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Biomedical subjects

M J Butel

Publications and source records attributed to M J Butel.

14 recordsLinked to original sources
PubMed1999

Oligofructose contributes to the protective role of bifidobacteria in experimental necrotising enterocolitis in quails.

Bifidobacteria are dominant in the gut of full-term infants, although colonisation by them is often delayed in preterm neonates. Bifidobacteria are recognised to have beneficial effects on digestive disorders and they might prevent neonatal necrotising enterocolitis (NEC), a gastrointestinal disease that predominantly affects premature infants. They have been shown to protect gnotobiotic quails against NEC-like lesions when the birds were inoculated with faecal flora from preterm infants, decreasing the clostridial population. The present study was designed to investigate whether oligofructose, which stimulates the activity of bifidobacteria, may enhance their protective role. Experiments were done in eight groups of germ-free quails for 28 days. The groups differed as to their bacterial status, diet and environment. Quails were inoculated with one of two flora from premature twins. The first flora included Bifidobacterium pseudo-catenulatum, Escherichia coli and no clostridia. The second flora included clostridial species and was associated with B. infantis-longum. Caecal bacterial population and metabolism changes were investigated with a lactose (6%) diet versus a lactose-oligofructose (3%-3%) diet, either in a gnotobiotic environment or in an ordinary environment permitting post-colonisation by exogenous bacteria. In both environments and with both flora, oligofructose significantly increased the level of bifidobacteria and this was associated with a decrease of E. coli or C. perfringens and C. ramosum. The bacterial changes in the ordinary environment depended on the initial composition of the microflora and the colonisation resistance against exogenous bacteria was more efficient with the flora that included B. pseudo-catenulatum. The changes in caecal pH and short-chain fatty acids were minimal. It was demonstrated that, irrespective of the environmental conditions, the use of oligofructose helped to prevent the overgrowth of bacteria implicated in necrotising enterocolitis in preterm neonates.

Animals↗
PubMed1998

Synthesis of 2-hydroxy acid from 2-amino acid by Clostridium butyricum.

Cultures of Clostridium butyricum type strain in synthetic medium supplemented with various L-2-amino acids revealed the presence of the corresponding 2-hydroxy acid. This metabolite is able to produce the polyester poly(2-hydroxyalkanoic acid). The bioconversion is not stereoselective since D-2-amino acids were also converted. Chiral GC analysis demonstrated that only D-enantiomer is formed from L-leucine.

Amino Acids↗
PubMed1998

Clostridial pathogenicity in experimental necrotising enterocolitis in gnotobiotic quails and protective role of bifidobacteria.

The pathogenesis of neonatal necrotising enterocolitis (NEC) remains unclear. Gnotobiotic quails fed a lactose diet have been used to investigate the role of clostridial strains originating from faecal specimens of neonates through the intestinal lesions, the changes in microflora balance and the production of bacterial metabolites, i.e., short-chain fatty acids and hydrogen. Bifidobacteria are thought to exert various beneficial effects on host health, including interaction with the colonic microflora. Therefore, it was hypothesised that a protective role could be exercised through bifidobacterial colonisation. A Clostridium butyricum strain (CB 155-3) and a whole faecal flora including three clostridial species (C. butyricum, C. perfringens, C. difficile), each from premature infants suffering from NEC, caused caecal lesions in quails similar to those observed in man, i.e., thickening of the caecal wall with gas cysts, haemorrhagic ulceration and necrotic areas. Conversely, a whole faecal flora including bifidobacteria (identified as Bifidobacterium pseudo-catenulatum) and no clostridia, isolated from a healthy premature infant, was unable to produce NEC-like lesions. When the two clostridial groups were associated with a Bifidobacterium strain (B. infantis-longum, CUETM 89-215, isolated from a healthy infant), bifidobacterial colonisation suppressed all pathological lesions. This study is the first demonstration of a protective role for bifidobacteria against NEC via the inhibition of growth of C. butyricum or the disappearance of C. perfringens. C. difficile was not found to be responsible for the aetiology of the caecal lesions in quails. The main effect of bifidobacteria on lactose fermentation was either a dramatic decrease or a disappearance of butyric acid. The protective role was not associated with changes in H2 production. Therefore, a new step between colonic colonisation and its relevance to NEC is thought to involve the fermentation of unabsorbed lactose into butyric acid at the onset of the disease.

Animals↗
PubMed1992

[Neonatal digestive implantation of streptococcus group B. Influence of antibiotic therapy].

