In the adult dog, signs of zinc deficiency are confined mainly to the skin. In young animals growth may be retarded and other more generalised signs may be seen. Appetite may be depressed in affected animalsas a result of a diminished sense of taste and smell; prolongeddeficiency can result in weight loss, impaired wound healing,conjunctivitis and keratitis.
Typically a dog will develop areas of erythema, alopecia, crust and scale, which develop symmetrically aroundthe extremities, mucocutaneous junctions and pressure points ofthe limbs. Thick crusts are common overthe elbow, hock and other pressure points and, in some cases,the footpads may become thickened with deep fissures. Lesions may be mild presenting as callous formation or more severe requiring veterinary attention. The haircoat is typically dull and harsh, and secondary skin infectionswith bacteria or Malassezia pachydermatitis are common.
Due to the availability of zinc in commercial diets an absolute deficiency of zinc is very rare. However relativedeficiency can occur in some dogs when the availability of dietaryzinc is reduced through nutrient interactions or cases in whichintestinal absorption of zinc is impaired as a result of diseaseor genetic factors.
Syndrome I is associated with defective intestinal absorptionof zinc and occurs predominantly in Alaskan malamutes and Siberianhuskies, although other Northern breeds may be affected. Malamutes appear to have a genetic inability to absorb zinc from their diets. The appearanceof lesions frequently coincides with the onset of adulthood andduring periods of stress; it may be linked to higher metabolicrequirements in these dogs. Although dietary interactions with calcium or phytates in cereal maylimit zinc absorption in some affected animals, the conditionoccurs in many cases despite feeding a nutritionally completeand balanced diet. Oral zinc supplementation, together with the institution of a balanced diet where appropriate, brings rapid resolution of signsin most cases. Supplementation with elemental zinc at a dose of 1-3 mg/kg body weight daily in the form of zinc sulphate at a dose of 10 mg/kg daily is usually adequate,but lifelong therapy is normally required, and the dosage maybe adjusted for long-term maintenance.
Syndrome II is usually seen in rapidly growing puppies, particularly of the giant breeds, and may correspond with a high metabolicrequirement for zinc in affected animals. The condition is recognized when the diet is absolutely or relatively deficient in zinc. This most commonly occurs when the diet is high in phytate oris oversupplemented with calcium. Lesions resolve within 2-6 wkafter dietary correction, but the response time can be hastenedby oral supplementation with zinc which is given at the same dose rate as animals with syndrome I. In these cases, supplementationmay be discontinued once the clinical signs are in remission.