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Query: UMLS:C0740441 (acute diarrhea)
 2,275 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The microflora and pH of gastric contents were determined in breast-fed and in bottle-fed normal infants, in well nourished infants with acute diarrhoea and in infants with chronic diarrhoea and protein-calorie malnutrition. The last group of infants was reevaluated after recovery from diarrhoea and protein-calorie malnutrition. A bactericidal pH effect below 2-5 was observed. Bottle-fed controls had low pH values and low bacterial concentrations, whereas infants with chronic diarrhoea and protein-calorie malnutrition had high pH values and bacterial overgrowth, essentially of Gram-negative bacilli. After recovery, the only remaining alteration was the frequent isolation of yeast-like fungi in low concentrations. Infants with acute diarrhoea, except for the isolation more frequently of yeast-like fungi, presented no alterations; this seems to indicate that pH alterations and Gram-negative bacilli overgrowth occurred during the evolution of the disease to a chronic state. Breast-fed normal infants had hydrogen-ion concentrations similar to those of the chronic diarrhoea group, but without Gram-negative bacilli overgrowth, suggesting that other factors, besides pH, regulate bacterial growth in the gastric contents of these groups of infants.
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PMID:Gastric pH and microflora of normal and diarrhoeic infants. 0 Feb 74

During the last 10 years there has been a major break-through in understanding the pathogenic mechanisms of E. coli as a cause of acute diarrhoea. The current situation is briefly tabulated in Table 3. In the near future the field of interest is likely to centre on the investigation of adhesive factors and certainly on the possibility of using preparations of adhesive factors as vaccines. The successful use of such vaccines may have enormous benefit as intervention measures to break the acute diarrhoea--malnutrition syndrome which is so damaging to the life of infants and young children in developing countries.
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PMID:The role of Escherichia coli in gastroenteritis. 38 99

The reported incidence of "pathogenic" bacteria, as judged by serotype, in the stools of children with acute diarrhoea has varied from 4 to 33% over the last twenty years. Techniques such as tissue culture provide a means for detecting enterotoxin-producing strains of bacteria, strains which often do not possess "pathogenic" serotypes. "Pathogenicity" requires redefinition, and the aetiological importance of bacteria in diarrhoea is probably considerably greater than previous reports have indicated. Colonization of the bowel by a pathogen will result in structural and/or mucosal abnormalities, and will depend on a series of complex interactions between the external environment, the pathogen, and the host and its resident bacterial flora. Enteropathogenic bacteria may be broadly classified as (i) invasive (e.g. Shigella, Salmonella and some Escherichia coli) which predominantly affect the distal bowel, or (ii) non-invasive (e.g. Vibrio cholerae and E. coli) which affect the proximal bowel. V. cholerae and E. coli elaborate heat-labile enterotoxins which activate adenylate cyclase and induce small intestinal secretion; the secretory effects of heat-stable E. coli and heat-labile Shigella dysenteriae enterotoxins are not accompanied by cyclase activation. The two major complications of acute diarrhoea are (i) hypernatraemic dehydration with its attendant neurological, renal and vascular lesions, and (ii) protracted diarrhoea which may lead to severe malnutrition. Deconjugation of bile salts and colonization of the small bowel with toxigenic strains of E. coli may be important in the pathophysiology of the protracted diarrhoea syndrome. The control of bacterial diarrhoea requires a corrdinated political, educational, social, public health and scientific attack. Bacterial diarrhoea is a major health problem throughout the world, and carries an appreciable morbidity and mortality. This is particularly the case during infancy, and in those developing parts of the world where malnutrition is common. This paper is concerned mainly with acute bacterial diarrhoea, and reviews the problem as a whole.
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PMID:The problem of bacterial diarrhoea. 79 97

The aerobic flora of 2 groups of children (normal and with malnutrition) with acute diarrhoea was studied, by intubation of the upper and middle small intestine and by stool culture. All the 27 children studied presented bacterial concentrations of 10(5) germs/ml at one or both levels studied. In 9 cases enteropathogen bacteria e were isolated from stools, and in 6 of these they were also found in the small intestine. The results show the elevated incidence of overgrowth of the small intestinal aerobic flora in children with acute diarrhoea. This fact is mentioned as another etiological factor to be taken into consideration in this pathology.
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PMID:Stool bacterial aerobic overgrowth in the small intestine of children with acute diarrhoea. 96 12

