Maternal-to-infant transmission of probiotics: concept validation in mice, rats, and pigs.

BACKGROUND: Postnatal introduction of probiotics results in a low incidence of colonization, whereas maternal fecal and vaginal bacteria colonize the gastrointestinal tract (GIT) of vaginally delivered infants. OBJECTIVE: We tested if probiotic bacteria, fed to three pregnant animal models, would colonize the GIT of offspring delivered vaginally. METHODS: Probiotic strains of Lactobacillus acidophilus and Bifidobacterium lactis were fed to pregnant mice, rats, and sows for at least 7 days prior to vaginal delivery. Cultural approaches and genotyping were used to determine if the probiotic bacteria colonized the GIT after birth. RESULTS: The probiotic bacteria were detected in the feces and vagina of maternal mice, rats, and sows after, but not before, administration. L. acidophilus was detected at postnatal day 14 in 22, 33, and 75% of the mice, rats, and pigs, respectively, and after weaning in 35% of the mice and 1 of 5 pigs. B. lactis was present at postnatal day 14 in 30 and 80% of the mice and pigs. Bacterial assemblages in the GIT of the colonized young differed from those in which the probiotics were not detected. CONCLUSIONS: Probiotic bacteria administered to mothers during late gestation are transferred to infants born vaginally and influence the assemblages of GIT bacteria. However, colonization of the neonatal GIT and persistence past weaning does not occur in all offspring and varies among probiotics and animal models.

Lactulose feeding lowers cecal densities of clostridia in piglets.

BACKGROUND: In order to understand the consequences of persistent enteral feeding in patients with carbohydrate malabsorption, we fed piglets lactulose in sufficient dosage to produce osmotic diarrhea or inulin, using a conventional dose, to determine if this prebiotic can modulate the effects of lactulose. Feeding lactulose increases cecal luminal synthesis of butyrate, with inulin having an intermediate effect. Because clostridia may be a major source of colonic butyrate production, we hypothesized that feeding piglets lactulose or inulin would increase cecal densities of clostridia. METHODS: Piglets were assigned to 3 formula study groups for 6 days: (1) control, fed only sow milk replacer (n = 12); (2) inulin, inulin supplement (3 g/L; n = 11); and (3) lactulose, lactulose supplement (66.7 g/L; n = 6). Cecal fluid for bacteriological studies was sampled intraoperatively. RESULTS: The wet/dry ratio of the cecal contents (mean +/- SEM) was 8.2 +/- 0.5, 6.2 +/- 0.5, and 18.8 +/- 5.5, respectively, in the control, inulin, and lactulose groups (p = .049, Kruskal-Wallis). There were no differences among the diet groups for cecal densities (10(6) colony-forming units [CFU]/g dry wt cecal contents) of total anaerobes, total aerobes, bifidobacteria, or lactobacilli. Densities of clostridia were markedly reduced in the lactulose group (1.14 +/- 0.41) vs the control (18.39 +/- 4.44; p = .001) or inulin groups (8.87 +/- 2.20; p = .04). CONCLUSIONS: In piglets, feeding lactulose at a dose known to cause diarrhea reduces cecal densities of clostridia.