Cutaneous vasculitis in dogs (Proceedings)

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.

Pathogenesis

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.

Presentation

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

Diagnosis is confirmed by skin biopsy and appropriate tests/withdrawal procedures to address suspected etiologic factors in Table 1.

Table 1. Etiologic Factors for Cutaneous Vasculitis in Dogs

Management

Treatment includes management/elimination of known triggering factors (see Table 1), and immunomodulatory drugs.3 Drugs that may be useful in cutaneous vasculitis include: (a) systemic glucocorticoids (prednisolone or methylprednisolone, 2 mg/kg/day initially); (b) pentoxifyilline (Trental,® generics) 25 mg/kg q12h with food (slow-starter); (c) dapsone (1 mg/kg q8h initially - slow-starter); colchicine (0.03 mg/kg q24h); (d) tetracycline and niacinamide (250 to 500 mg of each, q8h initially (slow-starter); (3) azathioprine (Imuran®) 2.5 mg/kg/day initially (slow-starter); and (f) cyclosporine (5 mg/kg q24h with food (slow-starter).

References

Malik R, Foster SF, Martin P, et al. Acute febrile neutrophilic vasculitis of the skin of young Shar-Pei dogs. Australian Veterinary Journal 2002; 80:200.

Manning TO, Scott DW. Cutaneous vasculitis in a dog. Journal of the American Animal Hospital Association 1980; 16:61.

Scott DW, Miller WH, Griffin CE. Muller & Kirk's Small Animal Dermatology, 6th ed. WB Saunders, Philadelphia, 2001; p 742.

Tellier LA. Immune-mediated vasculitis in a shar-pei with swollen hock syndrome. Canadian Veterinary Journal 2001; 42:137.

Tonelli EA, Benson CJ, Scott DW, et al. Hereditary pyogranuloma and vasculitis of the nasal plane in Scottish terriers: two new cases from Argentina and the United States. Japanese Journal of Veterinary Dermatology 2009; 15:69.

Torres SMF, O'Brien TO, Scott DW. Dermal arteritis of the nasal philtrum in a giant schnauzer and three Saint Bernard dogs. Veterinary Dermatology 2002; 13:275.