Hypervitaminosis A

Cats require preformed vitamin A in the diet because beta-carotene, the plant precursor of vitamin A, cannot be converted to vitamin A by cats (see Chapter 15).⁶ 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 neurologic deficits as a result of nerve entrapment from hyperostoses.^{10,16,44,51,52} It occurs when excessive vitamin A is present in the diet in the form of raw liver or cod liver oil or as a vitamin supplement.* Hyperostoses resulting from hypervitaminosis A include primarily 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 pelvis. Ankylosis of cervical vertebrae and elbow joints may occur. Affected cats typically have an unkempt appearance because of an inability to groom. On presentation adult cats typically have a prolonged history of malaise, poor appetite, and a diet consisting mainly of liver or other concentrated source (or sources) of vitamin A. Physical examination often reveals muscle wasting, cutaneous hyperesthesia, inability to move neck, and a tendency to sit on the hindlimbs in a “kangaroo” position. Cervical radiography is diagnostic for ankylosing spondylosis. Plasma vitamin A can be measured. Normal plasma vitamin A concentrations are 960 ± 770 ng/mL²; plasma concentrations of vitamin A in cats with hypervitaminosis A have been reported to be higher than 4500 ng/mL.^9,16,44,51 Treatment for hypervitaminosis A includes discontinuing the high vitamin A diet or supplement, changing the diet to one containing recommended vitamin A levels, and administering an analgesic and possibly antiinflammatory 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 because of their inability to flex their neck. It may be necessary for the owner to provide food and water at a height that does not require neck flexion, or a feeding tube may be required.

Hypervitaminosis D

The dietary vitamin D requirement of adult cats is fairly low, although cats require a dietary source because sunlight is not required for activation of vitamin D.⁴⁶ Hypervitaminosis D is uncommon 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 because of excessive levels of vitamin D₃ contained in the vitamin–mineral premix. Affected cats developed gastrointestinal signs, hypercalcemia, and renal disease. More commonly, hypervitaminosis D results from 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 31). Chronic hypervitaminosis D results in musculoskeletal deformities, although cats appear to be relatively resistant.⁵³

Excessive Intake of Polyunsaturated Fatty Acids

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.* Although this condition is uncommon, it may occur if the antioxidant activity of the food is not adequate, if the food is fed beyond the effective time of included antioxidants, or with homemade diets that are stored for long periods without added antioxidants. Fish oil is particularly susceptible to oxidation and requires higher levels of antioxidants compared with vegetable or animal fat sources. Treatment involves analgesic therapy, antioxidant supplementation, and possibly surgical excision of necrotic fat.

Thiamin

Thiamin is a B vitamin that is involved with neurologic function. Classic thiamin deficiency occurs with ingestion of large amounts of raw fish that contain thiaminase, an enzyme that destroys thiamin. Cooking the fish destroys thiaminase and eliminates the problem. Thiamin deficiency has been reported with sulfur dioxide preservation of dietary meat and in cats fed commercial cat food.^{11,30,31,55,57} A small cluster of thiamin-deficiency cases associated with commercial cat foods occurred in the eastern part of the United States in 2009, and another limited precautionary recall of canned cat foods owing to inadequate thiamin content occurred in 2010. Clinical signs of thiamin deficiency include decreased food intake, hypersalivation, ventral flexion of the neck (see Figure 26-19), and seizures. Myocardial degeneration has also been associated with thiamin deficiency.¹ Fundic examination may reveal retinal venous dilation and hemorrhages. Treatment includes discontinuing the offending diet, changing to a complete and balanced cat food, and supplementing with thiamin (5 mg orally or 1 mg parenterally). Thiamin supplementation results in resolution of clinical signs, usually within 24 hours.

Vitamin E

Ingestion of large quantities of raw fish may also result in vitamin E deficiency. Fish contains polyunsaturated fatty acids that are easily oxidized. Vitamin E is an antioxidant that prevents oxidation of fatty acids in cell membranes. Signs of vitamin E deficiency include pansteatitis (discussed previously), decreased appetite, hyperesthesia, fever, and myositis.^13,15,64 Treatment consists of changing the diet with vitamin E supplementation (vitamin E acetate 100 mg/kg daily by mouth). Glucocorticoids may help decrease inflammation.

Taurine

Taurine is a beta-sulfonic amino acid that is an essential nutrient for cats, and deficiency has been associated with heart disease. Cats cannot make taurine from other amino acids and lose taurine in bile. Taurine is found primarily in animal-based products, and commercial cat foods have added taurine. Taurine deficiency occurs in cats when loss exceeds intake. This usually 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 (see Figures 29-61 and 29-62), dilated cardiomyopathy (see Figure 18-1), reproductive problems, and abnormal skeletal development in kittens.* 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.

With dilated cardiomyopathy the diagnosis of taurine deficiency is made by radiography and echocardiography (see Chapter 20). In cats with retinal degeneration, a thorough ophthalmic examination should be performed (see Chapter 29). If reproductive problems are present, evaluation for other causes of decreased conception rates or stillbirths is undertaken (see Chapter 40). In kittens with skeletal abnormalities, radiography should be performed. In cats plasma taurine concentration can decrease below the normal range after less than 24 hours of fasting; therefore whole blood is preferred for evaluation of taurine levels.^22,36,54 Although taurine deficiency is now a rare cause of dilated cardiomyopathy in cats, taurine is inexpensive and safe and is often empirically administered (250 to 500 mg orally every 12 hours) for 8 weeks to patients with presumed deficiency. Commercial dry cat foods are required to contain 0.1% taurine on a dry matter basis, and canned foods are required to contain 0.2% on a dry matter basis. Canned diets are required to contain more taurine than dry diets because canned diets promote bacterial growth in the intestines that degrade taurine.