The performance of piglets in nurseries may vary depending on body weight, age at weaning, management, and pathogenic load in the pig facilities. The early events in a pig’s life are very important and may have long lasting consequences, since growth lag involves a significant cost to the system due to reduced market weights and increased barn occupancy. The present review evidences that there are several strategies that can be used to improve the performance and welfare of pigs at weaning. A complex set of early management and dietary strategies have been explored in sows and suckling piglets for achieving optimum and efficient growth of piglets after weaning. The management strategies studied to improve development and animal welfare include: (1) improving sow housing during gestation, (2) reducing pain during farrowing, (3) facilitating an early and sufficient colostrum intake, (4) promoting an early social interaction between litters, and (5) providing complementary feed during lactation. Dietary strategies for sows and suckling piglets aim to: (1) enhance fetal growth (arginine, folate, betaine, vitamin B₁₂, carnitine, chromium, and zinc), (2) increase colostrum and milk production (DL-methionine, DL-2-hydroxy-4-methylthiobutanoic acid, arginine, L-carnitine, tryptophan, valine, vitamin E, and phytogenic actives), (3) modulate sows’ oxidative and inflammation status (polyunsaturated fatty acids, vitamin E, selenium, phytogenic actives, and spray dried plasma), (4) allow early microbial colonization (probiotics), or (5) supply conditionally essential nutrients (nucleotides, glutamate, glutamine, threonine, and tryptophan).

An experiment was designed to evaluate the effects of 3 different additives on the gastrointestinal microbiota of early-weaned pigs. Early-weaned (18 to 22 d; n = 32) pigs (6.0 ± 0.10 kg of BW) from 8 litters were randomly distributed into 8 pens. Each pen was assigned 1 of 4 dietary treatments: a prestarter or control diet, the control diet with 0.04% avilamycin (AB), with 0.3% sodium butyrate, or with 0.03% plant extract mixture (XT; standardized mixture with 5% (wt/wt) carvacrol extracted from Origanum spp., 3% cinnamaldehyde extracted from Cinnamonum spp., and 2% capsicum oleoresin from Capsicum annum). At the end of the experimental period, 8 pigs per treatment were killed, and samples of their intestinal content were taken. The total bacterial load along the gastrointestinal tract (GIT; stomach, jejunum, cecum, and distal colon) and the lactobacilli and enterobacteria in the jejunum and cecum were measured by quantitative PCR. The total microbial counts along the GIT did not differ among the diets, but there was an increase in the lactobacilli:enterobacteria ratio in the cecum of the piglets on the XT diet (P = 0.003). Restriction fragment length polymorphism of the PCR-amplified V3, V4, and V5 regions of the 16S rDNA gene showed changes in the structure of the microbial community in the jejunum. Dendrograms grouped animals by diets; control with 0.3% sodium butyrate was the treatment that promoted the biggest changes in the microbial ecosystem, followed by AB and then XT. Biodiversity increased when using additives compared with the control diet (P = 0.002). Microbial metabolic activity along the hindgut was studied using the concentration of purine bases and carbohydrase activities. Different patterns for purine bases were observed between diets (diet × intestinal section, P = 0.01). The control diet reached a maximum purine base concentration at the end of the colon, whereas that of the AB diet was reached at the cecum. We could not detect any cellulase or xylanase activities in animals of this age. Appreciable amylase and amylopectinase activities were found, but they did not differ between diets. The results suggest that the effects of avilamycin, butyrate, or the plant extract would not be related to a reduction in the number of total bacteria inhabiting different sections of the GIT but rather to changes in the ecological structure and metabolic activity of the microbial community. Copyright © 2006. . Copyright 2006 Journal of Animal Science

β-1,4-Mannanases (mannanases), which hydrolyse mannans and glucomannans, are located in glycoside hydrolase families (GHs) 5 and 26. To investigate whether there are fundamental differences in the molecular architecture and biochemical properties of GH5 and GH26 mannanases, four genes encoding these enzymes were isolated from Cellvibrio japonicus and the encoded glycoside hydrolases were characterized. The four genes, man5A, man5B, man5C and man26B, encode the mannanases Man5A, Man5B, Man5C and Man26B, respectively. Man26B consists of an N-terminal signal peptide linked via an extended serine-rich region to a GH26 catalytic domain. Man5A, Man5B and Man5C contain GH5 catalytic domains and non-catalytic carbohydrate-binding modules (CBMs) belonging to families 2a, 5 and 10; Man5C in addition contains a module defined as X4 of unknown function. The family 10 and 2a CBMs bound to crystalline cellulose and ivory nut crystalline mannan, displaying very similar properties to the corresponding family 10 and 2a CBMs from Cellvibrio cellulases and xylanases. CBM5 bound weakly to these crystalline polysaccharides. The catalytic domains of Man5A, Man5B and Man26B hydrolysed galactomannan and glucomannan, but displayed no activity against crystalline mannan or cellulosic substrates. Although Man5C was less active against glucomannan and galactomannan than the other mannanases, it did attack crystalline ivory nut mannan. All the enzymes exhibited classic endo-activity producing a mixture of oligosaccharides during the initial phase of the reaction, although their mode of action against manno-oligosaccharides and glucomannan indicated differences in the topology of the respective substrate-binding sites. This report points to a different role for GH5 and GH26 mannanases from C. japonicus. We propose that as the GH5 enzymes contain CBMs that bind crystalline polysaccharides, these enzymes are likely to target mannans that are integral to the plant cell wall, while GH26 mannanases, which lack CBMs and rapidly release mannose from polysaccharides and oligosaccharides, target the storage polysaccharide galactomannan and manno-oligosaccharides.

The potential of a prebiotic oligosaccharide lactulose, a probiotic strain of Lactobacillus plantarum , or their synbiotic combination to control postweaning colibacillosis in pigs was evaluated using an enterotoxigenic Escherichia coli (ETEC) K88 oral challenge. Seventy-two weanlings were fed four diets: a control diet (CTR), that diet supplemented with L. plantarum (2 × 10 ¹⁰ CFU · day ⁻¹ ) (LPN), that diet supplemented with 10 g · kg ⁻¹ lactulose (LAC), or a combination of the two treatments (SYN). After 7 days, the pigs were orally challenged. Six pigs per treatment were euthanized on days 6 and 10 postchallenge (PC). Inclusion of lactulose improved the average daily gain (ADG) ( P < 0.05) and increased lactobacilli ( P < 0.05) and the percentage of butyric acid ( P < 0.02) in the colon. An increase in the ileum villous height ( P < 0.05) and a reduction of the pig major acute-phase protein (Pig-MAP) in serum ( P < 0.01) were observed also. The inclusion of the probiotic increased numbers of L. plantarum bacteria in the ileum and colon ( P < 0.05) and in the total lactobacilli in the colon and showed a trend to reduce diarrhea ( P = 0.09). The concentrations of ammonia in ileal and colonic digesta were decreased ( P < 0.05), and the villous height ( P < 0.01) and number of ileal goblet cells ( P < 0.05) increased, at day 10 PC. A decrease in plasmatic tumor necrosis factor alpha (TNF-α) ( P < 0.01) was also seen. The positive effects of the two additives were combined in the SYN treatment, resulting in a complementary synbiotic with potential to be used to control postweaning colibacillosis.