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Lameness in Poultry - Role of Nutrition

S. Venkata Ramarao, M.V.L.N. Raju. M.M. Chawak & NX. Praharaj
Project Directorate on Poultry, Hyderabad .

Nutritionally well balanced diet together with good management is required to obtain optimum performance in terms of high body weight gain and livability in broilers and high egg production with low layer house mortality in layers. Breeding primarily for high growth rate in broilers, as has been practiced by many breeders, has the inherent major drawback of concomitant increase in the incidence of leg abnormalities (Wise and Jennings, 1972). Selection for meat yield or increased meat to bone ratio is probably an indirect negative selection for the absolute amount of skeleton. Thus, the incidence of leg weakness has alarmingly increased in today's fast growing commercial broiler flocks. Therefore, the need for provision of adequate dietary levels of various nutrients that influence the leg weakness has acquired greater significance.

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Birds affected with lameness weighed approximately 25% less than normal birds at 8 weeks of age (El Boushy, 1974), mainly due to reduced feed and water consumption. The anatomical difficulty in free movement and dominance of normal birds make the lame birds deprived of normal feeding and watering.

Further, broilers with lameness were difficult to eviscerate properly with the automatic eviscerating machines (Burton et al., 1981), thereby rendering them liable for discard, despite better body weights.

Chondrodystrophy, Tibial Dyschondroplasia and Rickets, are the most commonly encountered conditions responsible for lameness in commercial Poultry.

Chondrodystrophy (Perosis / Slipped Tendon)

Chondrodystrophy which was otherwise popular as Perosis is a condition characterized by enlargement of hock joint, twisting or bending of the distal end of tibia and proximal end of metatarsus and the frequent slipping of Achilles tendon from its position in the intercondyloid fossa, found at the rear to the hock joint (Norris and Scott, 1965). Wolbach and Hegsted (1953) described Perosis as an affliction of the epiphyll seal cartilage whereby a significant increase in the width of the cartilage plate occur in conjunction with reduction in visualization. This condition is precipitated by a wide range of nutritional deficiencies primarily like manganese (Wilgus et al., 1936), zinc (Young et al., 1958) and choline (Jukes, 1940). Deficiency of Vitamin E (Scott, 1953).niacin (Hunt and Me Ginnis. 1959). Biotin (Jukes and Bird, 1942), folic acid (Darnel et al., 1946) and pyridoxine (Gries an& Scott, 1972) also induced this condition. Perosis may also occur in Vitamin B deficient chicks, when the sources of methyl groups like choline, methionine or beanie are also inadequate in the diet. Contrary to this concept Schaefer et al., (1950) showed that Vitamin B helped to prevent Perosis in chicks fed intermediate levels of folic acid but that folic acid at high levels was effective without the use of supplementary vitamin B,; and further concluded that Vitamin B can't be considered as an anti paretic factor.

The main difference between Niacin induced Perosis and the Perosis of Manganese or Choline deficiency is that in nicotinic acid deficiency the tendon of Achilles rarely slips from its condyle (Scott and Heuser, 1954), Marginal deficiency of Pyridoxine combined with 31% protein caused severe Perosis characterized by a disorganized Vesicular zone of the epiphysis cartilage of the tars metatarsal joint and uneven vascular invasion of the plate (Gries and Scott, 1972).

Perosis caused by choline deficiency is characterized by pinpoint hemorrhages and a slight puffiness around the hock joint, followed by an apparent flattening of the joint caused by a rotation of the metatarsus. The metatarsus continues to twist and may become bent or bowed so that it is out of alignment with the tibia, subsequently the tendon of Achilles slips from its condyle. Excessive amounts of MgCO 3 resulted in Perosis (Schaible et al., 1933).

The incidence of Chondrodystrophy can be greatly reduced but not completely prevented when higher levels of manganese (MnSo 4 5H 2O; or MnCO 3) are included in the diet. Wilgus et al., (1936) noticed substantial antiperotic activity of Manganese in chickens. Jukes (1940) and Wolbach and Hegsted, (1953) could prevent Chondrodystrophy by addition of choline to a diet deficient in choline and containing adequate levels of manganese. Injection of biotin could alleviate clinical Perosis (Jukes and Bird, 1942). Nicotinic acid supplementation has little or no effect on cases progressed to the extent of slipping of tendon from its condyle or on advanced cases of "enlarged hock disorder" in adult torn turkeys (Scott et al., 1978). Schaiable et al., (1933) observed Perosis (Slipped tendon) in chick fed excess amounts of Magnesium Carbonate. Schaefer et al.. (1950) showed that folic acid was required in addition to choline for the prevention of Perosis.

