Hen with weak legs

Discussion in 'Emergencies / Diseases / Injuries and Cures' started by MelissaB, Nov 5, 2007.

  1. MelissaB

    MelissaB New Egg

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    About three weeks ago I noticed one of my 6 month old RIR hens was looking funny. Her tail feathers were a mess and she was walking weird. She started to not be able to get up from the ground and would flap her wings and scoot backwards until she ran into something and then use it to help her stand. She seems to have trouble going from standing to sitting and vice versa. She spends most of the day laying in the run. I have called all the vets in my area and none see chickens. I called the feed shop where we got her and they suggest coccidiosis and we ran tiramissin. No change. We called Ohio State poultry science dept and they thought ricketts. We have been supplementing the water for the past week with vitamins and electrolytes and no change. Her color is good. She is eating and drinking and her stool is firm. She is still laying. She just seems to have really weak legs. When she flaps her wings they are in unison. Does anyone have any thoughts?
     
  2. eggchel

    eggchel Overrun With Chickens Premium Member

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  3. dlhunicorn

    dlhunicorn Human Encyclopedia

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    outside of a toxin or mycotoxin which may have caused this here is additional info:
    http://www.asasea.com/po15_95.html
    (excerpt)
    "Leg Weakness
    Disorders involving leg weakness are a persistent problem in commercial poultry operations around the world. Leg problems in poultry are associated with many causes including nutrition, genetics, virus infection, environment. The problem is widespread with 2 to 6% of all commercial chickens displaying some sort of problem. Descriptions of the more common problems are given:
    Viral arthritis
    Also called tenosynovitis. Reovirus infection is considered the main cause of the problem with secondary Staphylococcus aureus infection. The disease is not nutritional in origin but may occur along with malabsorption syndrome. The condition results in severe lameness that reduces ability of the bird to move causing malnutrition and stunting. Swelling of the shanks and hock can be observed as early as 10 days but usually develop at 4 to 6 weeks. The swollen area may be filled with clear or bloody fluid or may be hardened and fibrous.

    Femoral head necrosis
    This condition is also called "brittle bone disease". It appears to be related to reovirus and adenovirus as these are often isolated from affected flocks. Fusarium contamination of ingredients is often observed. Femoral head necrosis is characterized by a severe weakening or disintegration of the head of the femur such that upon necropsy the bone end is easily broken off between the fingers.

    Synovitis
    This is caused by infection with Mycoplasma synoviae. The major signs are lameness and swelling of the hock joints with cream colored fluid. Eradication has been successful through blood testing of the breeders. Egg transmission can be reduced by dipping of eggs with antibiotic.

    Osteomyelitis
    This condition is caused by bacterial infection. S. aureus is the major cause with secondary involvement of E. coli and Pasteurella multocida. Invasion of bacteria after toe trimming or by cuts and scratches produce toxins that prevent cartilage formation. Birds often have a hopping gait and the affected area is swollen and warm to the touch. Biosecurity, good hygiene and treatment with antibiotics will reduce problems if caught in the early stages.

    Tibial dyschondroplasia
    This abnormality occurs primarily at the growth ends of the tibia where a large amount or "plug" of unvascularized cartilage accumulates. TD does not appear to be related to virus infection. Faster growing flocks on a high plane of nutrition are often affected. Acid-base imbalance, high levels of salt, low calcium and excess nitrogen increase severity of TD (Waldroup, 1986). Fusarium mycotoxins such as fusarochromanone and contamination of corn with Fusarium moniliforme increases the incidence of TD (Cook, 1987). Aflatoxin reduces vitamin D absorption and liver damage prevents conversion to the active 25-OH form of vitamin D3. Experimentally, 1, 25- OH vitamin D3 has ben found to prevent TD. Vitamin C has also been found useful. Although TD occurs in other bones, it is most common at the proximal end of the tibia because of high stress at this point. A higher incidence of breast blisters is usually observed in birds with this condition probably because they are spending more time off their feet.

    Rickets
    A direct result of vitamin D deficiency and low or imbalanced calcium or phosphorus nutrition. Bones are decalcified and weakened causing bowing of the legs and other problems. The growth plate is increased in width and birds appear sluggish and are reluctant to walk. The bones and beaks are soft and rubbery. Mycotoxins are often involved.

    Perosis
    Also called chondrodystrophy or "slipped tendon". Symptoms include swelling of the hock joint, shortening of the leg bone and gastrocnemius tendon slippage off the condyle. This problem is mostly genetic but may be induced experimentally in diets deficient in one or more of the following nutrients: choline, manganese, zinc, copper, niacin, biotin, pyridoxine, vitamin E, vitamin B12, calcium and phosphorus.

    Twisted leg
    This very common ailment in broilers is often confused with other problems. One or both legs may be involved. The legs may be bent inward or outward. Litter quality and heat stress seem to play a role. Manganese deficiency worsens the condition whereas high doses of pyridoxine improve the condition (Waldroup, 1986). Dietary tannin from rapeseed meal and high tannin sorghum as well as the high sulfur content in rapeseed and Canola meal interfere with calcium metabolism and increase incidence of this condition (Summers, 1993).


    Strategies for reducing incidence of leg problems:
    Biosecurity and disease control to eradicate mycoplasma and reduce the indicence of reovirus.

    Monitor and reduce contamination of grains, groundnut meal and corn gluten meal with aflatoxin and Fusarium mold.

    Calcium and phosphorus sources should be highly bioavailable. Avoid dolomitic limestone containing more than 3% magnesium as this impairs calcium utilization. Phosphate sources should contain less than 0.25% fluoride and defluorinated rock phosphate should contain between 4 to 6% sodium to ensure solubility of phosphorus. Maintain a 2:1 ratio of calcium to available phosphorus for broilers and pullets and 12:1 ratio for layers.

    Ensure adequate available levels of all vitamins and trace minerals. Additional vitamin E (up to 150 ppm), biotin (up to 60 ppm) and supplementation with vitamin C (125 ppm) may be useful.

    Avoid excess sodium (above 0.30%) and chloride (above 0.40%) in feed.

    Avoid water with sodium above 500 ppm, chloride above 500 ppm, nitrogen (as NO3) above 50 ppm and sulfur (as sulfate) above 1000 ppm (Leeson and Summers, 1991).

    Monitor sulfur level in feed. This can be a problem when using high levels of rapeseed and/or Canola meals. Total feed sulfur should be less than 0.5%.

    Avoid high levels of tannins. Monitor the use of ingredients such as high tannin sorghum, sunflower meal, Canola and rapeseed meals.

    Reduce nutrient density in feed to slow growth when persistent problems occur. Avoid amino acid imbalances and excess protein. ...."
     
  4. DuckLady

    DuckLady Administrator Staff Member

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    Unless you are running a large commercial business, I would agree with Eggchel that it sounds like Marek's. I have heard of rare cases that survive it, but most of the birds I have know of having it have been put down.
    I am sorry this is happening to her. It is hard to watch.
     
  5. MelissaB

    MelissaB New Egg

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    Nov 5, 2007
    Thanks for the helpful info. I should also add that these chickens were vaccinated as day old chicks. Does that change your opinion of marecks disease?
     

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