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Background: Recent nutritional interventions have targeted colonic functions in patients with infectious diarrhea during rehydration and during recovery from malnutrition, with the assumption that the effects will be influenced by metabolism of complex carbohydrates by colonic bacteria. However, the diversity of colonic bacteria in patients with cholera is not known., Aim: To study the diversity of colonic bacteria in malnourished children with cholera before and during treatment with oral rehydration salt solutions containing 1 of these 3 substrates: glucose, rice, or amylase-resistant starch., Patients and Methods: Serial fecal samples were collected from 30 malnourished children with cholera until completion of rehydration and partial nutritional recovery; 11 malnourished children without diarrhea; and 6 better nourished children. Polymerase chain reaction, using universal primers for 16S rDNA, was performed on chromosomal DNA extracted from the stool samples, and the products were separated by temporal temperature gradient gel electrophoresis., Results: The Vibrio cholerae band was detected in all children at enrollment and disappeared within 2 days. On day 2, a rapid and significant increase in the band numbers was observed, which was followed by a steady increase until day 28. After full recovery from cholera and partial recovery from malnutrition, the number of bands (11.5+/-2.8) was lower than in healthy children (22.2+/-1.3). On day 3, the number of bands was greater with rice or amylase-resistant starch than with glucose (P<.05)., Conclusions: Bacterial diversity was markedly but transiently altered in severely malnourished children with cholera receiving therapy.

Objective: To test the safety and effect on faecal microbiota of a formula with prebiotic oligosaccharides alone or in combination with acidic oligosaccharides in infants at the age of partial formula feeding., Patients and Methods: The study was a double-blind, placebo-controlled, randomised intervention trial in which 82 healthy, full-term, partially breast-fed children, from 1 week to 3 months old, were given 1 of the following formulae: whey-based formula (control group), whey-based formula with galacto- and long-chain fructo-oligosaccharides (scGOS/lcFOS group), or whey-based formula with galacto- and long-chain fructo-oligosaccharides added with pectin-derived acidic oligosaccharides (scGOS/lcFOS/pAOS group). Children were studied for the duration of the partial formula feeding period and every 2 weeks for 2 months after breast-feeding cessation. The total bacteria count and the proportion of 7 bacterial families were determined using in situ hybridisation coupled to flow cytometry., Results: The total bacterial count did not alter with time or type of feeding (9.9 +/- 0.1 log10 cells per gram wet weight). Compared with the control group, there was an increase of the Bifidobacterium genus (P = 0.0001), and a decrease of proportions for the Bacteroides group (P = 0.02) and the Clostridium coccoides group (P = 0.01) in both oligosaccharide groups. The proportion of bifidobacteria was significantly higher in the scGOS/lcFOS/pAOS compared with the scGOS/lcFOS group (P < 0.01)., Conclusions: Infant formulae appear to be clinically safe and effective on infant microbiota. They minimize the alteration of faecal microbiota after cessation of breast-feeding and promote bifidobacteria proportions, with a stronger effect when acidic oligosaccharides are present.

Background: The respective effect of milk and fermented milks on intestinal barrier capacity and on sensitization to beta-lactoglobulin was studied using a guinea pig model of cow's milk allergy., Methods: Guinea pigs were fed a control diet or the same diet supplemented with milk, fermented milk (Streptococcus thermophilus and Bifidobacterium breve), or dehydrated fermented milk. Intestinal barrier capacity to macromolecules was assessed in an Ussing chamber, and sensitization to cow's milk proteins was measured by systemic anti-beta-lactoglobulin immunoglobulin G1 titers and by intestinal anaphylaxis, the latter assessed by the beta-lactoglobulin-induced increase in short-circuit current of jejunal fragments (deltaIsc(beta-LG))., Results: The electrical resistance of jejunum was similar in the four groups (approximately 80 omega/cm2) suggesting the same paracellular permeability. The transport of 14C-beta-lactoglobulin from mucosa to serosa was significantly decreased in the animals fed dehydrated fermented milk (403+/-131 ng / hr x cm2) compared with that in control animals or animals fed milk (767+/-250 ng / hr x cm2 and 749+/-475 ng / hr x cm2, respectively; p < 0.05). Milk fermentation did not modify native beta-lactoglobulin concentration but anti-beta-lactoglobulin immunoglobulin G1 titers were higher in fermented milk and dehydrated fermented milk (log10 titer = 2.86 and 2.79, respectively) than in guinea pigs fed milk (log10 titer = 2.5; p < 0.007). However, beta-lactoglobulin-induced intestinal anaphylaxis remained the same in the three groups (deltaIsc(beta-LG), 9.6+/-4.1 microA/cm2, 8.5+/-4.3 microA/cm2, and 8.5+/-3.4 microA/cm2 in milk-fed, fermented milk-fed, and dehydrated fermented milk-fed guinea pigs, respectively)., Conclusions: The intestinal barrier capacity to milk proteins seems to be reinforced by dehydrated fermented milk, but milk and fermented milks are equally efficient in inducing cow's milk allergy in guinea pigs.

Yogurt has been shown to inhibit, by various mechanisms, pathogenic bacterial growth in vitro, including that of the rabbit Escherichia coli strain RDEC-1. To determine whether this in vitro inhibition by yogurt has an in vivo counterpart, 60 newly weaned New Zealand rabbits were randomly assigned to receive a diet supplemented with either milk or yogurt. Four days later, rabbits were infected intragastrically with 10(8) E. coli strain RDEC-1. During the 30 days postinfection, animals were checked regularly for weight, stool characteristics, and fecal excretion of bacteria. Results show that the duration of diarrhea as well as bacterial excretion were the same in the milk and yogurt groups, indicating that in vivo, yogurt did not interfere with the growth of the pathogenic E. coli strain RDEC-1. The pattern of the survival curves was significantly different in the two groups (p less than 0.03), but the difference between their mortality at 30 days postinfection was not significant (80% in the milk group versus 67% in the yogurt group). These results indicate that the bactericidal activity of yogurt observed in vitro against the E. coli strain RDEC-1 does not have an in vivo counterpart in the model of the just-weaned rabbit infected by RDEC-1.

Although the pathophysiology of persistent diarrhea in children remains unclear, it has been suggested that it may be related to the composition of the food ingested. Since lactase deficiency and cow's milk protein intolerance are often identified in children with persistent diarrhea, replacement of milk with yogurt should be beneficial. We, therefore, compared the clinical outcome of children (aged 3-36 months) with persistent diarrhea randomly assigned to receive either milk or yogurt for 5 days. Preliminary results on 45 of the 100 children indicated clinical failure, which was determined after a 5% loss of body weight per day or the persistence of diarrhea after 5 days, in only 14% of the children fed yogurt compared to 42% of those fed milk (p less than 0.05). These preliminary results strongly suggest a clinical advantage of feeding yogurt rather than milk in children with persistent diarrhea.