Page 1248 - Veterinary Immunology, 10th Edition

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FIG. 37.11 Skin lesion in a case of dermatomyositis. Note the
diffuse ischemic hair follicle atrophy and multifocal basal
keratinocyte degradation in the epidermis. (Courtesy Dr. J. Mansell.)

Muscle disease follows the onset of skin disease, but there is poor

correlation between the severity of the two lesions. The most
common sign of myositis is masseter and temporal muscle atrophy.
Some severely affected puppies may have difficulty eating as a

result of the myositis and thus grow poorly. If the muscles of the
esophagus are affected, megaesophagus may develop, and
secondary aspiration pneumonia results. Generalized lymphoid
hyperplasia may also occur in these dogs. Many dogs outgrow the
disease and are left with moderate hyperpigmentation, some

hypopigmentation and alopecia, and atrophy of the muscles of
mastication. Other dogs develop a progressive disease with severe
dermatitis and myositis. Dogs with progressive disease may also

develop signs of immunodeficiency, especially pyoderma and
septicemia, as well as demodicosis. On necropsy, myositis may be
seen in the esophagus and arteritis in the skin, muscle, and bladder.
The key autoimmune target in dermatomyositis is capillary
endothelium. The skin and muscle lesions are a result of ischemic

vasculopathy. Thus there are swollen endothelial cells,
vacuolization, capillary necrosis, inflammation, and ischemia. The
onset and progression of the disease correlate with a rise in

circulating immune complexes and serum IgG, but the reason for
these increases is unclear. Immune complexes and IgG levels return
to normal as the disease resolves, suggesting a causal association.
Muscle biopsy, especially of the temporal muscle, shows multifocal

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