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Introduction 112 How I treat: equine vasculitis ACVSC Proceedings Dermatology Chapter Science Week 2005 Linda Vogelnest Vasculitis is an uncommon disease in the horse that most frequently affects the skin, however may affect multiple body organs. Cutaneous vasculitis can occur in a variety of clinical forms and is characterised by lesions of purpura, urticarial wheals, or necrosis and ulceration. Similarly to cutaneous vasculitis in other animals and humans, disease aetiology and pathogenesis are complex and incompletely understood. A diverse range of triggering primary aetiological events underlies this disease in humans, including inflammatory, autoimmune and malignant diseases, although ~50% cases remain idiopathic. In the horse, clearly identified aetiological agents include bacterial infections (Streptococcus equi or zooepidemicus [“strangles”], Salmonella spp., and Corynebacterium pseudotuberculosis); and viral infections (equine influenza and equine viral arteritis). Drugs (eg phenylbutazone, vaccines), immunemediated colitis, cholangiohepatitis, omphalitis in foals, photo-activation, and neoplasia have also been implicated in disease aetiology, however many cases of equine cutaneous vasculitis remain idiopathic. Disease Pathogenesis Both immunological and non-immunological mechanisms have been implicated in disease pathogenesis; however immune-complex deposition and damage to small vessels, most often postcapillary venules, is reportedly the most common mechanism in humans and of proposed importance in animals. A complex series of events leading to disease may include initial antigenic stimulation, local immune complex deposition & inflammatory-mediator release (TNF-α, IFN-γ, IL-1, IL-4, IL-8), complement activation, increased local endothelial cell adhesion molecule expression (LFA-1, ICAM-1, E-selectin, P-selectin), coagulation (enhanced by plasminogen activator inhibior-1 [PAI-1]), and immunological response to initial inflammation (eg dermal dendritic cells, LH cells and T cells) further enhancing inflammation. Disruption to blood flow in affected vessels may result from inflammatory cell attack of vessel walls (which may be neutrophilic, lymphocytic or rarely eosinophilic or granulomatous, classically resulting in leukocytoclastic changes), inflammatory mediator damage to endothelial cells (producing primarily hyalinisation), or thrombogenic or hypercoagulable states (where thrombosis predominates).
Clinical Disease The clinical result of disruption to blood supply from cutaneous vasculitis is lesions that range in severity from wheals, papules, purpura, erythema and oedema if acute; to alopecia and scarring if mild and chronic; to areas of well-demarcated necrosis, ulceration and crusting if severe. Lesions occur most commonly on the distal limbs, pinnae, lips and periocular areas. Diascopy confirms purpura as erythemic lesions that will not blanch. Signs of systemic illness, including pyrexia, lethargy, decreased appetite and weight loss may accompany cutaneous lesions. Forms of cutaneous vasculitis recognised in horses include: 1. Purpura Haemorrhagica - is reported as the most common form of cutaneous vasculitis in the horse. It is an acute disease characterised by extensive oedematous swelling of the distal limbs, ventral abdomen, and sometimes face and muzzle, and typically concurrent signs of systemic illness. Incidence is low and sporadic, with most affected horses greater than 2 years of age, and no apparent breed or sex predispositions. This syndrome may occur within 2-4 weeks of a respiratory infection (Streptococcus equi or zooepidemicus), or other potential triggering factors or disease. Urticaria may occur initially, and progress to oedema that is usually well-demarcated, painful, symmetrical, and involving all four limbs. Severely affected areas may have surface serum exudation and progress to necrosis and ulceration. Petechiae and ecchymoses may be present on mucous membranes. Most affected horses have obvious signs of depression and are reluctant to move, anorexic, tachycardic, tachypnoeic, and often pyrexic. There is a wide variation in severity and clinical course. 2. Subacute Pastern Vasculitis – is proposed to be a relatively common although poorly characterised entity in the horse. Lesions primarily occur on nonpigmented lower limbs, and may be more prevalent in animals on pasture. Sunlight exposure and photactivation are proposed aetiological factors in some cases, however appear uninvolved in others. Early lesions include erythema and oedematous swelling, which progress to serum exudation, necrosis, crusting and ulceration. Pain on palpation is often present, and pruritus absent. Chronic lesions may be alopecic, scaling, lichenified, and proliferative. Diagnosis Definitive diagnosis of cutaneous vasculitis requires consistent history, clinical lesions, and histopathological changes. In acute disease varying degrees of specific vessel wall changes may be identified, including disproportionately more leukocytes within vessel walls than surrounding perivascular areas, leukocytoclasis within or adjacent to walls, fibrinoid necrosis, and vessel thrombosis. Less specific supportive changes include intense oedema, red cell extravasation, and endothelial cell swelling. There may be evidence of cutaneous infarction if severe, and follicular atrophy (“faded follicles”) with chronic disease. Clear histological support for a diagnosis of ACVSC Proceedings Dermatology Chapter Science Week 2005 113
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Australian College of Veterinary Sc
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Australian College of Veterinary Sc
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3.00 Afternoon tea 3.30 How I treat
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Dr Jennifer A. Charles BVSc MVS Dip
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Scientists in Feline Medicine in 19
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IgE-bearing cells have been demonst
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years, median age 6.5 years, with a
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dusts, grain smuts, moulds, danders
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References: Evans AG, Paradis MR, &
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Comparatively simple, cheap and eff
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TABLE 1: CURRENT ALLERGENS SELECTED
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AmericanCockroach Cockroach mix
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Patient Preparation Drug Withdrawal
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Each injection site is visually exa
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References 1. Scott DW, Miller WH:
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Intradermal Testing (IDT) in Horses
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TABLE 2 Additional allergens used i
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Allergen Positive reactions Mosquit
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much higher and corresponded to the
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and this and other uncontrolled tri
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Introduction Diagnostic Approach to
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Wheals vary in size and shape and q
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References Evans AG, Paradis MR & O
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Introduction: Equine Chronic Urtica
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Acute treatment - Epinephrine 1:100
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anecdotal success with use of human
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an 80:20 mixture of evening primros
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Clinical approach to the horse with
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identify plants in a pasture that m
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Equine sarcoidosis Sonya Bettenay T
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Page 65 and 66: 12. LeGall, F., Loeuillet, L., Dela
Page 67 and 68: Introduction The equine sarcoid: an
Page 69 and 70: Clinical Presentation Small fibrous
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Page 77 and 78: Owen LN & Barnett KC (1983) - Treat
Page 79 and 80: any anatomic location but commonly
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Page 83 and 84: References D.C. Knottenbelt, S. Edw
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Page 89 and 90: 2. Affect on the horse and 3. Affec
Page 91 and 92: Affected horses usually scratch and
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Page 95 and 96: How I treat: equine pemphigus folia
Page 97 and 98: Treatment of pemphigus foliaceus in
Page 99 and 100: SCOTT, D.W., WALON, D.K., SLATER, M
Page 101 and 102: Diagnosis History of access of hors
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Page 105 and 106: References Alfaro AA & Mendoza L (1
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Page 109 and 110: Authors recommendations: 1. Both Im
Page 111: chorioptic mange by the author (Lit
Page 115 and 116: treatment options have been used. P
Page 117 and 118: Notes ACVSC Proceedings Dermatology
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