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An optimal balance of intestinal microbiota is necessary for digestive and immune health. Poor performance, susceptibility to infections, and decreased growth rate can be signs of an imbalanced microbiome. Dietary strategies to establish and maintain an optimal balance of microbiota include prebiotics (food for indigenous microbiota in the gastrointestinal tract) and probiotics (beneficial microbiota consumed by the animal). Recent research regarding use of probiotics and prebiotics in reproducing and growing livestock and companion animals is summarized. Documented benefits include prevention of diarrhea, decreased mortality, establishment of a healthy microbiota balance, and improved immune function.

The gut microflora play a crucial role in several physiologic functions of the host, including maturation of the gut-associated lymphoid tissues during the first months of life. Oral administration of probiotic lactic acid bacteria (LAB) modulates the immune system of humans and some laboratory animals. This effect has never been examined in dogs; therefore, our aim was to study the capacity of a probiotic LAB to stimulate immune functions in young dogs. Puppies were allotted to two groups receiving either a control diet or a diet supplemented with 5 x 10(8) colony forming units (cfu)/d of probiotic Enterococcus faecium (SF68) from weaning to 1 y of age. Fecal and blood samples were collected from the dogs at different time points for the measurement of fecal immunoglobulin (Ig)A, circulating IgG and IgA, and the proportions of lymphoid cell subsets. Fecal IgA and canine distemper virus (CDV) vaccine-specific circulating IgG and IgA were higher in the group receiving the probiotic than in controls. There were no differences in the percentages of CD4(+) and CD8(+) T cells between the groups, but the proportion of mature B cells [CD21(+)/major histocompatibility complex (MHC) class II(+)] was greater in those fed the probiotic. These data show for the first time that a dietary probiotic LAB enhance specific immune functions in young dogs, thus offering new opportunities for the utilization of probiotics in canine nutrition.

Two iron repletion experiments using hemoglobin as a response criterion were conducted to assess effects of hemicelluloses on iron bioavailability to chicks. In Experiment 1, iron bioavailability from intact fiber sources was determined by adding tomato pomace (14.6% hemicelluloses), soybean hulls (20.6% hemicelluloses), beet pulp (21.5% hemicelluloses), orchard grass (24.1% hemicelluloses) and corn fiber (55.2% hemicelluloses) to a casein dextrose basal diet providing 0.4-4.1% hemicelluloses to the diet. Test foods were analyzed for iron, total dietary fiber, neutral detergent residue, neutral detergent fiber, acid detergent fiber, acid detergent lignin, pectins and uronic acids. Hemicelluloses were determined by the difference of neutral detergent residue minus acid detergent fiber. Iron bioavailability was determined by the standard curve method to be (percent relative to ferrous sulfate using hemoglobin as the response criterion) as follows: tomato pomace, 82.0; soybean hulls, 94.0; beet pulp, 26.5; orchard grass, 68.9; corn fiber, 69.4. Iron bioavailability was not related to hemicellulose content of test foods or diets. In Experiment 2, the effect of psyllium husk (a fiber source that contains predominantly hemicelluloses) on iron bioavailability from ferrous sulfate was assessed. Bioavailability was determined by the slope ratio method where treatments consisted of graded levels of ferrous sulfate in the presence and absence of 5% dietary psyllium. Although iron intrinsic to psyllium was unavailable, bioavailability of ferrous sulfate iron was not affected (P > 0.05) by the presence of psyllium. Thus, there was no clear effect of hemicelluloses on iron bioavailability. However, some feeds that contained high levels of hemicelluloses had low intrinsic iron bioavailabilities, suggesting that other dietary factors are primarily responsible for determining iron bioavailability from these feed components.

An estimate of the dietary requirement for iron (Fe) has never been made for the growing canine or feline. Therefore, two assays were conducted in which weanling puppies or kittens were fed a casein-based, fiber-free diet containing 5, 30, 55, 80, 105, or 130 mg/kg Fe (supplied as FeSO4 X 7H2O) for 30 d. Blood samples were obtained and body weight measured at 10-d intervals. Hemoglobin concentration and hematocrit were determined and a one-slope broken-line model analysis of these two parameters was used to estimate the dietary Fe requirement for each species. For the puppy, 84 +/- 6.1 mg dietary Fe/kg was necessary to maximize hemoglobin concentration, whereas 81 +/- 5.0 mg dietary Fe/kg was the requirement estimate using hematocrit as the response criterion. For the kitten, requirement estimates were 77 +/- 8.1 and 80 +/- 7.2 mg dietary Fe/kg for maximizing hemoglobin concentration and hematocrit, respectively. We conclude that at least 80 mg dietary Fe/kg is required by growing dogs and cats fed a purified casein-dextrose diet.

Cysteine, via chelation reactions, ameliorates biochemical lesions caused by excessive ingestion of several trace elements. Because oral cysteine per se is considerably more protective than the in vivo metabolic cysteine precursors, methionine or cystine, chelation of cysteine with trace elements likely occurs primarily in the gut, thereby decreasing absorption of both cysteine and the trace element in question. Hence, using copper as an example, orally administered cysteine markedly improves growth and reduces liver copper deposition in chicks or rats fed a high level of inorganic copper. Likewise, excessive copper ingestion impairs sulfur amino acid (SAA) utilization and increases the dietary requirement for SAA. Cobalt and selenium toxicities are also ameliorated by oral cysteine ingestion, with the responses being even more striking than those occurring with copper toxicity. While inorganic arsenic poisonings are generally ameliorated by administering cysteine or a cysteine derivative (e.g., dimercaptopropanol), organic pentavalent arsenic toxicity is exacerbated by cysteine administration. Cysteine in this instance acts as a reducing agent, facilitating conversion of organic pentavalent arsenicals such as roxarsone and arsanilic acid to the more toxic trivalent state.