Deleted - that was an old recall. Sorry.
-Kathy
-Kathy
Last edited:
Chicken can't walk
- Thread starter Olson
- Start date
Welcome to BYC. It's possible that your chicks may be dealing with a vitamin deficiency, or a disease called avian encephalomyelitis. Mareks is also a possibility, but they may be on the young side for symptoms of that to show up. I would go get some poultry vitamins from your feed store, and start putting them in the water every day. Here is some reading about avian encephalomyelitis and a good long link on Mareks Disease:
http://www.merckmanuals.com/vet/pou...itis/overview_of_avian_encephalomyelitis.html
https://www.backyardchickens.com/a/the-great-big-giant-mareks-disease-faq
http://www.merckmanuals.com/vet/pou...itis/overview_of_avian_encephalomyelitis.html
https://www.backyardchickens.com/a/the-great-big-giant-mareks-disease-faq
Here are some videos of chicks with Avian encephalomyelitis:
-Kathy
-Kathy
This is what I would look at:
http://www.merckmanuals.com/vet/pou..._poultry/vitamin_deficiencies_in_poultry.html
Vitamin D3 Deficiency
Abnormal development of the bones is discussed under calcium and phosphorus imbalances (see Calcium and Phosphorus Imbalances) and manganese deficiency (see Manganese Deficiency). Vitamin D3 is required for the normal absorption and metabolism of calcium and phosphorus. A deficiency can result in rickets in young growing chickens or in osteoporosis and poor eggshell quality in laying hens, even though the diet may be well supplied with calcium and phosphorus.
Laying hens fed a vitamin D3-deficient diet show loss of egg production within 2–3 wk, and depending on the degree of deficiency, shell quality deteriorates almost instantly. Using a corn-soybean meal diet with no supplemental vitamin D3, shell weight decreases dramatically by about 150 mg/day within 7 days. The less obvious decline in shell quality with suboptimal supplements is more difficult to diagnose, especially because it is very difficult to assay vitamin D3 in complete feeds.
There is a significant increase in plasma 1,25(OH)2D3 of birds producing good versus poor eggshells. Feeding purified 1,25(OH)2D3 improves the shell quality of these inferior layers, suggesting a potential inherent problem with metabolism of cholecalciferol.
Retarded growth and severe leg weakness are the first signs noted when chicks are deficient in vitamin D3. Beaks and claws become soft and pliable. Chicks may have trouble walking and will take a few steps before squatting on their hocks. While resting, they often sway from side to side, suggesting loss of equilibrium. Feathering is usually poor, and an abnormal banding of feathers may be seen in colored breeds. With chronic vitamin D3 deficiency, marked skeletal disorders are noted. The spinal column may bend downward and the sternum may deviate to one side. These structural changes reduce the size of the thorax, with subsequent crowding of the internal organs. A characteristic finding in chicks is a beading of the ribs at the junction of the spinal column along with a downward and posterior bending. Poor calcification can also be seen at the epiphysis of the tibia and femur. By dipping the split bone in a silver nitrate solution and allowing it to stand under an incandescent light for a few minutes, the calcified areas are easily distinguished from the areas of cartilage. Adding synthetic 1,25(OH)2D3 to the diet of susceptible chicks reduces the incidence of this condition. Although the response is variable, results suggest that some leg abnormalities may be a consequence of inefficient metabolism of cholecalciferol.
In the laying hen, signs of gross pathology are usually confined to the bones and parathyroid glands. Bones are soft and easily broken, and the ribs may become beaded. The ribs may also show spontaneous fractures in the sternovertebral region. Histologic examination shows deficiency of calcification in the long bones, with excess of osteoid tissue and parathyroid enlargement.
Enough vitamin D is added to commercial diets to provide 3 times the normally recommended level for a period of ~3 wk. Dry, stabilized forms of vitamin D3 are recommended to treat deficiencies. In cases of severe mycotoxicosis, a water-miscible form of vitamin D is administered in the drinking water to provide the amount normally supplied in the diet.
Vitamin E Deficiency
The 3 main disorders seen in chicks deficient in vitamin E are encephalomalacia, exudative diathesis, and muscular dystrophy. The occurrence of these conditions depends on various dietary and environmental factors.
