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Many can have an annular to arciform or serpiginous pattern. Additional lesions include urticarial plaques, and vesicles and bullae that progress to ulcers. Mucosal lesions are generally erythematous and can also progress to vesicular, bullous and ulcerative lesions; crusting may be associated with some lesions. The most commonly affected sites include the ventrum, axillae, mucocutaneous junctions, oral cavity, pinnae and footpads. With such variation in clinical signs and a large differential diagnosis to consider based on clinical signs (bacterial folliculitis, demodicosis, dermatophytosis, urticaria, other vesicular and bullous disorders), biopsy with histopathology is needed for diagnosis. The most characteristic histopathologic feature with EM is panepidermal apoptosis with lymphocyte satellitosis and an interface dermatitis. Response to treatment and perhaps permanent remission is contingent upon identifying and eliminating a trigger where one can be found, as elimination of the etiology can result in spontaneous resolution within weeks of correcting and treating. A hypoallergenic elimination diet trial should be performed in cases with no identifiable trigger, as food hypersensitivity can be a potential cause. In more severe cases, and for those cases where a trigger cannot be identified, immunosuppressants such as corticosteroids, azathioprine, and cyclosporine have been effective. In life-threatening cases, hIVIg has been utilized to improve and expedite treatment outcome. Cutaneous vasculitis There are a variety of vascular diseases that affect dogs. Cutaneous vasculitis is a disease process whereby blood vessel walls are targeted by an inflammatory response, resulting in subsequent destruction of blood vessels and ischemic necrosis of the affected tissue. It is important to note that cutaneous vasculitis is more a cutaneous reaction pattern rather than a specific diagnosis, as there are multiple causes that trigger vasculitis. Cutaneous vasculitis has been associated with other coexisting diseases, including food hypersensitivity, insect bites, malignancies, and infectious diseases including tick-borne diseases. Additionally, numerous drugs have been implicated as causing vasculitis. In many cases, an underlying etiology is not readily identifiable and the disease is considered idiopathic. In most cutaneous vasculitides, the pathomechanism is suspected to be a type III hypersensitivity reaction, whereby immune complexes formed following antigen exposure are deposited in vessel walls. However, additional factors may be involved, including genetics, defects in immune complex clearance, and autoantibodies.
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