial function may contribute significantly to bacteremia and to subsequent mortality in the early postsplenectomy period.
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PMID:Characterization of the defects in murine peritoneal macrophage function in the early postsplenectomy period. 760 13

Fifty-nine episodes of bacteremia due to Aeromonas species occurred within a 5-year period in one medical center in southern Taiwan. Underlying diseases in the 58 patients included hepatic cirrhosis (36%) and cancer (24%). Patients with aeromonas bacteremia more often had underlying hepatic cirrhosis than did those with bacteremia due to other gram-negative bacilli. Males (67%) outnumbered females. The cases appeared to cluster in the summer and fall months. Thirty-two percent were polymicrobial infections; often the Aeromonas pathogens were accompanied by other gram-negative bacilli. Aeromonas hydrophila was the most common species isolated (69%). In addition to fever, hypotension and jaundice were the common clinical manifestations of aeromonas sepsis. In cirrhotic patients, spontaneous bacterial peritonitis, altered mental status, and jaundice were most common, and aeromonas bacteremia in such patients was monomicrobial and community-acquired more often than in noncirrhotic patients. In vitro aeromonads were generally susceptible to aminoglycosides, cefuroxime, the third-generation cephalosporins, and quinolones. The overall crude fatality rate was 36%. Predictors of fatal outcome for cirrhotic patients included spontaneous bacterial peritonitis, hypotension on admission, diabetes mellitus, and high Pugh scores.
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PMID:Aeromonas bacteremia: review of 59 episodes. 762 14

Sepsis due to Streptococcus pneumoniae has a high mortality. We report a retrospective review of 40 episodes of S pneumonia sepsis in adult patients during a two year period in a general hospital, that represented 11.3% of all sepsis observed in such hospital. Ninety two percent of infections were community acquired and in 95%, the portal of entry was the respiratory tract. Eighty five percent of patients had at least one risk factor such as alcohol abuse, unconsciousness or chronic pulmonary disease. Nine patients had suppurative complications (empyema in 4 cases, spontaneous bacterial peritonitis in 2, septic arthritis in 2 and meningitis in 1 case) and 12 (30%) died. The potential benefit of antipneumococcal vaccine as prevention should be considered in high risk subjects.
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PMID:[Streptococcus pneumoniae septicemia. Analysis of 40 cases]. 765 13

We presented a case of critical illness polyneuropathy after bacterial peritonitis. A 62-year-old male was received an emergency colectomy because of perforation of the sigmoid colon five days after the endoscopic polypectomy. He developed sepsis from peritonitis after operation in spite of the antibiotics therapy. On 15-th hospital days he developed muscle weakness and numbness of all limbs. He needed an artificial ventilator due to respiratory failure. Hematological and blood chemical findings showed a leukocytosis and metabolic acidosis with renal dysfunction because of sepsis. Serum anti-Campylobacter antibody was negative. Serial CSF examinations failed to show any abnormalities including albuminocytologic dissociation. Electrophysiological studies revealed a primary axonal degeneration, mainly in the motor, but also in the sensory nerve. Compound muscle and sensory action potentials were not elicited or markedly reduced without conduction velocity prolongation. Microscopic findings of the left sural nerve biopsy showed a primary axonal degeneration without evidence of inflammation. His prognosis was poor and three months later, he still required ventilatory assistance. Because of these clinical findings this patient was thought to have a critical illness polyneuropathy after excluding various etiologies of polyneuropathies. This case suggests that sepsis may be one of a cause of primary axonal polyneuropathy. The certain mechanism of this disease is still unknown. However cytokine, tumor necrotic factor(TNF) and/or Platelet activating factor(PAF) that secreted during sepsis may have an important role for the primary axonal degeneration.
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PMID:[A case of critical illness polyneuropathy in association with peritonitis after sigmoid colon perforation]. 766 19

Although lymphocyte-derived cytokines are known to augment macrophage cytokine production in vitro, their effect on macrophage tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) secretion during gram-negative bacterial sepsis has not been characterized. The purpose of this study was to examine the effect of lymphocyte-derived cytokines on macrophage TNF-alpha and IL-6 secretion during gram-negative bacterial peritonitis. To examine this problem, uninfected and infected mice were studied. Mice were infected with Escherichia coli O111:B4 and two subgroups were examined consisting of those pretreated iv 1 hr prior to bacterial challenge with either (1) saline or (2) anti-E. coli O111:B4 LPS mAb 2A3, the latter administered to abrogate the effects of LPS in vivo. Thus, three groups of mice were studied in relation to pretreatment and infectious challenges: (1) saline/saline (control); (2) saline/E. coli (saline); and (3) mAb 2A3/E. coli (mAb 2A3). Nonadherent splenocytes (> 95% lymphocytes by histologic staining criteria) harvested 16 hr later from mice in each group were incubated in culture ex vivo for 3 hr to obtain supernatants containing lymphocyte-derived cytokines. These supernatants containing lymphocyte-derived cytokines then were incubated in vitro with naive splenic macrophages with or without E. coli O111:B4 LPS. Macrophage TNF-alpha and IL-6 levels were determined using L929 and B9 bioassays.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lymphocyte-derived cytokines augment macrophage tumor necrosis factor-alpha and interleukin-6 secretion during experimental gram-negative bacterial sepsis. 779 54

Non 0-1 Vibrio cholerae infection is often associated with ingestion of contaminated seafood and its common presentation is gastroenteritis. Septicemia may be found in immunocompromised hosts resulting in mortality approaching 50%. A case is reported of non 0-1 Vibrio cholerae infection presenting with septicemia in a patient with neutrocytic ascites suggestive of spontaneous bacterial peritonitis.
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PMID:Non 0-1 Vibrio cholerae septicemia and culture negative neutrocytic ascites in a patient with chronic liver disease. 779 72


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