Tufts University, Cummings School of Veterinary Medicine, North Grafton, Massachusetts
There are hundreds of conditions that are considered heritable in dogs and cats, and certainly many dermatologic conditions for which breed predispositions are recognized. However, there are relatively few dermatologic disorders for which actual genetic documentation is available.
Sebaceous adenitis is a periappendageal inflammatory process directed against hair follicles and glands. It is presumed autosomal recessive in Standard poodles but the condition in other breeds may be quite different. An immune-mediated process is suspected which, in turn, is influenced by other conditions such as atopy, food allergy, vaccination, and season (estrus). Clinical signs include non-inflammatory hair loss and scaling. Most dogs are young adults when first affected. There is extreme variability between breeds suggesting that this is a common end-result of potentially very different processes.
The diagnosis is confirmed with biopsies for histopathology, which should be taken from normal, mildly-affected and severely-affected skin. Carriers can sometimes be predicted by early biopsy.
The condition responds to anti-inflammatory therapies, and the best approach is frequent anti-seborrheic shampoos (including dishwashing liquid) and emollients (e.g., baby oil, propylene glycol, urea, lactic acid) and oral supplementation with high-dose marine oil. In rare cases, dogs can go into spontaneous (if only transitory) remission.
Dermatomyositis has a definite hereditary component (autosomal dominant with variable expressivity), but is also believed to be affected by infections (viral particles recovered) and an immune-mediated process. The list of breeds affected continues to grow.
Clinical signs tend to become evident by 12 weeks of age and consist of erosions and scarring on face, elbows, ears and hocks; muscle wasting is seen in some cases. Some dogs have difficulty eating, drinking and swallowing and megaesophagus may result in aspiration pneumonia. The diagnosis can be confirmed with histopathology and electromyography.
Some cases spontaneously improve so all therapies must be based on individual assessment. Vitamin E is recommended to help decrease scarring. Corticosteroids are of little benefit. Other therapies include pentoxifylline and avoiding sun exposure.
Demodex mites are obligatory parasites. The whole life cycle takes place in the skin (in the hair follicle and sebaceous glands or on the skin surface, depending on species). The mite is typically acquired from the dam during nursing in the first few days of life, but propagation of the mite probably occurs throughout the animal's life.
Demodicosis is usually arbitrarily designated as localized demodicosis, juvenile-onset generalized demodicosis, adult-onset demodicosis and demodectic pododermatitis. Juvenile-onset generalized demodicosis may be the result of heritable or non-heritable immune dysfunction. Adult-onset cases are often associated with underlying disease or immunosuppressive drug therapy, but in about 30-40% of cases, no underlying disease or drug is identified.
Demodicosis is usually diagnosed by deep skin scrapings, but superficial scrapings are often needed to find the short-bodied variety that resides on the skin surface. There are many treatment options for demodicosis. For very mild cases, using a follicle-flushing shampoo (e.g., benzoyl peroxide shampoo), a 3-4 week course of bactericidal antibiotic and a nutritious diet rich in antioxidants (or supplemented with vitamin E) is sufficient to achieve resolution. For more persistent cases, those often referred to as generalized demodicosis, specific miticidal therapy is often needed, in addition to searching for underlying causes of immune suppression. Therapies of most use in this regard are topical amitraz (250 ppm), or macrocyclic lactones such as ivermectin, milbemycin or moxidectin.
Ivermectin belongs to the avermectin class of antiparasitic agents and is certainly not a new parasite-control treatment. In most mammals, the blood-brain barrier prevents access of ivermectin to the central nervous system. However, there are some animals that have genetic mutations of the mdr1 (ABCB1) gene, making them particularly sensitive to the neurological effects of ivermectin. Affected breeds include collie, Shetland sheepdog, Australian shepherd, Old English sheepdog, white German shepherd dog, and longhaired whippets. Homozygotes for the deletion seem to show toxicity to ivermectin at 100 mcg/kg, while heterozygotes are relatively tolerant of doses up to 600 mcg/kg. Animals that are sensitive to ivermectin may also have adverse reactions to a variety of medications, including loperamide (Imodium®), cyclosporine, digoxin, vinca alkaloids, and doxorubicin. Fortunately, a genetic test is now available to detect susceptibility to ivermectin toxicity.
1. Ackerman, L: The Genetic Connection: A Guide to Health Problems in Purebred Dogs. AAHA Press, 2000.
2. Nesbitt, G; Ackerman, L: Canine & Feline Dermatology, Veterinary Learning Systems, 1998, 498pp.