Encephalomalacia is seen in commercial flocks if diets are low in vitamin E, if an antioxidant is either omitted or is not present in sufficient quantities, or if the diet contains a reasonably high level of an unstable, unsaturated fat. For exudative diathesis to occur, the diet must be deficient in both vitamin E and selenium. Signs of muscular dystrophy are rare in chicks, as the diet must be deficient in both sulfur amino acids and vitamin E. Because the sulfur amino acids are necessary for growth, a deficiency severe enough to induce muscular dystrophy is unlikely to occur under commercial conditions. Signs of exudative diathesis and muscular dystrophy can be reversed in chicks by supplementing the diet with liberal amounts of vitamin E, if the deficiency is not too advanced. Encephalomalacia may respond to vitamin E supplementation, depending on the extent of the damage to the cerebellum.
The classical sign of encephalomalacia is ataxia. The results from hemorrhage and edema within the molecular and granular layers of the cerebellum, with pyknosis and eventual disappearance of the Purkinje cells and separation of the molecular and granular layers of the cerebellar folia. Due to its inherently low level of vitamin E, the cerebellum is particularly susceptible to lipid peroxidation. In prevention of encephalomalacia, vitamin E functions as a biologic antioxidant. The quantitative need for vitamin E for this function depends on the amount of linoleic acid and polyunsaturated fatty acids in the diet. Over prolonged periods, antioxidants have been shown to prevent encephalomalacia in chicks when added to diets with very low levels of vitamin E or in chicks fed vitamin E-depleted purified diets. Chicks hatched from breeders that are given additional dietary vitamin E are also less susceptible to lipid peroxidation in the brain. The fact that antioxidants can help prevent encephalomalacia, but fail to prevent exudative diathesis or muscular dystrophy in chicks, strongly suggests that vitamin E is acting as an antioxidant. Exudative diathesis results in a severe edema caused by a marked increase in capillary permeability. Electrophoretic patterns of the blood show a decrease in albumin levels, whereas exudative fluids contained a protein pattern similar to that of normal blood plasma.
Vitamin E deficiency accompanied by sulfur amino acid deficiency results in severe muscular dystrophy in chicks by ~4 wk of age. This condition is characterized by degeneration of the muscle fibers, usually in the breast but sometimes also in the leg muscles. Histologic examination shows Zenker's degeneration, with perivascular infiltration and marked accumulation of infiltrated eosinophils, lymphocytes, and histocytes. Accumulation of these cells in dystrophic tissue results in an increase in lysosomal enzymes, which appear to function in the breakdown and removal of the products of dystrophic degeneration. Initial studies involving the effects of dietary vitamin E on muscular dystrophy showed that the addition of selenium at 1–5 mg/kg diet reduced the incidence of muscular dystrophy in chicks receiving a vitamin E-deficient diet that was low in methionine and cysteine, but did not completely prevent the disease. However, selenium was completely effective in preventing muscular dystrophy in chicks when the diet contained a low level of vitamin E, which alone had been shown to have no effect on the disease.
Studies with chicks on the interrelationships between antioxidants, linoleic acid, selenium, and sulfur amino acids have shown that selenium and vitamin E play supportive roles in several processes, one of which involves cysteine metabolism and its role in the prevention of muscular dystrophy in the chicken. Glutathione peroxidase is soluble and is located in the aqueous portions of the cell, while vitamin E is located mainly in the hydrophobic environments of membranes and in lipid storage cells. The overlapping manner in which vitamin E and selenium function in the cellular antioxidant system suggest that they spare one another in the prevention of deficiency signs.
Only stabilized fat should be used in feeds. Adequate levels of stabilized vitamin E should be used in conjunction with a commercial antioxidant and up to 0.3 ppm selenium. Signs of exudative diathesis and muscular dystrophy due to vitamin E deficiency can be reversed if treatment is begun early by administering vitamin E PO or through the feed. Oral administration of a single dose of 300 IU of vitamin E per bird usually causes remission.
Riboflavin Deficiency
Many tissues may be affected by riboflavin deficiency, although the epithelium and the myelin sheaths of some of the main nerves are major targets. Changes in the sciatic nerves produce “curled-toe” paralysis in growing chickens. Egg production is affected, and riboflavin-deficient eggs do not hatch. When chicks are fed a diet deficient in riboflavin, their appetite is fairly good but they grow slowly, become weak and emaciated, and develop diarrhea between the first and second weeks. Deficient chicks are reluctant to move unless forced and then frequently walk on their hocks with the aid of their wings. The leg muscles are atrophied and flabby, and the skin is dry and harsh. In advanced stages of deficiency, the chicks lie prostrate with their legs extended, sometimes in opposite directions. The characteristic sign of riboflavin deficiency is a marked enlargement of the sciatic and brachial nerve sheaths; sciatic nerves usually show the most pronounced effects. Histologic examination of the affected nerves shows degenerative changes in the myelin sheaths that, when severe, pinch the nerve. This produces a permanent stimulus, which causes the curled-toe paralysis.