Since over half of the children aged 5 years and under in the developing world suffer from mild-moderate malnutrition, means of correcting nutrition deficiencies are essential. In the case of the child with diarrhea, malnutrition is exacerbated by a number of disease-related factors including anorexia, cultural or medical withdrawal of food, and purgation. It was discovered, in a study among Apache children, that early and rapid replacemtnt of volume loss and correction of electrolyte imbalance using glucose-electrolyte solutions administered orally can restore physical well-being and appetite to children suffering from acute diarrhea, and hence enhance these children's nutritional status. The solution recommended contained, in millimolar concentrations per liter: sodium, 81; potassium, 18; choride, 71; HC03, 28; and glucose, 139. A field trial of oral therapy for acute diarrhea in children is called for tod etermine the extent of effects on nutrition and mortality, as well as to indicate some of the cultural and logistical problems which remain to be solved.
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PMID:Oral glucose-electrolyte therapy for diarrhea: a means to maintain or improve nutrition? 105 11

Growth of bacteria greater than 10-5 organisms/ml was found in 22 children, of whom 17 gave a histroy of chronic diarrhoea. The other 8 children had either no diarrhoea or where having an acute attack lasting for a few days. In those with chronic diarrhoea, Esch. coli, bacteroides, and enterococci tended to occur more frequently, whereas streptococci occurred more frequently in those with acute diarrhoea. Bacilli, staphylococci, micrococci, klebsiellas, pseudomonads, and candidas often occurred in both groups and in large numbers in those with chronic diarrhoea. This confirms previous reports in other parts of the world that some children with malnutrition have considerable bacterial contamination of the jejunum, and that this may be of aetiological significance as a cause of much of the diarrhoea seen in malnourished children. It is possible too that this may be important in the pathogenesis of malnutrition. The presence of intestinal parasites in these malnourished children is also noted. A double-blind trial in the use of antibiotics in this condition is advocated to determine whether it is possible to break the diarrhoea-malabsorption-malnutrition cycle. At the same time the effect of simply removing the child to a more sanitary environment, together with an estimate of the natural clearance of bacteria from the upper intestine, should be evaluated.
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PMID:Jejunal microflora in malnourished Gambian children. 109 72

Two hundred and seventy-one infants with acute diarrhoea were studied for the presence of carbohydrate malabsorption and 110 infants (40.6%) were found to have carbohydrate intolerance. Malnutrition and severe diarrhoea were found to increase the predisposition to carbohydrate intolerance. The incidence of major complications, protracted diarrhoea and mortality were significantly higher in the carbohydrate intolerant infants as compared to those with carbohydrate tolerance.
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PMID:Carbohydrate intolerance in infants with acute diarrhoea and its complications. 115 66

Previous evaluation of diagnostic tests for acute renal failure in children demonstrated that osmolality urine/plasms (U/P) ratio below 1.3, urea ratio below 4.8 and a negative mannitol test (absence of a diurteic response within one hour after intravenous administration of 60 ml/m2 of 12.5% mannitol solution) may be considered as valuable factors in this diagnosis. However, the validity of those ratios were in doubt in selected populations such as newborns and in severe malnourished children in whom an impairment in concentrating urine capacity can be anticipated. With the purpose to test the validity of these parameters, a group of 53 newborns and 68 children with severe malnutrition were studied. They were admitted to the hospital with dehydration secondary to acute diarrhea presenting oliguria and hyperpnea and before any treatment was given, urine and blood samples were taken to determine urea and osmolality U/P ratios besides routine chemistries. Mannitol test was performed when urine could not be obtained and in some cases in whom U/P results deserved confirmation with the biological test. Seven of the 53 newborn patients developed acute renal failure with negative mannitol test and further clinical course of persistent oliguria. Urea and osmolality U/P ratios were 3.0 +/- 1.5 and 1.07 +/- 0.01 respectively, whereas the remaining 46 newborns had afterwards an uneventful recovery presenting U/P ratios of 12.4 +/- 8.5 for urea and 1.32 +/- 0.57 for osmolality. The difference between the average values of urea U/P ratio of the patients with acute renal failure and those with functional oliguria, were statistically significant at the level of p less than 0.01, but there was no significant difference between osmolality ratio values.
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PMID:[Evaluation of the urinary and plasma urea ratio and osmolarity in newborn infants and malnourished children with pathological and normal renal function]. 127 67

