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Metabolic Bone Disease in Wild and Exotic Felines, by Gail Hedberg
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Metabolic bone disease is a general term for conditions that develop as a result of prolonged deficiencies of calcium, vitamin D, or an improper ratio of calcium to phosphorous in the diet.

Felines and canines are highly susceptible to MBD. General signs first appear as lameness caused by fractures or painful joints.

Metabolic bone disease is diagnosed by a combination of clinical signs, radiographic studies and a thorough diet evaluation.







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Introduction

Metabolic bone disease is a general term for conditions that develop as a result of prolonged deficiencies of calcium, vitamin D, or an improper ratio of calcium to phosphorous in the diet. Many names are given to this syndrome, such as osteoporosis, rickets, cage paralysis, paper bone disease, nutritional secondary hyperparathyroidism. Metabolic bone disease should be considered to be a disease caused by dietary and husbandry mismanagement (Fowler 1986; White 1988; Wisman 2003). The disease is erroneously thought by some to be the result of too much protein in the diet. In fact, a simple adjustment of the mineral balance will correct the absorption and retention rate of calcium (Wallach 1983).

Mother reared cubs initially receive a balanced diet from their motherís milk but at weaning a cub or kitten becomes dependent on solids for continued growth and development. In the wild, cats would consume the whole prey-skin, fur, feathers, bones, intestines, and intestinal contents. The overall intake provides a balanced nutrition. Meat alone contains a relatively small amount of calcium. It also has high levels of another mineral called phosphorous which further depresses body calcium levels. Calcium deficiency is usually associated with diets of skeletal muscle and viscera, but not bone, or diets of neonatal prey (baby chicks for example).

When carnivores are fed a muscle meat without bone, calcium intakes are deficient calcium to phosphorous ratios are inverse (aprrox 1:20) and nutritional secondary hyperparathyroidism may result. Excessive vitamin A intakes from the consumption of liver may interfere with vitamin D metabolism, which can affect uptake of calcium from the diet. True rickets is a disease where there is a reduced density of bones at the points of growth and it is caused by a deficiency of vitamin D (Wallach 1983).

Mineral oil is often used as an oral laxative. When mineral is used orally for more than two weeks it coats the the mucosa of the small intestine and reduces absorption of vitamins. As a result, calcium and phosphorous utilization is reduced, possibly leasing to a deficiency (USDA 2002).

Pathophysiology

Metabolic bone disease occurs as a result of biochemical reactions regulated by the parathyroid glands, small glands located near the thyroid glands in the neck. Calcium regulation is not a simple process. The body uses three specific hormones together for bone development. A delicate balance by the interaction of parathyroid hormone (PTH), calcitonin (TCT), and the active form of vitamin D (1.25-di-hydroxy cholcalciferol) must be maintained throughout the process for proper uptake and distribution of nutrients to tissue, and for bones to develop normally. Major organs involved in this process include the intestine, liver, kidney, parathyroid gland, thyroid gland and bone.

Calcium

Calcium is required for normal muscle function, including the heart. Other functions for which calcium is essential include blood clotting, cell membrane permeability and activation of enzymes (Fowler 1986). It provides structural framework for the skeleton. The majority of the body calcium is stored in bones.

Calcium absorption occurs during the digestive process with the help of vitamin D and the parathyroid hormone. Any disease of the small intestine such as chronic diarrhea, or complications from liver disease, can interfere with calcium absorption. Ingestion of a high fat diet may reduce calcium absorption and impact vitamin D effectiveness.

Phosphorous

Phosphorous is required for proper acid-base levels in the body fluids. Together with calcium it is an essential nutrient for bone formation and affects calcium metabolism. The nutritional relationship between calcium and phosphorous is expressed as a ratio. Calcium is always listed first then phosphorous. In the body, calcium and phosphorous are in a ratio of 2:1. The optimal ratio in the diet should be between 1:1 to 2:1(Wallach 1983; Fowler 1986; Allen 1996). Most dietary errors involve too much phosphorous which causes low calcium. Adding too much calcium to the diet can throw the imbalance the other direction producing a phosphorous deficiency.

Bone

Bone is composed of living cells. Proper nutrition allows bone formation to be complete. A mammal is still growing and developing proper bone formation for a full year (or longer-like humans!!). The mineral composition of bone is calcium and phosphorous.

Vitamin D

Cats do not effectively convert precursors of vitamin D to active isomers, but nonetheless appear to have an extremely low dietary requirement for vitamin D provided that they have exposure to some sunlight and are otherwise well nourished.

Vitamin D controls calcium and phosphorous levels in the blood stream and also the absorption of dietary calcium. Vitamin D occurs in two forms, vitamin D2 (ergocalciferol) and vitamin D3 (cholecalciferol). This vitamin, when given as a supplement in excess, results in a condition called hypervitaminosis D (Hoskins 1990). Adding oral vitamin D3 will cause withdrawal of calcium from the bones of a felid fed a calcium deficient diet. Vitamin D toxicity can be produced relatively easily and is usually the result of overzealous dietary supplementation with, for example, cod-liver oil. As with all fat-soluble vitamins, excesses are stored in the body and their effects are cumulative.