Group B streptococcus (GBS) is an important cause of neonatal infection. Early-onset diseases are due to perinatal contamination. The epidemiology of late-onset infections is poorly known. Maternal colonization may be responsible for some of them. The relationships between neonatal colonization and late disease could be a colonization of the gut. The purpose of this 3 year-prospective study was to analyse the kinetics of gut colonization in neonates and the influence of antibiotherapy. One hundred and nineteen infants less than one month of age were included because of the presence of GBS in their gastric aspirates or GBS infection. Depending on the therapeutic strategy, the infants were separated into 3 groups: 1) amoxicillin plus aminoside greater than or equal to 10 days because of neonatal infection (28 infants), 2) same combination less than or equal to 5 days because a GBS infection was suspected but not confirmed (17 infants), 3) no antibiotics (77 infants). Fecal flora was regularly analysed by differential count. Antibiotics caused rapid disappearance of GBS from the gut. However, the same strain reappeared after stopping the antibiotics at a rate of 13.5%. Without antibiotics, GBS was implanted in 33% of cases. This difference of implantation rate is statistically significant (p less than 0.05). No GBS infection was observed in any infant after a follow-up examination of 6 months to 2 years. Among the clinical and bacteriological factors studied, adhesion only was correlated with the GBS implantation. These results allow to discuss therapeutic abstention in colonized infants without any signs of infection.

Ampicillin↗
PubMed1991

[Epidemiology and prevention of perinatal group B streptococcal infections].

Neonatal group B streptococcal infection is frequent and may be responsible for lethal neonatal septicaemia. Its preventive treatment is still hotly debated. Digestive and genital tracts colonization is frequent in mother (15-20% of the cases) but it is unstable. About one out of two infants born of a colonized woman becomes colonized or infected. Neonates can also be colonized during their stay in maternity hospitals. Colonization is much more frequent than infection which strikes 0.2 to 0.6 per cent of neonates (at a very early period in two-thirds of the cases), but it jeopardizes their prognosis for life and later their functional prognosis. Prematurity and chorioamnionitis are the two main infection facilitating factors. Some of the various measures proposed to prevent infection in neonates, such as antibiotic therapy of colonized mothers during pregnancy and of symptomatic colonized neonates, do not seem to be effective, but others are interesting, including administration of antibiotics to mothers during delivery in high-risk situations, combined with early detection and immediate bactericidal treatment of neonatal infections.

Anti-Bacterial Agents↗
PubMed1986

[Effect of erythromycin on the fecal flora of infants less than 1-year old].

Erythromycin ethyl succinate is an antibiotic frequently administered in pediatrics. According to some authors, this drug sharply decreases the fecal count of enterobacteria. The fecal flora of 12 infants less than one year old, treated by erythromycin ethyl succinate for 7 to 10 days was studied by differential count. A variable effect was observed on enterobacteria: a 10(3) to 10(5) fold reduction in 9 cases with a final count superior or equal to 10(4) per gram of feces, with or without coming back to the initial count; in 3 cases no modification. MIC of enterobacteria and concentrations of erythromycin in feces were not predictives of flora variation. Anaerobic flora was weakly modified. No implantation of potentially-pathogenic bacteria or multi-resistant or highly erythromycin resistant enterobacteria occurred. Thus, erythromycin ethyl succinate is valuable in pediatrics as it does not disturb barrier effects. But its use for selective decontamination of gut must be discussed depending on pharmacologic form and posology administered.

Enterobacteriaceae↗
PubMedDate not supplied

Diet, length of gestation, and fecal short chain fatty acids in healthy premature neonates.

BACKGROUND: Excretion of fecal short-chain fatty acids (SCFAs) may indicate changes in colonic or colonocyte metabolism. The aim of this study was to detect the influence of gestational age and feeding practices on SCFA concentrations and profiles in healthy preterm infants. METHODS: A total of 198 fecal samples (28 infants) were collected from 8 to 21 days of age from 3 groups of preterm infants born at 33 to 37 weeks of gestation and fed either breast milk (group I) or Nutramigen, a lactose-free formula (group II), and extremely preterm infants born before 33 weeks of gestation and fed breast milk (group III). Total SCFA concentrations and SCFA profiles were analyzed using a gas chromographic (GC) procedure. RESULTS: Total fecal SCFA excretion did not differ significantly between group I (mean, 24.0 micromol/g; range, 1.3 to 118.8 micromol/g) and group II (mean, 23.0 micromol/g; range, 3.0 to 73.3 micromol/g). Conversely, differences occurred between SCFA profiles and became significant after day 17. The main differences were a significant increase in the butyric acid concentration (12% versus 30%) with group II. Compared with group I, fecal SCFA concentrations were 3.2-fold lower (7.4 micromol/g; range, 0.3 to 37.4 micromol/g) in group III with no significant changes in the profiles. CONCLUSIONS: Fecal SCFA excretion may vary in absence of any digestive disease. During this study, in terms of gestational age, total SCFA concentrations were significantly lower in extremely premature infants compared with infants born less premature, despite their known higher deficiency in intestinal lactase activity. In terms of diet, the absence of lactose did not lead to a decrease in colonic fermentation and induced changes in SCFA patterns. These new baseline data may offer clues to further development of milk formulas.

Age Factors↗