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fibroblastic variant, particularly on the elbow or jaw. Differential diagnoses for such lesions include various forms of chronic infectious lymphangitis/lymphadenitis (e.g. glanders, epizootic lymphangitis and cutaneous histoplasmosis) and metastasising carcinomas. Why biopsy? Histopathology usually permits confirmation of a clinical diagnosis of equine sarcoid and elimination of the considerable list of differential diagnoses. However, nonexcisional biopsy may provoke transition of a quiescent sarcoid into a rapidly growing aggressive one. For this reason, many equine practitioners are loath to interfere, particularly with large or poorly demarcated lesions or when a suitable method of treatment is unlikely to be available once the diagnosis is confirmed. Diagnostic histological features of equine sarcoids Histologically, most sarcoids are characterised by dermal fibroblastic proliferation and intimately associated, pseudoepitheliomatous hyperplasia of the epidermis. There is usually some degree of hyperkeratosis and there may be mild parakeratosis. Long, narrow, anastomosing rete pegs of hyperplastic and at least focally acanthotic epidermis extend into the proliferating spindle cell component in the dermis. The infiltrative and poorly demarcated dermal component is usually of moderately high cell density, with the superficial portion tending to be more cellular than the deep part. The dermal fibroblasts are slender to plump fusiform cells with poorly defined cytoplasmic boundaries. The nuclei may be slender and elongate or enlarged and of irregular shape. Mitotic figures are usually infrequent (0-1 per high power field) but may be more numerous (up to 2-3 per high power field) in superficial than in deep areas of sarcoids and adjacent to areas of ulceration. Mitoses and fibroblastic nuclear pleomorphism, anisokaryosis and nucleolar enlargement may be observed in rapidly growing or recurrent sarcoids; cellular anaplasia is, however, rare. The fibroblasts are typically arrayed in tight whorls, interweaving bundles, haphazard tangles and occasionally herringbone and basket weave patterns, with a small to moderate amount of intercellular collagen. In recently developed sarcoids, the volume of intercellular collagen may be minimal. In chronic lesions, the collagen content increases and the dense fibres may appear hyalinised. Plump dermal fibroblasts usually directly abut the epidermis and, in a high percentage of sarcoids, are characteristically oriented perpendicular to the epidermal basement membrane in a picket-fence arrangement. Hair follicles enveloped by fibroblasts may undergo cystic dilation. Histological variants Prominent hyperplasia of the epidermis with formation of long rete pegs is not invariably present in sarcoids. It is usually observed in verrucous and mixed forms and at the margins of ulcerated areas in fibroblastic sarcoids. In occult sarcoids, the 80 ACVSC Proceedings Dermatology Chapter Science Week 2005
epidermis may be histologically normal, minimally hyperplastic or atrophic; hyperkeratosis, if present, is often mild. Epidermal thinning is a common finding in nodular sarcoids but the epidermis may be normal if the fibroblastic component is confined to the subcutis or involves the dermis but does not directly underrun the epidermis. All sarcoids are characterised by an increased density of fibroblasts but occult sarcoids are usually less cellular than other forms. Some occult sarcoids are characterised by only a subtle increase in the density of fibroblasts in the superficial to mid dermis and a localised reduction in the number of adnexal structures. The fibroblasts are frequently not in typical whorling patterns or oriented as subepidermal picket-fences in occult tumours. Picket-fence alignment is also commonly absent in nodular sarcoids. In some sarcoid variants, hyperplasia of the epidermis is more pronounced than the dermal fibroblastic proliferation. These variants may histologically mimic a squamous papilloma. Non-diagnostic biopsies Excisional biopsies are more likely to be diagnostic than are punch biopsies, particularly if the excisional biopsies are histologically sectioned perpendicular to the skin surface to reveal the epidermal component of the lesion and the epidermaldermal interface. If punch biopsies are taken, it is important to avoid ulcerated or superficially inflamed areas in which diagnostic features may be obliterated or obscured. The typical epidermal component of sarcoids may not be demonstrable in ulcerated lesions. In the absence of a hyperplastic epidermis, the dermal component of the sarcoid may be misdiagnosed as granulation tissue, a fibroma, a fibrosarcoma or a peripheral nerve sheath tumour. Superficial dermal fibroblast proliferation may also be obliterated by ulceration or obscured by granulation tissue in traumatised lesions. Differential diagnoses Sarcoids are usually readily distinguished from squamous papillomas histologically by virtue of their dermal fibroblastic component. Granulation tissue may be present within ulcerated sarcoids and is characterised by orderly proliferation of both fibroblasts and endothelial cells, with the new capillaries aligned in parallel and at right angles to the fibroblasts and new collagen fibres. A maturation face may be apparent in older granulating lesions, with collagen of low cellularity in deeper areas and ongoing fibrovascular proliferation superficially. Fibromas can be distinguished from sarcoids by being expansively growing, well circumscribed nodules which compress adjacent structures. They are mainly ACVSC Proceedings Dermatology Chapter Science Week 2005 81
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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
Page 29 and 30: References 1. Scott DW, Miller WH:
Page 31 and 32: Intradermal Testing (IDT) in Horses
Page 33 and 34: TABLE 2 Additional allergens used i
Page 35 and 36: Allergen Positive reactions Mosquit
Page 37 and 38: much higher and corresponded to the
Page 39 and 40: and this and other uncontrolled tri
Page 41 and 42: Introduction Diagnostic Approach to
Page 43 and 44: Wheals vary in size and shape and q
Page 45 and 46: References Evans AG, Paradis MR & O
Page 47 and 48: Introduction: Equine Chronic Urtica
Page 49 and 50: Acute treatment - Epinephrine 1:100
Page 51 and 52: anecdotal success with use of human
Page 53 and 54: an 80:20 mixture of evening primros
Page 55 and 56: Clinical approach to the horse with
Page 57 and 58: identify plants in a pasture that m
Page 59 and 60: Equine sarcoidosis Sonya Bettenay T
Page 61 and 62: described as a possible feature of
Page 63 and 64: others 2001), isotretinoin(Waldinge
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
Page 71 and 72: Assessment should be made on the fo
Page 73 and 74: (ix)Bone becomes devitalized if inc
Page 75 and 76: and mitomycin C have been used. All
Page 77 and 78: Owen LN & Barnett KC (1983) - Treat
Page 79: any anatomic location but commonly
Page 83 and 84: References D.C. Knottenbelt, S. Edw
Page 85 and 86: indicated. Each sample for culture
Page 87 and 88: Proper dosage and proper duration a
Page 89 and 90: 2. Affect on the horse and 3. Affec
Page 91 and 92: Affected horses usually scratch and
Page 93 and 94: • Cattle ear tags impregnated wit
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
Page 103 and 104: These vaccines are not manufactured
Page 105 and 106: References Alfaro AA & Mendoza L (1
Page 107 and 108: y a variety of fungal metabolites.
Page 109 and 110: Authors recommendations: 1. Both Im
Page 111 and 112: chorioptic mange by the author (Lit
Page 113 and 114: Clinical Disease The clinical resul
Page 115 and 116: treatment options have been used. P
Page 117 and 118: Notes ACVSC Proceedings Dermatology
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