Signs of riboflavin deficiency in the hen are decreased egg production, increased embryonic mortality, and an increase in size and fat content of the liver. Hatchability declines within 2 wk when hens are fed a riboflavin-deficient diet, but returns to near normal when riboflavin is restored. Affected embryos are dwarfed and show characteristically defective “clubbed” down. The nervous system of these embryos shows degenerative changes much like those described in riboflavin-deficient chicks.
Signs of riboflavin deficiency first appear at 10 days of incubation, when embryos become hypoglycemic and accumulate intermediates of fatty acid oxidation. Although flavin-dependent enzymes are depressed with riboflavin deficiency, the main effect seems to be impaired fatty acid oxidation, which is a critical function in the developing embryo. An autosomal recessive trait blocks the formation of the riboflavin-binding protein needed for transport of riboflavin to the egg. While the adults appear normal, their eggs fail to hatch regardless of dietary riboflavin content. As eggs become deficient in riboflavin, the egg albumen loses its characteristic yellow color. In fact, albumen color score has been used to assess riboflavin status of birds.
Chicks receiving diets only partially deficient in riboflavin may recover spontaneously, indicating that the requirement rapidly decreases with age. A 100-μg dose should be sufficient for treatment of riboflavin-deficient chicks, followed by incorporation of an adequate level in the diet. However, when the curled-toe deformity is longstanding, irreparable damage occurs in the sciatic nerve, and the administration of riboflavin is no longer curative.
Most diets contain up to 10 mg riboflavin/kg. Treatment can be given as two 100 μg doses for chicks or poults, followed by an adequate amount of riboflavin in feed.
-Kathy
http://www.merckmanuals.com/vet/pou..._poultry/vitamin_deficiencies_in_poultry.html
Vitamin D3 Deficiency
Abnormal development of the bones is discussed under calcium and phosphorus imbalances (see Calcium and Phosphorus Imbalances) and manganese deficiency (see Manganese Deficiency). Vitamin D3 is required for the normal absorption and metabolism of calcium and phosphorus. A deficiency can result in rickets in young growing chickens or in osteoporosis and poor eggshell quality in laying hens, even though the diet may be well supplied with calcium and phosphorus.
Laying hens fed a vitamin D3-deficient diet show loss of egg production within 2–3 wk, and depending on the degree of deficiency, shell quality deteriorates almost instantly. Using a corn-soybean meal diet with no supplemental vitamin D3, shell weight decreases dramatically by about 150 mg/day within 7 days. The less obvious decline in shell quality with suboptimal supplements is more difficult to diagnose, especially because it is very difficult to assay vitamin D3 in complete feeds.
There is a significant increase in plasma 1,25(OH)2D3 of birds producing good versus poor eggshells. Feeding purified 1,25(OH)2D3 improves the shell quality of these inferior layers, suggesting a potential inherent problem with metabolism of cholecalciferol.
Retarded growth and severe leg weakness are the first signs noted when chicks are deficient in vitamin D3. Beaks and claws become soft and pliable. Chicks may have trouble walking and will take a few steps before squatting on their hocks. While resting, they often sway from side to side, suggesting loss of equilibrium. Feathering is usually poor, and an abnormal banding of feathers may be seen in colored breeds. With chronic vitamin D3 deficiency, marked skeletal disorders are noted. The spinal column may bend downward and the sternum may deviate to one side. These structural changes reduce the size of the thorax, with subsequent crowding of the internal organs. A characteristic finding in chicks is a beading of the ribs at the junction of the spinal column along with a downward and posterior bending. Poor calcification can also be seen at the epiphysis of the tibia and femur. By dipping the split bone in a silver nitrate solution and allowing it to stand under an incandescent light for a few minutes, the calcified areas are easily distinguished from the areas of cartilage. Adding synthetic 1,25(OH)2D3 to the diet of susceptible chicks reduces the incidence of this condition. Although the response is variable, results suggest that some leg abnormalities may be a consequence of inefficient metabolism of cholecalciferol.
