Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017160 (gastroenteritis)
11,398 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of gastroenteritis caused by a urea-hydrolyzing strain of Vibrio parahaemolyticus is presented. Urea-hydrolyzing strains of Vibrio parahaemolyticus have rarely been reported and have not been described previously as a cause of gastroenteritis in the United States. With the exception of urea hydrolysis and the methyl red test, the isolate had all the characteristics of V. parahaemolyticus. The need to screen suspicious non-lactose-fermenting colonies from stool specimens with the oxidase test is emphasized.
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PMID:Urea-hydrolyzing Vibrio parahaemolyticus associated with acute gastroenteritis. 713 Mar 72

A bacterium with an unusual ultrastructure and possessing a fusiform protoplasmic cylinder, spiral periplasmic fibers, and bipolar tufts of sheathed flagella was identified in the intestinal mucosae of laboratory mice. The organism was cultured under microaerophilic conditions and was found to rapidly hydrolyze urea. On the basis of 16S rRNA gene sequence analysis, the organism was shown to be "Flexispira rappini." "F. rappini" is closely related to members of the genus Helicobacter and has been reported to be associated with human gastroenteritis and ovine abortion. "F. rappini" has not previously been observed in the gastrointestinal tracts of mice.
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PMID:Isolation and characterization of "Flexispira rappini" from laboratory mice. 750 85

A disease syndrome similar to the hemolytic uremic syndrome of people is described in three dogs with acute renal failure. In each dog, hemorrhagic gastroenteritis preceded the onset of anuric acute renal failure. Evidence of microangiopathic hemolytic anemia (schizocytes, thrombocytopenia, and increased concentrations of fibrin split products) was present in the three dogs. Serum chemistry results showed increased concentrations of blood urea nitrogen, creatinine, and phosphorus. Ultrasound examination performed in one dog revealed increased echogenicity of the renal cortices. Treatment for anuric acute renal failure using a continuous dopamine and furosemide infusion established urine production in one of three dogs. Microscopic examination of tissue from the two dogs that underwent necropsy showed occlusion of the renal vasculature by fibrin thrombi consistent with microangiopathic arteriolar thrombosis. The pathophysiology and current knowledge of human hemolytic uremic syndrome is compared with hemolytic uremic syndrome in these dogs.
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PMID:Hemolytic uremic syndrome in dogs. 824 11

One hundred and twenty patients with a mean age of 38 years (range 12-85 years; M 91, F 37) were studied over a period of 5 years in a teaching hospital in Dhaka. Sixty-two patients presented with probable anuria with 1-4 days' duration, 63 patients presented with oliguria, and 3 were nonoliguric. The causes of acute renal failure were medical (94), surgical (22), obstetrical (13). Of the medical cases, the causes were gastroenteritis in 42 cases, gastroenteritis with CNS involvement in 11 cases, rapidly progressive glomerulonephritis in 10 cases, acute viral hepatitis in 8 cases, and septicemia in 8 cases. Of 22 surgical cases, postoperative acute renal failure was the cause in 9, road traffic accident in 6, and renal calculus disease in 7. There were 13 cases in the obstetrics group, of whom 9 were due to abortion, 2 were due to preeclampsia, and the other 2 were postoperative. The mean blood urea of all cases was 35 mmol/L and serum creatinine was 988 mumol/L. Dialysis was required in 105 cases; of these, 72 were medical cases, 21 were surgical cases, and 12 were obstetric cases. The overall survival rate was 75%. The improved survival is probably due to timely referral and prompt medical management.
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PMID:Outcome of acute renal failure in adults in a teaching hospital in Bangladesh. 829 Jul 6

The hemolytic-uremic syndrome (HUS) is an acute disorder, characterized by the triad of microangiopathic hemolytic anemia, nephropathy and thrombocytopenia. The great majority of patients are children, usually under 4 years of age, although adults can be affected. The onset is abrupt and usually follows gastroenteritis or upper respiratory infection. Later, clinical manifestations based on the triad, such as pallor, jaundice, edema, hypertension and purpura soon develop. The urinary output is reduced and the urine may appear dark yellow or tea-colored. Laboratory tests of peripheral blood show severe hemolytic anemia associated with fragmented red blood cells and thrombocytopenia, usually below 50,000/microliters. The blood urea nitrogen, serum creatinine and lactate dehydrogenase concentrations are elevated. Proteinuria and microscopic hematuria, which are indicative of active glomerular damage are also seen. Profound understanding of these manifestations is sufficient to permit an early diagnosis of HUS.
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PMID:[Diagnosis and clinical features of hemolytic uremic syndrome]. 843 21

