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Seven hundred and twenty hatchling broilers were allotted to 12 treatment groups. Groups 1 and 2 were fasted for 48 h posthatch; groups 3 and 4 were fasted for 48 h followed by ad libitum access to a 1% glutamine (Gln) diet; groups 5 and 6 had ad libitum access to a common diet; groups 7 and 8 had access to a 1% Gln diet posthatch; groups 9 and 10 were fed regular Oasis hatchling supplement; and groups 11 and 12 were fed Oasis sprayed with 1% Gln for the first 48 h posthatch. The birds in treatment groups 2, 4, 6, 8, 10, 11, and 12 were vaccinated with Eimeria maxima posthatch, and all birds were orally challenged with high dose E. maxima on d 22. During the first 2 wk, birds in group 7 had the highest gain and feed efficiency among treatments (P < 0.01). Compared with birds in the nonGln groups, birds in the Gln group had higher gain, feed efficiency, and livability (P < 0.05). Among the Fast (groups 1 to 4), Feed (groups 5 to 8), and Oasis (groups 9 to 12) groups, birds in the Feed groups had the highest gain during d 0 to 21 (P < 0.01). During d 22 to 28, birds in the Fast groups had the lowest BW and livability (P < 0.01), and the nonvaccinated birds had lower gain and feed efficiency relative to vaccinated birds (P < 0.01). Birds in the Feed and Oasis groups had higher villus height (VH) of mid small intestine than Fast groups at d 2 and 7 (P < 0.05), and nonvaccinated birds had higher VH than vaccinated birds (P < 0.01) at d 7 after hatch. On d 14, there were differences in serum interferon-gamma (P < 0.05) levels among treatments. During d 22 to 28, vaccinated birds had lower lesion scores in the mid small intestine than nonvaccinated birds (P < 0.01), and birds in the Feed or Oasis groups had lower lesion scores compared with the Fast groups (P < 0.02). These results indicated the importance of immediate access to feed posthatch, the beneficial effects of feeding Oasis hatching supplement and Gln after hatch, as well as the necessity of the vaccination program against coccidiosis challenge.

Two experiments were conducted to compare the effects of feeding organic acids and antibiotic growth promoters in weaned pigs. In Exp. 1, 96 nursery pigs (Large White×Landrace; initial weight 7.80±0.07 kg) were randomly allotted into one of four dietary treatments. Pigs in treatment 1 were fed a complex starter diet. Treatments 2 to 4 were the same as treatment 1 but supplemented with antibiotics (200 ppm chlortetracycline plus 60 ppm Lincospectin), 0.5% potassium diformate or 0.5% dry organic acid blend ACTIVATE Starter DA (ASD). During the 4-week post-weaning period, pigs fed ASD or antibiotics had better gain (p = 0.03) and feed efficiency (p = 0.04) than pigs fed the control diet. On d 14 post-weaning, pigs fed the control diet had the lowest fecal lactobacilli count among all dietary treatments (p = 0.02), whereas pigs fed ASD or antibiotics had a trend for lower fecal E. coli count compared to the control pigs (p = 0.08). Serum insulin-like growth factor-1 (IGF-1) of pigs fed ASD did not differ from pigs fed the control diet (p>0.05) at d 14 after weaning. In Exp. 2, 24 weaned pigs (Large White×Long White; initial weight 5.94±0.33 kg) were allotted into four groups and housed individually. Pigs were fed a control diet or diets supplemented with antibiotics (100 ppm colistin sulfate, 50 ppm Kitasamycin plus 60 ppm Olaquindox), 0.5% or 1% ASD. All pigs were orally challenged with E. coli K88 + on d 5. During d 5 to 14 after challenge, pigs fed antibiotics, 0.5% or 1% ASD had better gain (p = 0.01) and feed efficiency (p = 0.03) than pigs fed the control diet. On d 14, compared to the control pigs, pigs fed 0.5% ASD had higher lactobacilli in the duodenum and pigs fed 1% ASD and antibiotics had a trend for higher lactobacilli in the ileum (p = 0.08). Pigs fed antibiotics, 0.5% or 1% ASD diets tended to have decreased ileal E. coli count compared to those fed the control diet (p = 0.08). Serum interleukin-6 and cortisol and digesta pH values were not affected by treatment or time. These results indicate that feeding ASD can improve the growth performance of weaning pigs, mainly via modulating intestinal microflora populations without affecting gastrointestinal pH or immune indices.

Primary Audience: Nutritionists, Veterinarians SUMMARYThe microbial community of the gastrointestinal system has an enormous impact on the vertebrate host. The relationship begins at birth or hatch and evolves to a stable ecosystem in which diverse, and unique, niches are created and inhabited by microorganisms. These microbial populations tend to be similar within a host species (and even across host species), but each system is a unique construct resulting from its individual history of mutual influence. The development of the system, both microbial and host, begins in the perinatal animal. The timing of this developmental process is suggestive of imprinting, the process of epigenetic evolution of somatic stem cells. (Imprinted changes are thought not to involve the germ line, i.e., are not inherited by the next generation of the host animal, but are genetic changes that can be passed on to the daughter cells of the imprinted proliferative stem cell.) This review briefly discusses the development of the gastrointestinal system, including both the microbiota and its perinatal host. The effects of the microflora on enteric and immune cells are described. Effects of attempts to restrict contact between the mucosal immune system and the microbiota are addressed, along with further data that would be required to demonstrate that the effects of the gut microbiota on mucosal immune development are restricted to an ontogenetic window. Finally, the consequences of a failure to achieve a relationship of mutual tolerance between the microbiota and the host and some mechanisms to facilitate this process are discussed.

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