Lactobacillus rhamnosus JYLR-005 Prevents Thiram-Induced Tibial Dyschondroplasia by Enhancing Bone-Related Growth Performance in Chickens.

Tibial dyschondroplasia (TD) is a leg disorder caused by the abnormal development of the tibia in fast-growing poultry. Lactobacillus rhamnosus (L. rhamnosus) strains have been reported to have effects on increasing bone growth and improving osteoporosis in animals. However, whether L. rhamnosus JYLR-005 can improve bone growth in TD chickens remains unclear. In this study, we noted that L. rhamnosus JYLR-005 could not reduce the suppression of the production performance of TD broilers (p > 0.05) but had a slight protective effect on the broiler survival rate (χ2 = 5.571, p = 0.062). However, for thiram-induced TD broiler chickens, L. rhamnosus JYLR-005 could promote tibia growth by increasing tibia-related parameters, including the tibia weight (day 11, p = 0.040), tibia length (day 15, p = 0.013), and tibia mean diameter (day 15, p = 0.035). Moreover, L. rhamnosus JYLR-005 supplementation improved the normal growth and development of the tibial growth plate by maintaining the morphological structure of the chondrocytes and restored the balance of calcium and phosphorus. Taken together, these findings provide a proof of principle that L. rhamnosus JYLR-005 may represent a therapeutic strategy to treat leg disease in chickens.

Dietary supplementation with glycosaminoglycans reduces locomotor problems in broiler chickens.

This study aimed to assess the influence of glycosaminoglycan (chondroitin and glucosamine sulfates) supplementation in the diet on the performance and incidence of locomotor problems in broiler chickens. A completely randomized design was carried out in a 3 × 3 factorial scheme (3 levels of chondroitin sulfate -0, 0.05, and 0.10%; and 3 levels of glucosamine sulfate -0, 0.15, and 0.30%). Each treatment was composed of 6 replications of 30 broilers each. The performance of broilers (average weight, weight gain, feed intake, feed conversion, and productive viability) was assessed at 7, 21, 35, and 42 d of age, whereas the gait score, valgus and varus deviations, femoral degeneration, and tibial dyschondroplasia were assessed at 21 and 42 d of age. Increasing levels of glucosamine sulfate inclusion linearly increased the weight gain from 1 to 35 and from 1 to 42 d of age of broilers (P = 0.047 and P = 0.039, respectively), frequency of broilers with no femoral degeneration in the right and left femurs, and the proliferating cartilage area of proximal epiphysis at 42 d of age (P = 0.014, P < 0.0001, and P = 0.028, respectively). The increasing inclusion of chondroitin and glucosamine sulfates led to an increase in the frequency of broilers on the gait score scale 0 (P = 0.007 and P = 0.0001, respectively) and frequency of broilers with no valgus and varus deviations (P = 0.014 and P = 0.0002, respectively) also at 42 d of age. Thus, chondroitin and glucosamine sulfates can be used in the diet of broiler chickens to reduce their locomotor problems.

Protective effect of Astragaloside IV to inhibit thiram-induced tibial dyschondroplasia.

Tibial dyschondroplasia (TD) is most the common tibiotarsal bone disease in rapidly growing birds throughout the world. There is accumulating evidence that COX-2 abnormal expression in tibia plays an important role in TD progression. So, the regulation of COX-2 is an ever more appealing target for therapeutic intervention in TD. Astragaloside IV has an indispensable role in maintaining COX-2 expression in many diseases. So, we designed this study to use Astragaloside IV (AST-IV) against TD-affected chickens. A total of 180 Arbor Acres chickens were randomly divided in the control group, TD group, and Astr (AST-IV-treated chickens) group. During the experiment, mortality, feed conversion ratio, physiological changes, biochemical criterion, liver antioxidant enzymes, and gene expression of COX-2 were examined in all the chicken groups at various days. The results showed that AST-IV administration restored the growth performance and tibia lesions and decreased the mortality as compared with TD chickens. The biochemical criterion (ALP, AST, and ALT) of serum and liver antioxidant enzymes (SOD, GSH-Px, MDA, and T-AOC) improved after the administration of AST-IV. The COX-2 gene was upregulated significantly (P < 0.05) in TD chickens. Whereas, AST-IV treatment downregulated both gene and protein expression of COX-2 significantly (P < 0.05) in TD-affected chickens. AST-IV recovered tibial dyschondroplasia chickens by increasing the growth performance, ameliorating tibial cartilage damage, and decreasing COX-2 expression. In conclusion, AST-IV can be used to prevent thiram-induced TD in chickens.