The concentration of nitrate (the stable oxidation product of nitric oxide) in plasma and its excretion in urine was measured in 20 patients with a diagnosis of gastroenteritis. On day 1 of the illness plasma nitrate concentration was significantly elevated compared with a healthy control population (92.7 +/- 17.0 mumol/l vs. 33.1 +/- 1.6 mumol/l; P < 0.001) and continued to be elevated on days 2 and 3. Urinary nitrate excretion was also elevated. The plasma nitrate concentration correlated with disease severity as assessed by stool frequency and plasma urea concentration. Plasma nitrate concentration may be a sensitive and clinically useful indicator of severity of gastroenteritis.
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PMID:Plasma nitrate concentration and urinary nitrate excretion in patients with gastroenteritis. 852 41

Co-existence of trh gene and urea-hydrolysing property in one of 44 marine water isolates of Vibrio parahaemolyticus correlates strongly with both genotypic and phenotypic characteristics of the bacterium. Thus, urease-producing phenotype can be considered a marker of virulence for the production of thermostable direct haemolysin-related haemolysin (TRH) (i.e. possession of trh gene). The same isolate also possessed the tdh gene. An environmental isolate possessing all the characteristics of a pathogenic V. parahaemolyticus in this marine environment suggest that there is a likelihood of the occurrence of clinical cases of gastroenteritis caused by V. parahaemolyticus in the Andamans.
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PMID:Detection of tdh and trh genes in a urea-hydrolysing environmental isolate of Vibrio parahaemolyticus from the Andamans. 980 14

Gastroenteritis in children is a common reason for visits to family physicians. Most cases of gastroenteritis have a viral etiology and are self-limited. However, more severe or prolonged cases of gastroenteritis can result in dehydration with significant morbidity and mortality. This is often the scenario in third-world countries, where gastroenteritis results in 3 million deaths annually. A proper clinical evaluation will allow the physician to estimate the percentage of dehydration and determine appropriate therapy. In some situations, laboratory studies such as determination of blood urea nitrogen and serum electrolytes may be helpful. Stool studies are indicated if a child is having bloody diarrhea or if an unusual etiology is suspected, such as Escherichia coli O157:H7 or Cryptosporidium. Most children with gastroenteritis can be treated with physiologically balanced oral rehydration solutions. In children who are hypovolemic, lethargic and estimated to be more than 5 percent dehydrated, initial treatment with intravenous boluses of isotonic saline or Ringer's lactate may be required. Children with severe diarrhea need nutrition to restore digestive function and, generally, food should not be withheld.
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PMID:Gastroenteritis in children: principles of diagnosis and treatment. 1020 99

In a clinical prospective 3-year study of 158 children aged 2 weeks to 14 years with hypernatraemic dehydration (serum sodium 150 mmol/l or more), infants predominated (61.4%). The 158 children with hypernatraemia accounted for 13.7% of all children admitted with gastroenteritis over the same period, and significant aetiological factors included the use of artificial feeds, differences between the children with hypernatraemia and those with normo- or hyponatraemia, P < 0.001, P < 0.001, respectively; the use of breast milk, P < 0.001, P < 0.001, respectively; nutritional status, P < 0.001, P < 0.001, respectively; and clinical state of mild to moderate dehydration P < 0.001; P < 0.001, respectively; but not with patients considered severely dehydrated. There was also a significant difference between the presence of neurological features in hyper- and normonatraemic patients P < 0.001; in hyper- and hyponatraemic patients P < 0.05, and in mortality rate between hyper- and normonatraemic patients, P < 0.05 but not between hyper- and hyponatraemic patients. A history of refusal to feed or vomiting was obtained in 41 children (25.9%). The mean serum sodium was 155.5 mmol/l (range 150-189 mmol/l); mean serum urea 7.7 mmol/l (range 1-18.9 mmol/l). Hypernatraemic dehydration remains an important and serious complication of childhood gastroenteritis in our area of study. The use of artificial milk feeds is contributory, and well-nourished babies appear more at risk. We recommend more liberal water intake during gastroenteritis and the public should also be educated on and made more aware of this condition.
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PMID:A prospective clinical study of patients with hypernatraemic dehydration. 1045 91

The comparative effects of diazinon and malathion on Najdi sheep were described in sheep allotted as untreated controls, diazinon-treated at 25 mg/kg/d or 50 mg/kg/d, and malathion-treated at 25 mg/kg/d or 50 mg/kg/d. Although serum cholinesterase (ChE) activity was reduced, neither significant clinical signs nor severe pathological changes were produced in sheep dosed orally with 25 or 50 mg diazinon/kg/d for 21 d. Both oral dose levels of malathion were lethal to sheep between 1 and 6 d and caused, prior to death, hyperexcitability, tremors, clonic convulsions, salivation, nasal discharge, incoordination of movement, paresis of the limbs and recumbency. Lesions were widespread congestion and hemorrhage, patchy pulmonary cyanosis, gastroenteritis and hepatonephropathy. These changes were accompanied by increases in the activities of serum SDH and AST, in the concentrations of urea, triglyceride and cholesterol, and decreases in ChE activity and in RBC, PCV and Hb values.
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PMID:Comparative effects of diazinon and malathion in Najdi sheep. 1050 28


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