no help to offer for Elmer with the curled toes?

[Amiga]

I am thinking if the toe curling started at ten days if I read that correctly, I would be considering a nutrient deficiency (some ducklings are more sensitive to nutrient levels) although for some reason I would not entirely rule out an infection - but I would lean toward nutrient-related.

 

[casportpony]

I am thinking if the toe curling started at ten days if I read that correctly, I would be considering a nutrient deficiency (some ducklings are more sensitive to nutrient levels) although for some reason I would not entirely rule out an infection - but I would lean toward nutrient-related.

X2!

-Kathy

 

[casportpony]

I think I would talk to a vet about treating for this:


Treatment at bottom in red.

Source:http://www.merckmanuals.com/vet/pou..._poultry/vitamin_deficiencies_in_poultry.html


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