Hsp90 inhibitor celastrol reinstates growth plate angiogenesis in thiram-induced tibial dyschondroplasia.

Tibial dyschondroplasia (TD) is an important long bone defect of broiler chickens that disturbs the proximal growth plate and is characterized by non-vascularized cartilage, a distended growth plate and lameness. Celastrol, a medicinal root extract from the plant Tripterygium wilfordii, is reported widely as a well-known heat-shock protein 90 (Hsp90) inhibitor. Recently, Hsp90 inhibition in chondrocyte differentiation and growth-plate vascularization were effective in restoring the morphology of the growth plate. The present study was aimed at investigating Hsp90 inhibition in TD using celastrol. The broiler chicks were divided into three groups; Control; TD induced (40 mg/kg thiram) and celastrol treatment. Hsp90, vascular endothelial growth factor and Flk-1 expressions were evaluated by quantitative real-time polymerase chain reaction and the protein levels of Hsp90 were measured by Western blot analysis. Antioxidant enzymes were determined to assess the liver damage caused by thiram and the protective effects of the medicine were evaluated by levels of serum biomarkers. The expression levels of Hsp90 and vascular endothelial growth factor mRNA transcripts were increased while Flk-1 receptor was decreased in TD-affected chicks. Celastrol therapy inhibited Hsp90 mRNA and protein levels and up-regulated the expressions of receptor Flk-1 in TD-affected tibial growth plates significantly (P < 0.05) in addition to rectifying the damaging effects of thiram on the liver by decreasing the levels of aspartate aminotransferase, alanine aminotransferase and malondialdehyde and correcting the oxidative imbalance. In conclusion, administering celastrol to dyschondroplastic chicks prevented un-vascularized growth plate, lameness and reinstated angiogenesis. Celastrol may be efficacious for the treatment of TD through the inhibition of Hsp90 expression and limiting the liver damage caused by thiram in broiler chickens.

Preimplantation genetic diagnosis (PGD)--prevention of the birth of children affected with endocrine diseases.

OBJECTIVE: To develop a reliable and accurate preimplantation genetic diagnosis (PGD) method in six families with endocrine diseases: persistent hyperinsulinemic hypoglycemia of infancy (PHHI), congenital adrenal hyperplasia (CAH) salt-wasting form, Sanjat-Sakati syndrome and multiple endocrine neoplasia 2A (MEN 2A). METHODS: For each disease a battery of at least four informative markers surrounding the tested gene were identified and for each family a protocol of multiplex fluorescent markers was developed and performed on single cells. RESULTS: PGD for PHHI was performed in three families. In family 1 two healthy children were born from different cycles, in family 2 three healthy children were born from two cycles, and in family 3 a healthy boy was born. For CAH in one family a healthy girl was born. One PGD cycle for Sanjat-Sakati resulted in a clinical pregnancy that was terminated due to high nuccal translucency (46X0). For one family with MEN 2A disease, the eighth PGD cycle resulted in birth of healthy twins. In all children genetic confirmation of the healthy status was performed. CONCLUSIONS: PGD is an effective method for preventing birth of affected children with endocrine disorders. Increasing the awareness of clinicians to the availability of these methods is most important.

Effects of non-antibiotic feed additives on performance, tibial dyschondroplasia incidence and tibia characteristics of broilers fed low-calcium diets.

This experiment was conducted to investigate and compare the efficacy of different feed additives on performance, tibial dyschondroplasia (TD) incidence and tibia characteristics of male broilers fed low-calcium diets. A completely randomized design, with six treatments and five replicates of five chicks per each was used. Experimental treatments were: (i) Basal diet containing recommended level of calcium (0.9%) as control treatment (Ctrl), (ii) low-calcium (0.67%) diet without any additive (LC), (iii) low-calcium diet + probiotic (2 g/kg diet), (iv) low-calcium diet + prebiotic (2 g/kg diet), (v) low-calcium diet + synbiotic [mix of probiotic and prebiotic (each 2 g/kg diet)], (vi) low-calcium diet + organic acid (1.5 g/kg diet). Birds were reared in an open-sided house system under natural tropical condition until 21 days of age. Feeding with low-calcium diet negatively influenced broiler performance (body weight, body weight gain and feed conversion ratio) and tibia characteristics, whereas dietary inclusion of all feed additives had beneficial effects on above-mentioned parameters and helped the birds to overcome problems related to low-calcium diets. Different treatments had no effect on TD incidence.

