There are several enteric bacterial diseases and conditions of pigs that require control to prevent overt disease, to reduce morbidity and mortality, and to improve the efficiency of production. Traditionally, veterinarians, feed manufacturers and producers have relied upon antibiotics and minerals (for example, ZnO, CuSO 4 ) in diets for a large part of this control. However, recent trends, particularly in Europe, are to reduce antimicrobial use and seek alternative or replacement strategies for controlling enteric bacterial diseases. The majority of these strategies rely on 'nutrition', taken in its broadest sense, to reduce the susceptibility of pigs to these diseases. Evidence to date suggests that specific dietary interventions, for example feeding very highly-digestible diets based on cooked white rice, can reduce the proliferation of a number of specific enteric bacterial infections, such as post-weaning colibacillosis. No simple and universal way to reduce susceptibility to pathogens in the gastrointestinal tract has been identified, and the underlying basis for many of the reported positive effects of 'nutrition' on controlling enteric infections lacks robust, scientific understanding. This makes it difficult to recommend dietary guidelines to prevent or reduce enteric bacterial diseases. Furthermore, some diseases, such as porcine intestinal spirochaetosis caused by Brachyspira pilosicoli, are sometimes associated with other pathogens (co-infections). In such cases, each pathogen might have different nutrient requirements, ecological niches and patterns of metabolism for which a variety of dietary interventions are needed to ameliorate the disease. Greater understanding of how 'nutrition' influences gut epithelial biology and immunobiology, and their interactions with both commensal and pathogenic bacteria, holds promise as a means of tackling enteric disease without antimicrobial agents. In addition, it is important to consider the overall system (i.e. management, housing, welfare) of pig production in the context of controlling enteric bacterial diseases.

This review describes the pattern of intramuscular fat accretion in cattle and the potential for its manipulation during both the pasture (or backgrounding) and intensive grain-finishing phases of development. A growth curve for the development of marbling in British and Japanese Black type breeds is discussed with the conclusion that 3 phases of development exist: (i) a period of growth up to ~200 kg hot carcass weight where intramuscular fat does not increase; (ii) a period of linear development as carcass weight increases from 200 to 450�kg; and (iii) the attainment of mature body size (~500 kg carcass weight depending on genotype) at which intramuscular fat content appears to reachea maximum. Data are also presented to show that the intramuscular and other fat depots develop at similar rates indicating that intramuscular fat is not a late maturing depot. Pre-finishing growth checks reduce the initial intramuscular fat at the start of finishing and this is translated into lower levels at the end of finishing. It is argued that the greatest potential for the manipulation of intramuscular fat accretion during fattening is via an increase in the net energy of the ration. Increasing net energy can be achieved by increasing the cereal grain content of the diet (grain v. grass); by feeding processed cereal grain, which allows both maximal rumen fermentation and small intestinal digestion of starch, and by increasing the lipid content of the diet. In addition it is proposed that the substrate supply or hormonal milieu can also be optimised, along with the availability of net energy to maximise fat accretion. The role of lipolysis (fat turnover) as a regulator of fat accretion is also discussed.

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In order for livestock industries to consistently produce high quality meat, there must be an understanding of the factors that cause quality to vary, as well as the contribution of genetics. A brief overview of meat tenderness is presented to understand how genotype and environment may interact to influence this trait.Essentially, meat tenderness is determined from the contribution of connective tissue, sarcomere length determined pre-rigor and rate of proteolysis during ageing, as well as contributions from intramuscular fat and post-mortem energy metabolism. The influence of mutations in myostatin, the callipyge gene, the Carwell or ribe eye muscle gene as well as the calpain system on meat tenderness is presented. Specific examples of interactions between the production or processing environment and genetics are presented for both sheep and cattle. The day-to-day variation in tenderness is evident across experiments and this variation needs to be controlled in order to consistently produce tender meat.

Sources of viscous soluble fibre, such as barley and oats, have often been included in the weaning diet of the pig to accelerate development of the large intestine. Inclusion of a non-fermentable, viscous compound, sodium carboxymethylcellulose (CMC), in a low-fibre weaning diet was tested to assess the influence of digesta viscosity on the gut in the absence of increased fermentation. Two CMC sources, of low and high viscosity, were added to cooked rice-based diet at 40 g/kg total diet. A third control rice diet did not contain any CMC. Diets were fed for 13 d following weaning at 3 weeks of age. Addition of CMC to the diet significantly increased the intestinal viscosity of digesta within the small (P,0 : 001) and large (P,0 : 05) intestine. No simple association was found between increases in intestinal viscosity and effects on intestinal morphology and whole-body growth. The average empty-body-weight gain and the small intestinal villus height increased with low-viscosity CMC, but decreased with the high-viscosity CMC group. The full large intestinal weight increased in all pigs fed CMC. Dietary CMC (both low-and high-viscosity) increased the percentage moisture of digesta and faeces, and was associated with increased faecal shedding of enterotoxigenic haemolytic Escherichia coli. Feed ingredients in weaning diets that excessively increase the viscosity of the intestinal digesta may be detrimental to pig health and production.