In the laying hen, signs of gross pathology are usually confined to the bones and parathyroid glands. Bones are soft and easily broken, and the ribs may become beaded. The ribs may also show spontaneous fractures in the sternovertebral region. Histologic examination shows deficiency of calcification in the long bones, with excess of osteoid tissue and parathyroid enlargement.
Enough vitamin D is added to commercial diets to provide 3 times the normally recommended level for a period of ~3 wk. Dry, stabilized forms of vitamin D3 are recommended to treat deficiencies. In cases of severe mycotoxicosis, a water-miscible form of vitamin D is administered in the drinking water to provide the amount normally supplied in the diet.
Vitamin E Deficiency
The 3 main disorders seen in chicks deficient in vitamin E are encephalomalacia, exudative diathesis, and muscular dystrophy. The occurrence of these conditions depends on various dietary and environmental factors.
Encephalomalacia is seen in commercial flocks if diets are low in vitamin E, if an antioxidant is either omitted or is not present in sufficient quantities, or if the diet contains a reasonably high level of an unstable, unsaturated fat. For exudative diathesis to occur, the diet must be deficient in both vitamin E and selenium. Signs of muscular dystrophy are rare in chicks, as the diet must be deficient in both sulfur amino acids and vitamin E. Because the sulfur amino acids are necessary for growth, a deficiency severe enough to induce muscular dystrophy is unlikely to occur under commercial conditions. Signs of exudative diathesis and muscular dystrophy can be reversed in chicks by supplementing the diet with liberal amounts of vitamin E, if the deficiency is not too advanced. Encephalomalacia may respond to vitamin E supplementation, depending on the extent of the damage to the cerebellum.
The classical sign of encephalomalacia is ataxia. The results from hemorrhage and edema within the molecular and granular layers of the cerebellum, with pyknosis and eventual disappearance of the Purkinje cells and separation of the molecular and granular layers of the cerebellar folia. Due to its inherently low level of vitamin E, the cerebellum is particularly susceptible to lipid peroxidation. In prevention of encephalomalacia, vitamin E functions as a biologic antioxidant. The quantitative need for vitamin E for this function depends on the amount of linoleic acid and polyunsaturated fatty acids in the diet. Over prolonged periods, antioxidants have been shown to prevent encephalomalacia in chicks when added to diets with very low levels of vitamin E or in chicks fed vitamin E-depleted purified diets. Chicks hatched from breeders that are given additional dietary vitamin E are also less susceptible to lipid peroxidation in the brain. The fact that antioxidants can help prevent encephalomalacia, but fail to prevent exudative diathesis or muscular dystrophy in chicks, strongly suggests that vitamin E is acting as an antioxidant. Exudative diathesis results in a severe edema caused by a marked increase in capillary permeability. Electrophoretic patterns of the blood show a decrease in albumin levels, whereas exudative fluids contained a protein pattern similar to that of normal blood plasma.
Vitamin E deficiency accompanied by sulfur amino acid deficiency results in severe muscular dystrophy in chicks by ~4 wk of age. This condition is characterized by degeneration of the muscle fibers, usually in the breast but sometimes also in the leg muscles. Histologic examination shows Zenker's degeneration, with perivascular infiltration and marked accumulation of infiltrated eosinophils, lymphocytes, and histocytes. Accumulation of these cells in dystrophic tissue results in an increase in lysosomal enzymes, which appear to function in the breakdown and removal of the products of dystrophic degeneration. Initial studies involving the effects of dietary vitamin E on muscular dystrophy showed that the addition of selenium at 1–5 mg/kg diet reduced the incidence of muscular dystrophy in chicks receiving a vitamin E-deficient diet that was low in methionine and cysteine, but did not completely prevent the disease. However, selenium was completely effective in preventing muscular dystrophy in chicks when the diet contained a low level of vitamin E, which alone had been shown to have no effect on the disease.
Studies with chicks on the interrelationships between antioxidants, linoleic acid, selenium, and sulfur amino acids have shown that selenium and vitamin E play supportive roles in several processes, one of which involves cysteine metabolism and its role in the prevention of muscular dystrophy in the chicken. Glutathione peroxidase is soluble and is located in the aqueous portions of the cell, while vitamin E is located mainly in the hydrophobic environments of membranes and in lipid storage cells. The overlapping manner in which vitamin E and selenium function in the cellular antioxidant system suggest that they spare one another in the prevention of deficiency signs.