Effect of the level of cholecalciferol supplementation of broiler diets on the performance and tibial dyschondroplasia.

A study was conducted to evaluate four different cholecalciferol levels (NRC; modified), using diets supplemented with 200 (control), 1500, 2500 or 3500 IU/kg of cholecalciferol (VIT-D3). Each treatment was assigned to 3 pens of 17 broiler chicks of a commercial strain grown in an open-sided house with sidewall curtains. At 21 and 42 days, BW and feed conversion (FCR) were determined. At 42 days, five birds per pen were slaughtered to evaluate tibia and toe ash of the right leg, and incidence and severity of tibial dyschondroplasia (TD) of the left tibia and also measured dressing percentage and breast meat yield. Serum calcium and phosphorus concentrations were also determined. Haemagglutination inhibition antibody titre against Newcastle disease virus and lymphoid organs weight/body weight ratio were also determined. At both 21 and 42 days, the BW of birds fed 1500 IU/kg to 3500 IU/kg of VIT-D3 was significantly greater than birds fed 200 IU/kg. Similarly, better FCR was observed in birds those fed diets of high level of VIT-D3. No significant difference was observed for mortality at any age. Better dressing percentage and breast meat yield were noted in birds fed diets containing 2500 or 3500 IU/kg VIT-D3. Both tibia and toe ash contents were increased (p < 0.05) progressively with increased concentrations of cholecalciferol in feed. The incidence of TD (percentage of birds having TD scores greater than zero) was significantly (p < 0.05) influenced by level of 3500 IU VIT-D3/kg at 42 days. The severity of TD in birds fed diets containing 200 IU/kg VIT-D3 was apparently higher than birds fed diets with higher levels of VIT-D3. Concentrations of calcium and phosphorus minerals in the serum increased progressively with the high level of VIT-D3 supplementation to birds at both 21 and 42 days of age. Feeding levels of 1500 or 3500 IU of vitamin D3 did positively affect the immune system within the parameters measured. It may be concluded that performance, bone mineralization, blood chemistry and immunity against disease in broilers could be maintained when supplementing high level of VIT-D3 incorporated in broiler diets.

RNAi reduces expression and intracellular retention of mutant cartilage oligomeric matrix protein.

Mutations in cartilage oligomeric matrix protein (COMP), a large extracellular glycoprotein expressed in musculoskeletal tissues, cause two skeletal dysplasias, pseudoachondroplasia and multiple epiphyseal dysplasia. These mutations lead to massive intracellular retention of COMP, chondrocyte death and loss of growth plate chondrocytes that are necessary for linear growth. In contrast, COMP null mice have only minor growth plate abnormalities, normal growth and longevity. This suggests that reducing mutant and wild-type COMP expression in chondrocytes may prevent the toxic cellular phenotype causing the skeletal dysplasias. We tested this hypothesis using RNA interference to reduce steady state levels of COMP mRNA. A panel of shRNAs directed against COMP was tested. One shRNA (3B) reduced endogenous and recombinant COMP mRNA dramatically, regardless of expression levels. The activity of the shRNA against COMP mRNA was maintained for up to 10 weeks. We also demonstrate that this treatment reduced ER stress. Moreover, we show that reducing steady state levels of COMP mRNA alleviates intracellular retention of other extracellular matrix proteins associated with the pseudoachondroplasia cellular pathology. These findings are a proof of principle and the foundation for the development of a therapeutic intervention based on reduction of COMP expression.

Effect of diet with thiram on liver antioxidant capacity and tibial dyschondroplasia in broilers.

