Adolescent meat-type poultry and cage layers exhibit a high incidence of bone problems that include bone weakness, deformity, breakage, and infection and osteoporosis-related mortalities. These problems include economic and welfare issues. To improve bone quality in poultry, it is essential to understand the physiological basis of bone maturity and strength in poultry. A complex array of factors that include structural, architectural, compositional, physiological, and nutritional factors interactively determine bone quality and strength. Bone is approximately 70% mineral, 20% organic, and 10% water. Collagen is the major organic matrix that confers tensile strength to the bone, whereas hydroxyapatite provides compressional strength. In recent years, the roles of different collagen crosslinks have been shown to be important in the increase of bone mechanical strength. Similarly, age-related glyco-oxidative modifications of collagen have been shown to increase the stiffness of collagen. These posttranslational modifications of matrix can affect bone quality as it would be affected by the changes in the mineralization process. Our studies show that the growth in the tibia continued until 25 wk of age, which correlated with the increase in the content of hydroxylysylpridinoline (HP) and lysylpyridinoline (LP), the collagen crosslinks. The tibia from 5-wk-old chicks were strong but brittle because of low collagen crosslinks and high mineral content. Bone maturity may relate to its crosslink content. Compared to crosslink content, bone density and ash content showed moderate increases during growth. The bones from younger turkeys were more susceptible to corticosteroid-induced stunting of growth, which also resulted in decreased bone strength. This review discusses how different factors can compromise bone strength by reducing growth, altering shape, affecting mineralization, and affecting collagen crosslinking.

The effects of Salmonella typhimurium lipopolysaccharide (LPS) on the physiology of 3-wk-old broiler chickens were studied at 12, 24, and 48 h after a single intravenous injection of saline or LPS. Lipopolysaccharide elevated cloacal temperature by 3 h after injection, induced a diuretic response, and decreased BW gain. An increase in the relative liver weight was evident in LPS-treated birds at all time intervals, whereas a decrease in the relative weight of bursa of Fabricius was observed only at the 48-h time point. The plasma interleukin (IL)-6 and the blood heterophil concentrations were elevated at 12 and 24 h following LPS administration. These changes were not observed in control chickens or in LPS-treated chickens at 48 h. A decrease in the blood glucose concentration in LPS-treated birds at 12 h was accompanied by an elevation in the blood phosphate level. An increase in total plasma protein concentration was observed only at 24 and 48 h after LPS treatment. Comparative SDS-PAGE analysis of plasma proteins from these birds under nonreducing conditions showed some quantitative differences in four bands of proteins between saline and LPS-treated chickens. A protein corresponding to an approximate molecular weight (MW) of 65 kDa increased in LPS-treated chickens, and three other proteins with MW of approximately 39, 49, and 56 kDa showed reductions in concentration compared with saline-treated controls. These results show that LPS induces a number of physiological changes that may be responsible for the regulation of the acute phase response in chickens.

The progression of aflatoxicosis was evaluated in young broiler chickens (Hubbard X Hubbard). The experimental design consisted of four dietary treatments of aflatoxin (0, 1.25, 2.5, and 5.0 micrograms of aflatoxin/g of feed, ppm) and 11 replicates of 10 broilers/replicate. The broilers were maintained in electrically heated batteries with feed and water available ad libitum from hatching to 3 weeks of age. The broilers were weighed, bled, killed by cervical dislocation, and necropzied at 3, 6, 9, 12, 15, 17, and 21 days of age. Body weights were significantly decreased by 5.0 ppm aflatoxin at 6 days of age and by 2.5 ppm at 17 days of age. Aflatoxin induced a significant increase in the relative weight of the proventriculus, gizzard, spleen, and kidney. Liver atrophy was indicated in the early stages of aflatoxicosis by a decrease in the relative weight of this organ. As aflatoxicosis progressed, hepatomegaly became apparent due to lipid accumulation in the liver. Packed-cell volume and hemoglobin levels were significantly decreased by 5.0 ppm aflatoxin at 12 days and by 2.5 ppm aflatoxin at 21 days of age. Serum levels of albumin and total protein were significantly reduced at 5.0 and 2.5 ppm aflatoxin by 3 and 6 days of age, respectively. Serum levels of uric acid, triglycerides, and cholesterol were significantly decreased from control values from 12 through 21 days of age by 5.0 ppm aflatoxin and, to a lesser extent, by 2.5 ppm aflatoxin. The activity of serum lactic dehydrogenase was significantly decreased at all aflatoxin treatment levels from 12 through 21 days of age.(ABSTRACT TRUNCATED AT 250 WORDS)

The successful use of virulent (lytic) bacteriophages (phages) in preventing and treating neonatal enterotoxigenic Escherichia coli infections in calves, lambs and pigs has prompted investigation of other applications of phage therapy in food animals. While results have been very variable, some indicate that phage therapy is potentially useful in virulent Salmonella and E. coli infections in chickens, calves and pigs, and in control of the food-borne pathogens Salmonella and Campylobacter jejuni in chickens and E. coli O157:H7 in cattle. However, more rigorous and comprehensive research is required to determine the true potential of phage therapy. Particular challenges include the selection and characterization of phages, practical modes of administration, and development of formulations that maintain the viability of phages for administration. Also, meaningful evaluation of phage therapy will require animal studies that closely represent the intended use, and will include thorough investigation of the emergence and characteristics of phage resistant bacteria. As well, effective use will require understanding the ecology and dynamics of the endemic and therapeutic phages and their interactions with target bacteria in the farm environment. In the event that the potential of phage therapy is realized, adoption will depend on its efficacy and complementarity relative to other interventions. Another potential challenge will be regulatory approval.