Zinc is an essential nutrient because it is an important cofactor of many metalloenzymes involved in cell functions and is closely linked with essential fatty acids. This function is particularly important in the maintenance of epidermal integrity where the cells undergo rapid proliferation to replace those that are shed through desquamation. Zinc is also associated with immunity and neurological and intestinal functions.
Zinc-responsive dermatoses are clinical syndromes recognised in dogs, which respond to zinc supplementation. They are associated with either a metabolic abnormality (syndrome I), or a nutritional deficiency (syndrome II).
Syndrome I zinc-responsive dermatosis
This form of dermatosis has been associated with defective intestinal absorption and is breed associated – primarily in the Siberian Husky and Alaskan Malamute.
A syndrome associated with an autosomal recessive genetic defect that inhibits the absorption and utilisation of zinc is recognised in Bull Terriers with lethal acrodermatitis. Affected individuals develop signs as puppies and they fail to thrive; they normally don’t live beyond 18 months of age. Affected puppies were seen in the 1990s, but this genetic defect may now have been bred out in the UK. The author hasn’t seen any cases for over 15 years.
Syndrome II zinc-responsive dermatosis
Syndrome II is associated with a reduced availability in food; however, not all cases are linked with a dietary deficiency of zinc per se. Other nutritional factors that can reduce the availability of zinc include diets containing high levels of phytates, low levels of essential fatty acids, high levels of minerals such as calcium, phosphorus and magnesium and certain dairy products. Rapidly growing pups of certain large and giant breeds such as the Great Dane are also at risk if sufficient levels of zinc are not present in the diet.
Clinical signs
Cutaneous signs associated with syndrome I in the early stages include erythema, which is followed by alopecia, crusting and scaling around the mouth, eyes and ears (Figure 1). Other mucocutaneous areas such as the vulva, scrotum and anal areas may also be affected. Hyperkeratosis at pressure points such as the elbows, tarsi and footpads may be evident. Secondary infections are commonly seen.
Breeds more likely to be affected with syndrome II include: Great Danes, Dobermann Pinschers, German Shepherd Dogs, German Shorthaired Pointers, Labrador Retrievers and Standard Poodles. The signs associated with this syndrome vary between individuals. They may just present with recurrent bacterial or Malassezia infections, or may have hyperkeratotic plaques on areas of friction such as the pads. Severely affected individuals may have growth retardation, fever and depression.
Diagnosis
Diagnosis is based on history and clinical signs and supported by findings on skin biopsies. Histopathology generally reveals a marked epidermal and follicular parakeratosis and superficial perivascular dermatitis. Evidence of parakeratosis can be obtained by cytological examination of lesions. When large numbers of parakeratotic cells (nucleated keratinocytes) (Figure 2) are found on cytology, it may indicate a metabolic abnormality in the epidermal function.
The laboratory analyses for zinc levels in the serum or hair are unreliable for several reasons. Serum zinc concentrations can vary with age, season and breed and, unless matched with appropriate controls, the test results are difficult to interpret. Other reasons for inaccurate results include the presence of zinc in laboratory glassware and in the rubber stoppers of sample containers.
Treatment
The treatment depends on the syndrome. Dogs with syndrome I require oral supplementation of 2 to 3mg/kg of elemental zinc daily. The actual dosage will depend on the formulation of the supplement. For example, zinc sulphate is given at a dose of 10mg/kg once daily (Figure 3).
Some dogs that fail to respond to zinc supplementation alone benefit when also given a low dose prednisolone (0.1 to 0.5mg/kg q24 to 48h). The improvement in zinc availability may be due to increased absorption in the gut as the corticosteroids induce the production of metallothionein, a low molecular weight protein involved in zinc regulation. Omega-3 and omega-6 supplementation may also be beneficial to some dogs. Dogs with syndrome I require life-long supplementation.
Most dogs with syndrome II respond to a change in diet. In cases where a change in diet alone is not sufficient to reverse the clinical signs a short period of zinc supplementation may be required.
If secondary bacterial and Malassezia infections are identified, they must be treated accordingly to achieve a successful outcome.