1. An experiment was conducted to study the effect of thiram on liver antioxidant capacity and incidence of tibial dyschondroplasia in broilers. 2. One hundred and twenty Avian commercial broilers were allotted at random to three treatments: control group, low thiram group (50 mg/kg) and high thiram group (100 mg/kg). 3. Blood samples were collected to determine the activity of AST (aspartate aminotransferase). At the end of the trial, broilers were killed and liver samples were collected to determine the activity of SOD (superoxide dismutase), GSH-Px (glutathione peroxidase) and MDA (malondialdehyde) content, while the right proximal tibiotarsi were dissected in longitudinal section for assessment of tibial dyschondroplasia (TD) incidence and TD score. 4. The results showed that thiram increased the incidence of TD and TD scores, increased serum AST activity and MDA content of liver, and decreased the activity of SOD and GSH-Px in the liver. 5. They suggest that thiram causes TD in broilers by reducing liver antioxidation capability and damaging liver function; this may be one of the mechanisms by which thiram causes TD in broilers.

Evaluation of the efficacy of vitamin D3 or its metabolites on thiram-induced tibial dyschondroplasia in chickens.

Two trials were conducted to determine if thiram-induced tibial dyschondroplasia (TD) in chickens was linked to a vitamin D deficiency and calcium homeostasis dysregulation, and whether feeding vitamin D fortified diets may prevent it. Day-old chickens were given grower diets containing different vitamin D products throughout the experiment until necropsy on day 16. Half of the birds in each feed group received thiram at levels of 100 ppm (trial 1) or 50 ppm (trial 2) between days 7-9 to induce TD. The birds were weighed, bled, and euthanized to determine TD incidences and severity by examining the growth plates. Tibial bones were used to measure biomechanical strength and ash content. Blood concentrations of 25-hydroxyvitamin D, Ca, P, alkaline phosphatase, and creatine kinase were measured in serum that showed no differences between different groups. Thiram reduced body weight and induced TD regardless of any vitamin D treatment to the same extent as untreated birds.

Osteochondrosis and copper: histology of articular cartilage from foals out of copper supplemented and non-supplemented dams.

Copper (Cu) supplementation of dams in late gestation may be protective against articular cartilage abnormalities in foals. Articular cartilage was harvested from 22 Thoroughbred foals at 160 days of age, at sites predisposed to osteochondrosis (OC), and examined for evidence of early cartilage abnormalities and established dyschondroplastic (DCP) lesions to determine if there were any significant differences due to mare Cu supplementation by injection during late gestation, or foal liver Cu concentration. Cu supplemented mares received calcium Cu edetate injections in late gestation (250 mg at around 220, 248, 276 and 304 days gestation, then every two weeks until foaling). Foals were euthanased at 160 days of age and articular cartilage was harvested from four defined sites. Samples were examined for histological appearance of chondrocytes after staining with haematoxylin and eosin, and were also stained with toluidine blue to indicate proteoglycan content. Alkaline phosphatase (ALP) activity was detected by histochemistry, and histocytochemical techniques were used to determine the expression of cathepsin B. Cu supplementation of the dam, or liver Cu concentration of the foal at birth or 160 days of age had no statistically significant effect on the frequency of cartilage irregularities observed grossly, or abnormalities detected histologically at four defined sites. ALP expression was similar in all samples. Cathepsin B expression varied between sites, and was seen in chondrocyte clusters. The intensity of toludine blue staining varied between sites. Minor histological cartilage abnormalities were observed in cartilage from clinically normal animals. These abnormalities might be 'early' dyschondroplastic lesions, which could resolve or progress. The role of Cu in the development, resolution or progression of dyschondroplastic lesions is poorly understood.

The effect of maternal dietary vitamin D3 supplementation on performance and tibial dyschondroplasia of broiler chicks.