Only stabilized fat should be used in feeds. Adequate levels of stabilized vitamin E should be used in conjunction with a commercial antioxidant and up to 0.3 ppm selenium. Signs of exudative diathesis and muscular dystrophy due to vitamin E deficiency can be reversed if treatment is begun early by administering vitamin E PO or through the feed. Oral administration of a single dose of 300 IU of vitamin E per bird usually causes remission.
Riboflavin Deficiency
Many tissues may be affected by riboflavin deficiency, although the epithelium and the myelin sheaths of some of the main nerves are major targets. Changes in the sciatic nerves produce “curled-toe” paralysis in growing chickens. Egg production is affected, and riboflavin-deficient eggs do not hatch. When chicks are fed a diet deficient in riboflavin, their appetite is fairly good but they grow slowly, become weak and emaciated, and develop diarrhea between the first and second weeks. Deficient chicks are reluctant to move unless forced and then frequently walk on their hocks with the aid of their wings. The leg muscles are atrophied and flabby, and the skin is dry and harsh. In advanced stages of deficiency, the chicks lie prostrate with their legs extended, sometimes in opposite directions. The characteristic sign of riboflavin deficiency is a marked enlargement of the sciatic and brachial nerve sheaths; sciatic nerves usually show the most pronounced effects. Histologic examination of the affected nerves shows degenerative changes in the myelin sheaths that, when severe, pinch the nerve. This produces a permanent stimulus, which causes the curled-toe paralysis.
Signs of riboflavin deficiency in the hen are decreased egg production, increased embryonic mortality, and an increase in size and fat content of the liver. Hatchability declines within 2 wk when hens are fed a riboflavin-deficient diet, but returns to near normal when riboflavin is restored. Affected embryos are dwarfed and show characteristically defective “clubbed” down. The nervous system of these embryos shows degenerative changes much like those described in riboflavin-deficient chicks.
Signs of riboflavin deficiency first appear at 10 days of incubation, when embryos become hypoglycemic and accumulate intermediates of fatty acid oxidation. Although flavin-dependent enzymes are depressed with riboflavin deficiency, the main effect seems to be impaired fatty acid oxidation, which is a critical function in the developing embryo. An autosomal recessive trait blocks the formation of the riboflavin-binding protein needed for transport of riboflavin to the egg. While the adults appear normal, their eggs fail to hatch regardless of dietary riboflavin content. As eggs become deficient in riboflavin, the egg albumen loses its characteristic yellow color. In fact, albumen color score has been used to assess riboflavin status of birds.
Chicks receiving diets only partially deficient in riboflavin may recover spontaneously, indicating that the requirement rapidly decreases with age. A 100-μg dose should be sufficient for treatment of riboflavin-deficient chicks, followed by incorporation of an adequate level in the diet. However, when the curled-toe deformity is longstanding, irreparable damage occurs in the sciatic nerve, and the administration of riboflavin is no longer curative.
Most diets contain up to 10 mg riboflavin/kg. Treatment can be given as two 100 μg doses for chicks or poults, followed by an adequate amount of riboflavin in feed.
-Kathy
Last edited:
- Jun 20, 2013
- 10
- 0
- 22
Is your chick albino? I'm sorry to say I don't know what caused the lameness, but I'm curious because we had an albino RIR chick (she looked just like your chick) who had the same problem. She stopped being able to walk but would kick her legs when picked up. I would lay her on the grass next to me while I worked in the garden so she could peck around a little and feel the sunshine. She ate well for a while but eventually that stopped too and she just ceased to grow and ultimately didn't make it. If coccidiosis was the cause, I never saw any blood in her stool, so it must be very sneaky. Good luck with yours, hope you can find out what causes it and treat it.
Sorry for your loss... FWIW, I rarely see blood in the stool with coccidiosis.
-Kathy
Only 2 of the 4 bad strains of cocci affecting chickens (and 9 or more total) cause blood in the stools.
- Thread starter
- #19
- Aug 17, 2014
- 8
- 0
- 7
No he is not albino. They are mostly white with a few black spots.
- Thread starter
- #20
- Aug 17, 2014
- 8
- 0
- 7
Thanks so much for all of your help. This sounds like the most likely culprit, unfortunately.
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