Zinc is essential for more than 300 enzymes, structural proteins and hormones in the mammalian body. It is needed for diverse
physiological processes and metabolic functions including many aspects of the immune system, including iodine (thyroid) metabolism.
Lack of zinc is associated with atrophy of the thymus, a gland that has a role in the maturation of lymphocytes, and it seems
the function of T lymphocytes is especially vulnerable to deficiency of this mineral.
With zinc deficiency, there is a reduction in delayed type hypersensitivity, and other immune responses mediated by T cells.
Reduction in the production of antibodies and in the function of natural killer cells has also been reported in experimentally
induced zinc deficiency in animals.
In addition, zinc is needed for cell replication and is thus essential for the regeneration of the intestinal mucosa, the
healing of wounds and the turnover of epithelial cells necessary to maintain healthy skin, hair and nails.
It is also important in maintaining normal sexual function.
The combination of these essential functions explains why zinc plays such an important part in the protection against infections.
The first reported case of zinc-related disease in the dog was reported in the journal, Growth, in an Alaskan Malamute with chondrodysplasia. It was found that these Malamutes absorbed only 25 percent of zinc in the
small intestine compared to normal controls, and furthermore, the reduction in absorption was related to the inability to
release protein-bound zinc to the non-protein-bound status at the gut level. This transfer occurs in normal dogs. This zinc-related
disease (in this case, no skin problems were reported) in this breed has been later reported to cause skin lesions even with
animals on a well-balanced commercial dog food.
True zinc deficiency is quite rare; it only has been reported in the Bull Terrier with lethal acrodermatitis.
This condition demonstrates a dysfunctional zinc metabolism and probable malabsorption in the small intestines. Stunted growth,
diarrhea, numerous cutaneous or internal infections, and crusted and fissured paw pads are seen. The internal infection usually
manifests as pneumonia and is directly related to diminished cellular immunity. Puppies usually die or are euthanized.
The affected dogs do not respond to oral or intravenous zinc supplementation.
There are basically three other syndromes of zinc-related dermatoses in the dog.
Most cases have been well-documented and seen in the past, but less so recently. This may be due to better breeding and improvements
in the quality of canine commercial diets.
The first type occurs in Alaskan breeds including the Siberian Husky and Alaskan Malamute.
It has also been reported in Doberman Pinschers and Great Danes.
The affected dogs were all on a well-balanced commercial dog food that was sufficiently supplemented with zinc. It appears
the skin disease is a result of several causes, primarily related to a genetic defect in intestinal absorption. This has been
well documented in the Alaskan Malamute breed. The onset in the appearance of skin lesions has been also linked to estrus,
severe stress, or severe diarrhea.
Finally, diets that are supplemented with higher levels of calcium or phytates can reduce plasma levels of zinc by directly
binding or interfering with zinc uptake and absorption. Phytate is a plant-based protein source. Lesions start relatively
early in age and include thick crusts, erythema, scaling and occasional purulent exudation symmetrically around the eyes,
mouth, pressure points, muco-cutaneous junctions (vulva, prepuce) and scrotum (Figure 1).
Note the crusts and alopecia periocularly.
Also, the planum and the paw pad epithelium may also display similar changes as seen on the haired skin.