A series of experiments was conducted to investigate the effects of maternal dietary vitamin D3 supplementation at 4 different times during the laying cycle, on the performance and bone quality of broiler chicks fed a diet that induced tibial dyschondroplasia (TD) or an adequate diet. Ross x Ross broiler breeder hens were fed a corn-soy diet with various levels of vitamin D3 from 24 to 66 wk of age. Eggs were collected at 39, 44, 53, and 64 wk of age and hatched. Chicks from hens fed 250 IU of D3/kg (low maternal D3 or LMD3) and 2,000 IU of D3/ kg (high maternal D3 or HMD3) levels were placed in battery brooders and fed the diets from 0 to 16 d. At 16 d, the chicks were weighed and killed; the left tibias were used for bone ash determinations, and the right tibias were used to score the incidence and severity of TD (0, 1, 2, or 3, where 3 is the most severe). Body weight gain and feed intake were significantly lower for the LMD3 chicks at wk 44 and 64, although there was no difference in weight at hatch. For the first 2 hatches (wk 39 and 44), the LMD3 and HMD3 chicks demonstrated high average TD scores (2.03 and 1.57 vs. 2.05 and 1.75 for the LMD3 vs. HMD3 chicks, respectively) and high average incidences of severe TD (50 and 35% vs. 45 and 34% for LMD3 vs. HMD3 levels, respectively). However, results from the last 2 hatches (wk 53 and 64) showed that HMD3 chicks, compared with LMD3 chicks, had reduced average TD scores (1.39 and 1.47 vs. 1.01 and 0.44 for LMD3 vs. HMD3 levels, respectively) and severe TD incidence (36 and 40% vs. 17 and 8% for the LMD3 vs. HMD3 levels, respectively). In this experiment, as egg production declined toward the end of the laying cycle, hens fed the HMD3 might have been able to deposit sufficient quantities of vitamin D3 in the egg to maintain excellent body weight gain at 16 d of age and reduce the incidence and severity of TD. Hens fed the LMD3 diet were unable to produce similar improvements.

High vitamin D3 requirements in broilers for bone quality and prevention of tibial dyschondroplasia and interactions with dietary calcium, available phosphorus and vitamin A.

1. Two experiments were carried out to investigate responses in performance and bone compositional and structural characteristics in broilers fed diets containing 4 concentrations of vitamin D3 (5, 20, 125 and 250 microg cholecalciferol/kg) at different concentrations of calcium, available phosphorus and vitamin A. 2. In experiment 1, body weight and tibia breaking strength were maximised at 14d with 250 microg vitamin D3/kg, tibia ash was maximised with 125 microg vitamin D3/kg. A high incidence of tibial dyschondroplasia (TD) was decreased to very low levels with 125 microg vitamin D/kg. 3. At 42d, performance and bone characteristics showed no response to vitamin D3 concentrations above 20 microg/kg. 4. Dietary vitamin A within the range 2-4 to 4.5 mg retinol/kg did not show any interaction with vitamin D3 status at either age. 5. In experiment 2, responses to vitamin D3 were strongly influenced by dietary calcium/available phosphorus. With 13 g calcium and 5 g available phosphorus/kg, performance and bone characteristics responded to vitamin D3 concentrations up to 125 microg/kg but more was needed at less optimal concentrations of calcium and available phosphorus. TD incidence was minimised with 250 microg/kg. 6. This study shows that high dietary concentrations of vitamin D3 can prevent TD. It is concluded that the vitamin D3 requirement of broilers up to 14 d of age at optimal dietary calcium and available phosphorus concentrations may be in the range 35 to 50 microg/kg for cortical bone quality and up to 250 microg/kg for prevention of TD. The vitamin D3 requirement for cortical bone quality after 14 d is not higher than 20 microg/kg. These requirements are much higher than earlier estimates and may be related to higher calcium requirements of modern broiler genotypes. Current regulations limiting maximum vitamin D3 concentrations in broiler starter diets may need to be reviewed.

Effect of casein phosphopeptide and 25-hydroxycholecalciferol on tibial dyschondroplasia in growing broiler chickens.

1. An experiment was conducted to investigate the influence of dietary casein phosphopeptides and 25-hydroxycholecalciferol on the incidence of tibial dyschondroplasia (TD) in 14-d-old commercial broiler chickens. 2. Three hundred and twenty broiler chicks (one day old) were randomly allocated to one of 4 dietary treatments. A standard broiler diet was used as the control with the three experimental treatments receiving the control diet supplemented with 10 g casein phosphopeptide/kg, 14 g casein phosphopeptide/kg or 69 microg 25-hydroxycholecalciferol/kg. 3. Those birds fed the diets supplemented with 14g casein phosphopeptide/kg or 25-hydroxycholecalciferol had a lower incidence of TD than both the control and 10g casein phosphopeptide/kg treatments when assessed grossly. 4. The body weight of birds fed the 10 g casein phosphopeptide/kg diet or the 25-hydroxycholecalciferol diet was higher than birds fed the control diet. Although not significant, the body weight of birds fed the 14 g casein phosphopeptide/kg diet was also greater than the control birds. 5. The current experiment demonstrated that both casein phosphopeptide and 25-hydroxycholecalciferol can reduce the incidence of TD in the young broiler chicken. More research is required to explain the unexpected increase in body weight described above.

