Cutaneous vasculitis was first documented in a dog in 1980. Vasculitides can be apparently limited to the skin or, less commonly,
the skin may be one of multiple organ systems involved.
The pathomechanism of most cutaneous vasculitides is assumed to involve Type III (immune-complex) hypersensitivity reactions.3 However, multiple mechanisms likely play a role. Perhaps differences in membrane receptors (adhesion molecules, cytokines)
for immunoglobulin and complement on leukocytes account for the different histologic appearances of vasculitides (neutrophilic,
eosinophilic, lymphocytic). Additionally, initial neutrophilic -induced damage to endothelial cells could result in the expression
of "not self" antigens, whereupon dendritic cells and T lymphocytes could initiate a secondary cell-mediated immune response,
thus perpetuating the vascular disease and producing a lymphocyte-dominated infiltrate. Some cases/forms of vasculitis have
been associated with the presence of autoantibodies that react with neutrophil cytoplasmic structures (proteinase-3, myeloperoxidase)
or endothelial cells.
Cutaneous vasculitis may be associated with coexisting disease (infections, food allergy, insect bites, malignancies, systemic
lupus erythematosus), precipitating factors (drugs, vaccines, infections), or it may be idiopathic (about 50% of the cases).
Certain breeds may be predisposed, such as Parson (Jack) Russell terriers, Scottish terriers, German shepherd dogs, greyhounds,
dachshunds, and rottweilers. This may suggest genetic predilection. Vaccine reactions are more common in poodles, silky terriers,
Yorkshire terriers, Pekingese, Maltese, and bichon frise. This could reflect genetic, body size, or hair coat predilections.
Proposed etiologic factors for cutaneous vasculitis are listed in Table 1.
Cutaneous vasculitis was reported to account for 0.1% of all dogs with skin disease seen at a university clinic, and 0.76%
of all new patients at dermatology referral clinics. Skin lesions of vasculitis often occur on dependent areas of the body,
on areas of pressure and normal "wear and tear", and on extremities (pinnae, tip of tail, nasal planum, paw pads, scrotum,
and so forth) that are more susceptible to cold environmental influences. Perhaps the most common presentation of cutaneous
vasculitis is erythematous lymphedema, often affecting only one leg. Other reactions include: (a) palpable purpura; (b) erythematous
urticarial plaques; and (c) infarcts and "punched-out" ulcers. Acrocyanosis may be prominent in lightly-pigmented skin. Uncommon
lesions include hemorrhagic bullae and subcutaneous nodules/plaques (panniculitis due to septal vasculitis). Constitutional
signs may be present, including inappetence, depression, and pyrexia. Some vasculopathic syndromes include: (a) proliferative
thrombovascular necrosis of the pinnae; (b) cutaneous and renal vasculopathy ("Alabama rot" and so forth); (c) familial cutaneous
vasculopathy of German shepherd dogs; (d) familial pyogranuloma and vasculitis of Scottish terriers; (e) focal cutaneous vasculitis
and alopecia at the sites of vaccination (especially rabies); (f) widespread ischemic dermatopathy associated with vaccination;
(g) familial vasculitis ("swollen hock syndrome", and so forth) of Shar Peis; (h) acute febrile vasculitis of young Shar Peis;1 and (i) dermal arteritis of the nasal philtrum (especially St. Bernards).
Diagnosis is confirmed by skin biopsy and appropriate tests/withdrawal procedures to address suspected etiologic factors in
Table 1. Etiologic Factors for Cutaneous Vasculitis in Dogs