Supplementing a diet with vitamin B @ 1.9 mg/kg diet could reduce the incidence of Chondrodystrophy (Scott et al., 1978, dries and Scott, 1972; Beiroe and Jensen, 1981) and levels in excess of 3.1 mg/kg diet resulted in an almost elimination of perotic symptoms. It is suggested that Vitamin B is required in the formation of Picolinic acid. Which facilitate Zn absorption from intestine (Evans, 1980). By adding saturated fatty acids, high levels of Vitamin. E or Inclpmetbacin, Bettger et al., (1980) reduced Chondrodystrophy caused by Zn deficiency.

Tibial Dyschondroplasia (Osteochondrosis):

Tibial dyschondroplasia (TD) is characterized by the persistence of a cartilage plug in the proximal metaphysics of tibiotarsus Gone and associated faulty metanhyseal visualization. TD is often associated with Tibial fractures on the processing machine. This condition was first described by Leach and Nescheim (1965), who reported that the incidence was influenced by nutrition and genetic selection.

Although the cause of Tibial dyschondroplasia has been strongly linked to genetics, it is apparent that nutritional factors are also involved. Chicks fed a purified diet containing all known nutrients produced high incidence of tibial dyschondroplasia, which could be reduced by substituting, 20%- 30% of maize in a purified (net (Leach and Nescheim, 1965). The same workers later (1972) noticed rapid increase in the incidence of tibial dyschondroplasia following incorporation of ammonium chloride into the chick diet. Sauveur and Mongin (1974) reported that increasing the chloride content of diet enhanced the incidence of cartilage abnormalities when Sodium and Potassium levels were low. They felt that excess chloride induced metabolic acidosis and therefore influenced the occurrence of tibial dyschondroplasia. Sauveur et al., (1977) revealed that chronic metabolic acidosis did alter the renal metabolism of vitamin D. To prevent this condition chlorine requirement of 0.12% was found to be optimum with a purified diet containing 0.24% sodium and 0.4% potassium. Trace elements like copper deficiency also results in a cartilage defect similar to TD (Carlton and headperson, 1964).

The only known way of completely elimi­nating the occurrence of TD is to reduce growth rate, and it was first reported in literature by Wise and Nott (1975). Obviously, this is not a very acceptable solution for the economic production.

Poulos et al., (1978) observed that TD incidence and growth rate were significantly higher on the birds fed on high energy feed (3 090 Kcal, ME/Kg.) than those on low energy diet (2850 Kcal ME/Kg). This finding is in agreement with Yoshida et al, (1973), who prevented occurrence of twisted legs by decreasing dietary energy through addition of cellulose.

Hulan et al, (1980) observed reduced incidence of leg abnormalities without reduction of body weight in broilers reared to roaster weight using low protein levels.

Walser et al, (1980) obtained 90% of TD incidence by incorporating Fusarium roseum contaminated grain in a diet, at 2% level. Where as Aspergillus flavus Parasiticus ingrain did not cause increased incidence of TD. This might be due to decreased body weight of birds fed Altatoxin (Huff, 1980).

Edwards (1982) suggested that a low Ca/P ratio due to a low Ca level would increase the TD incidence. In support of this, Ulbrun et al., (1983) observed a consistent trend towards lower TD incidence when the Ca/P ratio was increased by reducing the available phosphorus level in the diet.

Rickets/ Osteomalacia:

Rickets is the term used to describe the symptoms associated with a deficiency of Vitamin D or calcium, and is characterized by widening and disorganization of the epiphysis cartilage accompanied by a decrease in blood supply to the region (Pierson and Hester, 1982). Tameness occurs when the ends of the long bones become enlarged and exceedingly flexible due to improper calcification. This often facilitates the development of a bowed appearance, most no­ticeable at the proximal end of tibia (Wise, 1975). During the periods of extreme leg weakness the hens show a characteristic posture which has been described as a "Penguin type Squat".

