Tibial Dyschondroplasia in Broilers

Tibial Dyschondroplasia in Broilers - A Review

M. M. Chawak. M. R. Reddy, M.V.L.N. Raju and S.V.R. Rao
Project Directorate on Poultry, Hyderabad .

Tibial Dyschondroplasia (TD) is a common cause of lameness in broilers. In the JUS it has been estimated that because of TD, monetary losses in the poultry industry were over S 200 mill­ion/year (Edwarda, 1983) In Australia . it has been reported that broilers with TD may lead to femora I head necrosis and Osteomyelitis in poultry (Lynch etal , 1992).

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The unique aspect of TD is that it occurs during the very early stages of growth, before other visible changes in bone structure or morphology occurs, which is associated with physiological changes because of enhanced early relative growth in broilers. In flocks of 36daysand over, 5-16% of chickens may o« affected. The chicken with severe lesions walks with difficulty.

The TD is grossly identified as large mass of unvascularized cartilage originating from the growth plate, primarily in the proximal tibia tarsus of young growing chickens, ducks and turkeys and the abnormal masses of cartilage in the proximal tibia tend to .be cone shaped,

Various factors responsible for development of TD in chickens are asfollows:

GENETIC FACTORS:

The available data indicate that TD Is positively correlated to increased rate of body weight gain. Sheridan et at (1978) suggested that the TD can be associated with e major sex linked recessive gene. The genetic influence on the incidence of TD has been dem­onstrated by selection for and against the presence of lesions (Laach and Nesheim, 1936. Riddell. 1976). Comparisons have also been made of the incidence of TD in commercially available broiler strains, broiler and leghorn strains and in mates and females (Leach and Nesheim, 1965). Sauveur and Mongin, (1976) reported that TD can be eliminated in broilers in Just 3 generations through selection. it is now well established that the susceptibility to skeletal deformities including TD can be influenced by genetic selection.

NUTRITIONAL FACTORS:

Lilburn et al. (1983) observed a consistent trend towards lower TD incidence where the Ca/P ratio was increased by reducing the available phosphorus level in the diet. It is thus possible that the Ca/P ratio is a factor in causing TD and a value of Cal avai­lable P lower than 2 would be critical. The electrolytes equilibrium has an imp­ortant role in TD. Metabolic acidosis induced by ammonium chloride (Leach and Neishelm. 1975) or by simple ex­cess of chloride relative to sodium and potassium (Sauveur and Mohgin, 1874, Riddell, 1975) increased the TD inci­dence. Sauveur et al. (1977) have shown that metabolic acidosis causes impairment in vitamin 03 metabolism which could be implied in TD

Dietary excesses of amino acids like homocystine, cystine and cystine but not methionine, were shown lo induce TD. Cysteine is found in poultry diets at various levels depending on dietary ingredient sources. For exam­ple, feather meal contains approxima­tely 4% cysteine. The addition of 5% feather meal in a diet would increase dietary cysteine above typical levels found in corn soyabean meal based diets (0.34% cysteine) and leads to a linear increase in the Incidence of TD (Orth et al.. 1992; Bal et al.. 1994).

Mycotoxins, particularly from Fusarium equiseti (Pathar et al., 1986) and Fusarium exysporium (Chuetal.,1993) causes TD. The compound Thirum which is used as antifungal agent for treatment of corn seed was also found to be potent inducer of the lesion. (Vargus et al 1983).

Rapid waiht gain has been impli­cated as one of the important causes of leg abnormalities ' including Tb/in meat type fowl (Nestor. 1984) Bata is available to both confirm and refute this hypothesis. Considering this hypothesis if steps are taken to reduce growth rate to less than the genetic potential, then incidence of TD can be reduced or eliminated. But obviously this is not an economically feasible solution for the problem. Still attempts can be made to reduce skeletal defects i by altering the growth through subject­ing the birds to quantitative (Edwards. and Sorenson.1987) or qualitative (Have and Simons. 1978) feed restriction programme in the early phase of growth. These will stow down rate of gain during the early stages of growth and thereby allow for optimum skeletal growth.

CONCLUSIONS:

Extensive research work has been conducted during the past fifty years towards the control and reduction of leg disorders in poultry. It is evident from the studies that there is no single solution to the problem. However, substantial gains have been made towards reducing the incidence of leg disorders especially through better understanding of the nutritional and pathological aspects of the issue. Nevertheless, continued research on multidisciplinary basis is needed involving geneticists, nutritionists, pathologists, physiologists and environmenital /managerial specialists for making the total elimination of leg disorders from the flock, a reality.