Cats require preformed vitamin A in the diet because β-carotene, the plant precursor of vitamin A, cannot be converted to vitamin A by cats (see Chapter 18: The Unique Nutritional Requirements of the Cat).³ Hypervitaminosis A is uncommonly seen, but results in ankylosing spondylosis particularly of the cervical vertebrae in cats; it can also induce growth retardation, abnormal dentition, and neurological deficits due to nerve entrapment from hyperostosis (Fig. 20.1).^4–8 It occurs when excessive vitamin A is present in the diet in the form of raw liver, cod liver oil, horse meat, or as a vitamin supplement.^4–10 Hyperostosis due to hypervitaminosis A primarily causes cervical stiffness and forelimb lameness. Affected cats resist movement, particularly neck flexion. Clinical signs are attributed to new periosteal bone formation at sites of ligament and tendon attachment, which restrict joint movements and may impinge on nerves exiting vertebral foramina. With continued exposure to high levels of vitamin A, bony changes may extend to sternebrae, ribs, scapulae, other long bones, and pelvic bones. Ankylosis of cervical vertebrae and elbow joints may occur. Affected cats typically have an unkempt appearance because of inability to groom. Adult cats present typically with a prolonged history of malaise, poor appetite, and a diet consisting mainly of liver or other concentrated source(s) of vitamin A. Physical examination often reveals muscle wasting, cutaneous hyperesthesia, inability to move the neck, and cats often sit on their hindlimbs in a “kangaroo” posture. Cervical radiography is diagnostic for ankylosing spondylosis. Plasma vitamin A can be measured. Normal plasma vitamin A concentrations are 960 ± 770 ng/mL;¹¹ plasma concentrations of vitamin A in cats with hypervitaminosis A have been reported to be >4500 ng/mL.^4,5,8,12 Treatment for hypervitaminosis A includes discontinuing the high vitamin A diet or supplement, changing the diet to one containing recommended vitamin A levels, analgesic administration, and possibly administration of anti-inflammatory medication. If caught early, changing the diet may result in resolution of early ankylosis; however, when ankylosis has been present for some time, it will not resolve. Affected cats may have difficulty eating and drinking due to inability to flex their neck. Food and water may need to be provided at a height where neck flexion is not required, or a feeding tube may be necessary.

The dietary vitamin D requirement of adult cats is fairly low although cats require a dietary source as sunlight is not required for activation of vitamin D.13 Hypervitaminosis D occurs uncommonly but may occur if complete diets are supplemented with vitamin D or when manufacturing errors occur. In 2006, a major pet food manufacturer recalled canine and feline canned diets due to excess levels of vitamin D3 contained in the vitamin–mineral premix.¹⁴ Affected cats developed gastrointestinal signs, hypercalcemia, and renal disease. More commonly, hypervitaminosis D occurs due to ingestion of vitamin D-containing rodenticides and causes an acute disease manifested as hypercalcemia, polyuria, polydipsia, muscle fasciculations, vomiting, diarrhea, anorexia, seizures, and possibly renal failure (see Chapter 34: Toxicology). Chronic hypervitaminosis D can result in musculoskeletal deformities although cats appear relatively resistant.¹⁵

Steatitis, a painful inflammatory condition of adipose tissue, may result from excessive intake of polyunsaturated fatty acids or ingestion of rancid fat. Hard, painful masses can be palpated in adipose tissue of affected cats (Fig. 20.2).^3,16–22 Although uncommon, this may occur if the antioxidant activity of the food is not adequate, if the food is fed after the antioxidants are no longer effective, or with homemade diets that are stored for long periods of time without added antioxidants. Fish oil is particularly susceptible to oxidation and requires higher levels of antioxidants when compared with vegetable or animal fat sources. Treatment involves analgesic therapy, antioxidant supplementation, and possibly surgical excision of necrotic fat.