Effectiveness of twenty-five-hydroxycholecalciferol in the prevention of tibial dyschondroplasia in Ross cockerels depends on dietary calcium level.

Five experiments were conducted to evaluate the efficacy of 25-hydroxycholecalciferol [25-(OH)D3] to minimize the development of tibial dyschondroplasia (TD) and improve phytate phosphorus retention in Ross cockerels during the starter period. In experiment 1, chicks were fed a TD-inducing (0.67% calcium) diet with or without exposure to ultraviolet light and no supplemental cholecalciferol. Dietary 25-(OH)D3 was added at 0, 10, or 70 microg/kg for both light treatments. In experiment 2, 25-(OH)D3 was added at 0, 10, 40, or 70 microg/kg to a TD-inducing diet containing 27.5 microg/kg added cholecalciferol. Experiment 3 was similar to experiment 2 except a diet marginal (0.85%) in calcium was fed, and cholecalciferol was added at 55 microg/kg. In experiments 4 and 5, 25-(OH)D3 was added at 0, 18, 36, 54, 72, or 90 microg/kg to a diet marginal in calcium. Dietary 25-(OH)D3 decreased the incidence of TD similarly at 40 and 70 microg/kg 25-(OH)D3 and improved phytate phosphorus retention when the TD-inducing diet was fed. The incidence of TD was decreased when 70 microg/kg 25-(OH)D3 was added to a diet marginal in calcium in experiment 3 only. Phytate phosphorus retention was generally not affected by dietary 25-(OH)D3 when a diet containing marginal calcium, adequate phosphorus, and high cholecalciferol was fed. The effectiveness of 25-(OH)D3 to reduce the incidence of TD in young broilers was higher when the dietary calcium level was below 0.85%. The incidence of TD in Ross cockerels was low (< 25%) when dietary calcium was greater than 0.85%.

Effects of u.v. irradiation of very young chickens on growth and bone development.

Six experiments were conducted to study the effects of exposure of young chickens to u.v. radiation. Chickens were fed a cholecalciferol (D3)-deficient diet and exposed to u.v. radiation from fluorescent lights giving total radiance (285-365 nm) at 0.15 m of 99.9 mJ/s per m(2). In Expt 1, chickens had increased body weight, bone ash and plasma Ca and decreased incidence of rickets and tibial dyschondroplasia (TD) when exposed to fluorescent light radiation 24 h per d, 24 h every 2 d, or 24 h every 3 d starting with exposure on day 1 after hatching. However, when not exposed on day 1, but on days 4, 7, 10, 13 and 16, the bone ash was reduced, and the incidence of TD and rickets was increased, compared with chickens exposed on day 1 after hatching. When chickens were exposed at 1 d of age to radiation from two lamps, each of which gave a radiance (285-365 nm) at 0.26 m of 856 mJ/s per m(2), both the length of time of radiation and location of the lamps (above or below the chicken) influenced the response as measured by body weight, bone ash, plasma Ca and incidence of rickets. When chickens that received a TD-inducing diet were exposed to 30 min u.v. radiation from below at 1 d of age they developed significantly less TD than did those not exposed when fed either 27.5 or 55.0 microg D3/kg diet.

Effect of antibiotics on in vitro and in vivo avian cartilage degradation.

Antibiotics are used in the livestock industry not only to treat disease but also to promote growth and increase feed efficiency in less than ideal sanitary conditions. However, certain antibiotic families utilized in the poultry industry have recently been found to adversely affect bone formation and cartilage metabolism in dogs, rats, and humans. Therefore, the first objective of this study was to determine if certain antibiotics used in the poultry industry would inhibit in vitro cartilage degradation. The second objective was to determine if the antibiotics found to inhibit in vitro cartilage degradation also induced tibial dyschondroplasia in growing broilers. Ten antibiotics were studied by an avian explant culture system that is designed to completely degrade tibiae over 16 days. Lincomycin, tylosin tartrate, gentamicin, erythromycin, and neomycin sulfate did not inhibit degradation at any concentration tested. Doxycycline (200 microg/ml), oxytetracycline (200 microg/ml), enrofloxacin (200 and 400 microg/ml), ceftiofur (400 microg/ml), and salinomycin (10 microg/ml) prevented complete cartilage degradation for up to 30 days in culture. Thus, some of the antibiotics did inhibit cartilage degradation in developing bone. Day-old chicks were then administered the five antibiotics at 25%, 100%, or 400% above their recommended dose levels and raised until 21 days of age. Thiram, a fungicide known to induce experimental tibial dyschondroplasia (TD), was given at 20 ppm. Birds were then killed by cervical dislocation, and each proximal tibiotarsus was visually examined for TD lesions. The results showed that none of these antibiotics significantly induced TD in growing boilers at any concentration tested, whereas birds given 20 ppm thiram had a 92% incidence rate.