This work argues that rapid intravenous rehydration is desirable in cases of acute diarrhea. It provides detailed instructions for preparing and administering the correct solutions and for recognizing patients who are hyponatremia or suffering from acute acidosis. With widespread use of oral rehydration therapy, i.v. rehydration is limited to patients with acute dehydration or contraindications to oral rehydration. For purposes of prognosis, dehydration is usually classified according to the concentration of serum sodium or the degree of fluid loss. The objectives of i.v., rehydration are to eliminate the deficits of water and electrolytes, replace losses so that the patient will not become dehydrated again, and permit early feeding. The water deficit is variable and may amount to 100-150 ml/kg in the severely dehydrated. The sodium deficit is 9-17 mmol/kg and the potassium deficit is 3-15 mmol/kg. Early feeding after no more than 8 hours of fasting is currently considered more effective in preventing malnutrition in children with diarrhea and dehydration. Since the presence of deficits prevents feeding, the initial period of dehydration should not be prolonged beyond 4 hours. In developed countries, i.v. rehydration takes place over 12-24 hours with periods of fasting of 24-48 hours, but the mortality associated with this method of treatment in dehydrated children with diarrhea is higher. To meet its objectives, i.v., rehydration should take place in 3 phases, a rapid initial phase followed by simultaneously occurring phases of maintenance and of replacement in which normal and abnormal losses are replaced. The initial rapid phase should restore the normal perfusion of vital organs by eliminating deficits of sodium and water in no more than 2 hours. All sings of dehydration should disappear. The weight of the child before dehydration and thus the weight loss is seldom known, but experience with the method allows adequate approximations to be made. The solution used in almost all patients is a mixture of physiological solution of NaCl .9% and 5% dextrose solution (PS:DS5% 1:1). The only exceptions are patients with very low sodium levels or severe acidosis, who can be recognized by the experienced practitioner based on their characteristic clinical symptoms. The final concentration of sodium in the solution is .45% of NaCl and that of dextrose 2.5%. The patient is always reevaluated after 1 hour of treatment to detect possible complications. Treatment of hyponatremia and acidosis requires adjusting levels in the 1st hour of treatment with special formulas so that the standard formula may be administered. Instructions are provided for calculating the quantity and content of fluids for the maintenance and replacement stages, which are customarily administered in segments of 6-8 hours.
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PMID:[Rapid intravenous rehydration in acute diarrhea]. 144 37

Between June 1989 and January 1990 in Ethiopia, health workers collected 2 gm diarrhea samples from 100 patients, 2-48 months old, at the oral rehydration unit of the Gondar College Medical Sciences Hospital to test for the presence of Cryptosporidium species' oocysts. Laboratory personnel used Loeffler's alkaline methylene-blue solution to isolate oocysts in 9 children. 6 of these children were 12 months old. None of the children with Cryptosporidium oocysts exhibited signs of severe protein energy malnutrition, but 31 other children did exhibit these signs. The presence of oocysts in the 9 children did not necessarily indicate that Cryptosporidium species were the only causes of their acute diarrhea. The 9% isolation rate may be an underestimate, because Baxby and Blonde have demonstrated that safranin-methylene blue yields a better Cryptosporidium oocyst isolation rate than does Loeffler's alkaline methylene-blue. A well-designed study is needed to determine the true prevalence of cryptosporidiosis, to describe its clinical profile, and to define its association with other diarrhea-causing enteropathogens and its association with malnutrition.
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PMID:Frequency of isolation of Cryptosporidium oocysts in Ethiopian children with acute diarrhoeal disease. 150 16


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