With the standardization of nutrient quantities in commercial food, thiamine deficiency and vitamin A toxicosis are generally uncommon findings in daily veterinary practice. However, the ever increasing popularity of feeding raw diets or all-organ meat diets to cats may increase the incidence of these conditions despite the well-meaning intentions of their owners.

Thiaminase in Fish

Thiamine or vitamin B1 is an essential nutrient for carbohydrate metabolism, especially in nerve tissue. Raw carp and herring are particularly rich in an enzyme called thaiminase that destroys thiamine. Experimental studies in cats fed diets consisting of raw carp or herring have shown that clinical symptoms can occur in as little as 23-40 days. Whitefish, pike, cod, goldfish, shark, flounder, and mullet also contain thiaminase. There are not the same confirmatory experiments with these fish types to determine if they contain sufficient quantities of thiaminase to produce toxicity. Perch, catfish, and butterfish do not contain active thiaminase.

Early symptoms are non-specific and consist of anorexia, weight loss, and decreased activity. Clinical signs of thiamine deficiency are primarily neurological. Dilated pupils, incoordination, weakness, falling, or circling may be early signs. Abnormal neck positions may precede seizures. Total collapse and prostration characterize the terminal stage of deficiency.

Diagnosis of thiamin deficiency is primarily based on feeding history, but increased blood levels of the carbohydrate metabolism products called pyruvate and lactate help confirm the diagnosis.

Supplementation with intravenous or subcutaneous thiamine will reverse the symptoms within days. Oral supplementation can then be initiated for several months. Animals without severe neurological damage can expect a full recovery. Those with neurological damage may have permanent posture or movement abnormalities that prevent normal physical exercise tolerance.

Thiaminase is deactivated by heat, so cooking carp or herring will prevent thiamine deficiency, provided adequate thiamine is included in the diet.

Vitamin A Toxicosis

Vitamin A is a fat soluble vitamin. Unlike the water soluble B-vitamins that are flushed daily into the urine, fat soluble vitamins are stored in large quantities in the liver and other body organs (kidney, heart, etc.). The inclusion of large quantities of organ meats, especially liver, or all-organ meat diets for cats is presently very popular. This significantly increases vitamin A ingestion and can easily result in excesses.

Vitamin A toxicocis affects the cervical or neck spine and front legs causing a syndrome called deforming cervical spondylosis. The cat’s growing and ever remodeling spine and leg bones, when subjected to excessive vitamin A, can develop outgrowths or exostoses on various areas of the vertebrae and long bones of the forelimbs. These symptoms occur over a long time period so the diagnosis is typically not made until much later in the cat’s life.

It is speculated that the repetitive movements of the cat’s normal grooming habits result in micro-injuries to the neck and spine skeleton, making them susceptible to the effects of excessive vitamin A, which explains the anatomical location of the abnormalities.

Pain and impaired mobility account for the symptoms. Initially, anorexia, weight loss, reluctance to exercise, and an unkempt coat may be the only signs. The unkempt coat is presumably a result of inability to groom due to the neck lesions. A “kangaroo” sitting position or exaggerated flexing of the back legs when walking may characterize more advanced disease. Eventually, forelimb lameness and reduced neck mobility become severely debilitating.

Since the symptoms cannot be reversed, treatment for the pain is the primary approach. Alternative treatments like laser therapy, acupressure, acupuncture, etc., may also be helpful but have not been studied exclusively for vitamin A toxicosis. Changing the diet to a more complete and balanced food may prevent further disease but will not reverse existing skeletal changes.

Dr. Ken Tudor

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