Influence of dietary phytase supplementation on incidence and severity in broilers divergently selected for tibial dyschondroplasia.

A study was conducted to determine the effect of dietary supplementation of phytase on the incidence and severity of tibial dyschondroplasia (TD) in chickens selected for high (HTD) and low (LTD) incidences of TD for 11 generations. By feeding a phosphorus-deficient diet (0.1% nonphytate phosphorous; nPP), HTD and LTD chickens were further identified as high-sensitivity birds (HS) and low-sensitivity birds (LS) to phosphorus deficiency based on mortality. Two hundred forty 1-d-old chicks from HTD and LTD lines (five replications of four birds per treatment) were randomly assigned to a control diet with 0.5% nPP and two treatment diets (0.1% nPP) with and without 600 phytase units (FTU) Natuphos phytase/kg. Feed consumption and growth rate were measured for 3 wk, and both tibiae were scored for TD incidence, average TD score, and total number of TD lesions with the most severe form of the abnormality (lesions that were scored 3). The addition of phytase had no influence on TD incidence and lesion scores of 3 in HTD chicks. However, a nonsignificant reduction in TD incidence (P = 0.07), TD score, and no. 3 lesions (P < or = 0.01) were observed in LTD chicks. Interactions between sensitivity (to P deficiency) and phytase (P < or = 0.01) and sensitivity and nPP (P < or = 0.01) were observed for no. 3 scores in LTD chicks. These results indicate that phytase was effective in reducing TD incidence and severity in LTD chicks but not in HTD chicks.

Nutrition and skeletal problems in poultry.

Several excellent reviews regarding nutrition and skeletal disorders have appeared in the last 20 yr. This review will cover several areas of vitamin D research, the area of feed deprivation, and bone abnormalities, because there has been considerable interest in these areas during the past 10 yr. Studies indicate that the quantitative requirement for cholecalciferol (D3) for broiler chickens is much greater than previously thought. Ascorbic acid may play a role in stimulating 1-hydroxylation of 25-hydroxycholecalciferol [25-(OH)D3], but the evidence is not clear under exactly what conditions this relationship is important in practical prevention of tibial dyschondroplasia. Studies indicate that dietary supplementation with 1,25-dihydroxycholecalciferol [1,25(OH)2D3] will reduce the incidence of tibial dyschondroplasia in three different strains of broilers bred to develop a high incidence of the disease. But it did not prevent the disease totally in the strains, unless high enough levels of 1,25-(OH)2D3 were fed to reduce growth rate. These studies indicate that these high tibial dyschondroplasia strains have a defect(s) in vitamin D metabolism. Studies continue to elucidate the role of ultraviolet light in preventing leg abnormalities. Only a few studies have been conducted on the efficacy of various vitamin D3 derivatives to prevent tibial dyschondroplasia. Feed deprivation continues to be an intriguing method of preventing tibial dyschondroplasia, and examination of exactly how this prevents the bone abnormality could open avenues for explaining the disease.

Nutrition: the integrative science.

1. Nutrition is a vitally important part of the production environment but also interacts with many other disciplines. 2. Modern breeding methods involving selection for a wider range of characteristics are likely to result in new genotypes with different nutritional needs. Geneticists and nutritionists will have to work closely together in the future to identify nutritional needs of these birds. 3. Collaboration between nutrition and other disciplines has been important in maintaining efficient poultry production and health and preventing or alleviating a number of metabolic disorders 4. There are many new challenges facing nutritionists to maintain health and performance in flocks under more exacting standards of bird welfare and human health. 5. A vigorous contribution from nutritional science and research will continue to be important for the future well-being of the poultry industry.