Thiamine is a B-vitamin that is involved with neurological function. Classic thiamine deficiency occurs with ingestion of large amounts of raw fish that contain thiaminase, an enzyme that destroys thiamine. Cooking the fish destroys thiaminase and eliminates the problem. Thiamine deficiency has been reported with sulfur dioxide preservation of dietary meat and in cats fed commercial cat food.23–27 In a study evaluating thiamine levels in canned cat foods, thiamine concentration was below minimum of the Association of American Feed Control Officials in 12 of 90 (13.3%) foods and below recommended allowance of the National Research Council in 14 of 90 (15.6%) foods.²⁸ Paté foods had significantly lower thiamine concentrations than did non-paté foods, and foods from smaller companies had significantly lower thiamine concentrations compared with concentrations in foods from larger companies. However, food flavor (such as fish) and country of manufacture were not correlated with dietary thiamine concentration.²⁸ Clinical signs of thiamine deficiency include decreased food intake, hypersalivation, altered mentation, blindness, seizures, and ventral flexion of the neck (Fig. 20.3).^29,30 On magnetic resonance imaging, cats with thiamine deficiency often show hyperintense signals on T1- and T2-weighted images in the areas of the lateral geniculate nucleus, caudal colliculi, medial vestibular nuclei, and cerebellar nodulus.^31–33 Polioencephalomalacia has been reported.³⁴ Myocardial degeneration has also been associated with thiamine deficiency.^34,35 Fundic examination may reveal retinal venous dilation and hemorrhages. Treatment includes discontinuing the offending diet, changing to a complete and balanced cat food, and thiamine supplementation (50–100 mg, parenterally, every 12 hours for 3–5 days, followed by oral administration for an additional 2–4 weeks).³⁶ Thiamine supplementation results in resolution of clinical signs usually within 24 hours.³⁶

Rickets is primarily due to vitamin D deficiency although it may also occur with dietary calcium or phosphorous deficiencies. Characteristic lesions of rickets are due to failure of vascular invasion and mineralization in the area of provisional physeal calcification resulting in pathology involving metaphyses of long bones. Clinical signs of rickets include bone pain, stiff gait, swelling in the area of metaphyses, difficulty rising, bowed limbs, and pathological fractures (Figs. 20.4 and 20.5). Radiographically, physeal width is increased and the nonmineralized physeal area is distorted. Rickets is primarily a disease of young, growing animals that are fed all-meat diets because these diets are often calcium and vitamin D deficient and/or have excess phosphorous.³⁷ Kittens fed exclusively beef heart developed locomotor problems within 4 weeks even though dietary digestible protein and fat content promoted normal growth. Rarely, there may be an inborn error of metabolism resulting in vitamin D-dependent rickets with clinical signs developing between 4 and 7 months of age.³⁸ Nutritional therapy includes discontinuing the diet associated with rickets and feeding a balanced diet.

Ingestion of large quantities of raw fish may result in vitamin E deficiency. Fish contains polyunsaturated fatty acids that are easily oxidized. Vitamin E is an antioxidant preventing oxidation of fatty acids in cell membranes. Signs of vitamin E deficiency include pansteatitis (see earlier), decreased appetite, hyperesthesia, fever, and myositis.39–41 Treatment consists of changing the diet and vitamin E supplementation (10–15 units/kg orally once daily). Glucocorticoids may help decrease inflammation.

Taurine is a beta-sulfonic amino acid that is an essential nutrient for cats and deficiency has been associated with heart disease and other problems. Cats cannot make taurine from other amino acids and lose taurine in bile.42 Taurine is found primarily in animal-based products and commercial cat foods have added taurine. Taurine deficiency occurs in cats when loss exceeds intake. Most commonly this occurs when homemade vegetarian diets are fed or when cats are fed primarily dog food. In cats, taurine deficiency is associated with retinal degeneration and blindness (Fig. 20.6), dilated cardiomyopathy (Fig. 20.7), reproductive problems, and abnormal skeletal development in kittens.^43–55 In pregnant queens, taurine deficiency is associated with abortions, stillbirths, and birthing of kittens that do not survive. If neonatal kittens are born live to queens that are taurine deficient, they often have skeletal abnormalities, such as curved spines and small stature.

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