Calcium (Ca) deficiency in layers results in depletion of Ca from mediullary bone, followed by cortical bone. Finally the bones be­come so thin that spontaneous fractures may occur, in long bones like tibia and femur. This condition may be called as "Cage layer fatigue" (Riddell et al, 1968). Isolated soybean protein and raw soybean meal were found to possess rachitogenic properties when fed to turkey pouts during first week of age (Carison et al. 1964). These effects could largely be eliminated by supplementation with 8 to 10 times the normal dietary level of Vitamin D or by autoclaving the Soybean fractions. Feeding a single massive dose of 15.000 IU Vitamin D cured rachitic chicks more promptly than using generous levels of Vitamin D, in diet (Hooper et al., 1942). Jensen (1968) reported that the occurrence of leg abnormalities among turkeys raised to 20 weeks of age was greater for those receiving 0.65% dietary phosphorus (P) during the first 8 weeks post hatch than those receiving 0.9% P. No malformation of the leg bones has been reported as a result of Magnesium (Mg) deficiency. However, excess of Mg increases the P requirement (Lee and Brittoh, 1980) and lead to shortened and bowed tibias with rachitic like lesions in the growth plates (Lee etal. 1980).

Rye grains contain a rachitogenic factor (Mac Auliffe et al., 1976) which can be largely overcome by either addition of a high level of Vitamin D in the diet, water extraction, acid auto claving or gamma irradiation. Additions of tallow or Penicillin also have a partial corrective effect,

Miscellaneous Leg Abnormalities:

Rapeseed meal (20 -30%) in a starter diet increased the frequency of leg deformities in broiler chicks (Holmes and Roberts, 1963; Seth and Clandinin, 1973) and turkey poults (Moody et al., 1978). The new low glucosinalate varieties of rapeseed induced less leg problems than the old ones (Moody etal-, 1978;). It is supposed that tannins orphytic acid contained in rapeseed meal act by binding some metal Ions (Zn.).

Leg weakness incidence in chicks increased with dietary lupine content (Vogt. et al., 1979; Lacassagne, 1982). This condition was not improved by treatment of the grains (extrusion, granulation or dehulling) or by tryptophan supplementation. Supplementation a lupindiet with 0.6 or I ppm of folic acid partly corrected the lupin effect on leg weakness (Lacassagne, 1982). Addition of yeasts or bacteria, riboflavin, vitamin mixture or histidin corrected leg weakness induced by lupin (Lacassagne, 1982).

According to Beime and Jensen (1979), the incidence of twisted legs in broilers de­creased from 29 to 18 when their mothers were fed on a diet containing 20% distillers dried grains. High tannin sorghum increased the incidence of leg problems characterized by enlarged hock and bending of the proximal tibial termini (Armstrong et al., 1973). Chicks fed diets infested with Aspergillus and Fusarium demonstrated a leg abnormality characterized as being "Knock-Kneed" or "Cow boy in appearance (Sharby et al., 1972). Aspergillus might act through libera­tion of aflatoxin, 1 ppm of which increases the Vitamin D, requirement by 9 lU/kg. of diet (Bird, 1978).

Leg abnormalities (bowed legs with swol­len nocks) were noted in chicks led high tannin sorghum grain diets (Rostagno et al., 1973; Armstrong etal., 1973). This action seems to be due to reduced rate of collagen synthesis (Elkin et al., 1978) and was almost suppressed after deactivation of sorghum tannins by high moisture storage (Blairand Mitaru, 1983).

Chlorine deficient birds, when startled fell forwards with their feet out stretched behind them and remained parlayed for several minutes, then appeared quite normal until they were frightened again. (Scot et al., 1978).


Nutrition plays a significant role in pre­venting and correcting the incidence of leg abnormalities in fast growing chicken. Chondrodystrophy, occur due to deficiency of Mn, Zn, Choline, Vitamin E niacin, biotin, folic acid and pyridoxine and also to some extent Vitamin B 12 presence of ammonium chloride, high toxic levels of chloride, copper deficiency, high energy and protein levels, contamination with fungi and low calcium/phosphorus ratio in the diet lead to tibial dyschondroplasia. Rickets/Osteomalacia is primarily a result of Ca and/or Vitamin D deficiency is primarily a result of Ca and/or Vitamin D 3 deficiency and feeding raw soyabean, rye or excess Mg also predispose the birds to the disease.

Provision of the required nutrients at optimum levels and elimination of predisposing factors are the effective measures in preventing lameness.