Rickets is the term used when bones of young, growing, vitamin D-deficient animals become soft and pliable. There may be neuromuscular abnormalities, including general weakness and poor motor reflexes, and resorption of bone resulting in pathological fractures (Fowler 1986). Cases are normally presented because of the most obvious signs of renal failure and the prognosis is always guarded (Hoskins 1990).

Clinical Signs

Felines and canines are highly susceptible to MBD. General signs first appear as lameness caused by fractures or painful joints. Often cage paralysis or a distinct hesitation to move is noted. Felines are prone to cataract formation and cross-eyes due to prolonged low calcium levels. Bowed legs are a common result of poor nutrition in the early stages of development (Fowler 1986).

Diagnosis

Metabolic bone disease is diagnosed by a combination of clinical signs, radiographic studies and a thorough diet evaluation. Blood levels of calcium and phosphorous will remain approximately normal until severe collapse is imminent (Wallach 1983). Further trauma and injury can result when restraining an animal suspected to have MBD. The bones are very brittle and can fracture easily.

Diet Summary

Muscle meat (chicken, beef) is notoriously low in calcium and phosphorous, especially calcium, resulting in an imbalance of the Ca: P ratio from 1:5 to 1:30 (Wallach 1983; Allen 1996). Organ meats such as liver, kidney and heart have an even worse ratio- 1:44 (Wallach 1983).

Conversion to a properly balanced diet is difficult but can be accomplished by mixing the old with the new. The composition of commercial diets may be found on the label or by direct communication with the manufacturer. Feeding commercial diets is the industry standard but it is always advisable to check with the manufacturer for a diet analysis report. Nutritional and metabolic bone disease has largely disappeared in zoo carnivores with the use of commercial meat-based diets (Allen et al., 1996).

Conclusion

Correcting the diet and husbandry practice is essential for reversing this disease. Offering a balanced diet with the addition of whole prey is a simple way to provide an excellent source of available calcium for many exotic felids. (See details in ww.nal.usda.gov/awic/zoo/WholePreyFinal02May29.pdf) New product resources are available to help meet the dietary requirements for calcium. These products are designed to use when skeletal muscle meat is used or in combination with whole prey and organ meat. Examples are Mazuri Carnivore Supplement, Oasis, and Meat Complete.

This disease is present in non-human primates, birds, iguanas, guinea pigs, ferrets, and in puppies and kittens. Letís all work together to educate owners of domestic and exotic animals regarding appropriate diets and husbandry practices. Metabolic bone disease takes just a few weeks to develop and within months, it is a life threatening condition and becomes catastrophic. It takes even longer to correct so it is important to diagnose it early. If clinical signs of lameness, reluctance to move or distorted limbs are present, seek immediate veterinary care for a complete physical exam and review nutritional history along with a radiographic evaluation. Then, hopefully, a treatment plan will help reverse this condition.

REFERENCES

Allen, M. A., Oftedal, O.T. (1996). Essential Nutrients in Mammalian Diets. Wild Mammals in Captivity. M. E. A. D.G. Kleiman, K.V.Thompson, S.Lumpkin.. Chicago, The University of Chicago Press: 117-128.

Allen, M. E., Oftedal, O.E., Baer, D.J. (1996). The Feeding and Nutrition of Carnivores. Wild Mammals in Captivity. M. E. A. D.G. Kleiman, K.V.Thompson, S.Lumpkin. Chicago, The University of Chicago Press: 139-147.

Fowler, M. E. (1986). Metabolic Bone Disease. Zoo and Wild Animal Medicine. M. E. Fowler. Philadelphia, W .B. Saunders: 70-90.

Hoskins, J. D. (1990). Nutrition and Nutritional Disorders. Veterinary Pediatrics Dogs and Cats from Birth to Six Months. J. D. Hoskins. Philadelphia, W.B. Saunders: 511-524.

Laboratories, W.-T. (2002). Report of Nutrient Analysis- Frozen Feline Diet (Miliken). G. Hedberg, Dunker, F. San Francisco, CA: 1.

USDA (2002). Mineral Oil, U.S. Department of Agriculture. CFNP TAP Review. http://www.ams.usda.gov/nop/NationalL/TAPReviews/MineralOil.pdf 2004.

Wallach, J. D., Boever, W.J. (1983). Felidae. Diseases of Exotic Animals Medical and Surgical Management. J. D. Wallach, Boever, W.J. Philadelphia, W.B. Saunders Company: 345-403.

White, J. (1988). Basic Wildlife Rehabilitation 1AB, An interpretation of existing biological and veterinary literature for the wildlife rehabilitator. Walnut Creek, CA USA, International Wildlife Rehabilitation Council: 50-61.

Wisman, M. A., Parsons, B. (2003). Metabolic Bone Disease in Exotic Pets, Exotic Pet Vet.Net. 2004.

Woodward, L. (2003). Nebraska Brand Analysis Reports. G. Hedberg. San Francisco, CA 94132.


Many thanks to Gail Hedberg for allowing the use of this article on ExoticCatz.com.com in cooperation with the Feline Conservation Federation. This article is copyrighted 2004 by Gail Hedberg, and originally appeared in the FCF Newsletter. All rights are reserved. FCF members receive a bi-monthly newsletter containing a wealth of articles like this one, and I highly recommend becoming an FCF member to learn more about exotic felines.







 

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© Jessi Clark-White, 2005
Metabolic Bone Disease in Wild and Exotic Felines