5 - ALOPECIAS INMUNEMEDIADAS

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1 5 - ALOPECIAS INMUNEMEDIADAS XVIII Congreso Internacional COMVEPE BC-IICV-UABC Mexicali, Junio 2017 Manon Paradis, DMV, MSCV, Dipl. ACVD, Departamento de Ciencias Clínicas, Facultad de Medicina Veterinaria, Université de Montréal, St-Hyacinthe, Québec, Canada. INTRODUCTION There are several immune-mediated dermatopathies causing alopecia in dogs. The aim of this presentation is to provide the clinician with an overview of selected immune-mediated skin disorders causing alopecia. These include sebaceous adenitis, dermatomyositis, post-rabies vaccine alopecia, adult onset generalized ischemic dermatopathy, alopecia areata (pelade) and isthmic lymphocytic mural folliculitis (pseudopelade). SEBACEOUS ADENITIS Sebaceous adenitis is an uncommon idiopathic skin disease in the dog The exact etiopathogenesis of this disease remains unknown. A genetically inherited cell-mediated immune reaction directed against a component of the sebaceous glands is suspected. Another theory is that the initial defect could be an abnormality in cutaneous lipid metabolism. The common feature of the disease is an inflammatory infiltrate affecting the sebaceous glands resulting in their destruction. Alopecia occurs by hair shafts breaking easily, most likely due to a decreased amount of sebum produced by the sebaceous glands. Sebaceous adenitis is most commonly seen in standard poodles and Akitas but has been diagnosed in various other breeds including Vizsla, German shepherd dog, Hovawart, Lhasa apso, Bernese mountain dog, and mongrels. Young adult to middle-aged dogs are most commonly affected. No sex predilection has been reported. There is a marked variability of clinical presentation depending on individual breeds and severity. Follicular casts (white scales adherent to hair shafts) is a common feature. They most likely result from the lack of sebum in the hair follicle infundibulum, where epidermis-like keratinization and desquamation occur. In long-coated dogs (e.g., standard poodles, Akitas) the first sign of disease is follicular casts protruding from the hair follicle. When hairs are plucked, the follicular keratinaceous debris cast the root of the hair shafts. In standard poodles, the disease starts most often on the dorsal muzzle and temporal region, spreading to the dorsal neck and thorax, whereas in Akitas the alopecia is typically more extensive. Broken hair shafts, dull and brittle hair coat, excessive scaling, change in hair colour, and musty odour may be seen. Pruritus is variable but may be marked, especially if secondary bacterial or yeast infection is present. In the Akita, where the disease can be more severe, fever, anorexia, and lethargy have been reported.

2 In short-coated dogs such as Vizsla, clinical presentation consist of coalescing patches of scaly alopecia with adherent scales developing more commonly on the face, head, and trunk. Presence of follicular casts and alopecia in a susceptible breed is highly suggestive of the disease. Skin biopsy and histopathological examination is necessary to confirm the diagnosis. In the early phase, dermatohistopathological changes are characterized by discrete perifollicular inflammation at the isthmus level of hair follicles. Later, nodular, granulomatous to pyogranulomatous inflammatory reaction around the sebaceous glands is seen. In addition, orthokeratotic hyperkeratosis and follicular plugging is observed in long-coated breeds. These hyperkeratotic changes tend to be milder in short-coated breeds. In advanced stages of the disease, the sebaceous glands are completely destroyed and the inflammatory reaction may disappear. Telogenization of hair follicles or follicular atrophy may occur. Suppurative folliculitis or furunculosis can be found when secondary staphylococcal infection is present. Skin scrapings and hair plucks (trichoscopy) are useful for ruling out ectoparasites. Casts of keratosebaceous material adherent to hair shafts can be seen on trichoscopic examination, which is suggestive of sebaceous adenitis, particularly in absence of Demodex mites. Cytologic examination to assess for presence of secondary bacterial or Malassezia infection, and Wood s lamp and dermatophyte culture to rule out dermatophytosis may also be required. Secondary sebaceous gland destruction with similar clinical hyperkeratosis can also occur with demodicosis, leishmaniasis, and severe granulomatous and histiocytic folliculitis. also includes dermatophytosis, bacterial folliculitis and various cornification disorders such as ichthyosis. Topical treatment with oil soaks, humectants (propylene glycol 50-75%) and shampoos are often effective but quite laborious. Oral cyclosporine (5 mg/kg q24h) has been shown to improve the clinical signs and to reduce inflammation greatly, as well has achieving regeneration of sebaceous glands. It is, however, an expensive treatment option. There is evidence of a synergistic benefit on both scaling and alopecia if topical therapy is combined with oral cyclosporine. Isotretinoin has been reported to be effective in Vizsla. However, it is difficult to comprehend why considering they are known to reduce sebaceous gland size and decrease sebum secretion. DERMATOMYOSITIS Canine dermatomyositis is a hereditary, idiopathic inflammatory skin and muscle disease wellcharacterized in Collies and Shetland Sheepdogs. of dermatomyositis is still unknown, although an autosomal dominant mode of inheritance with variable expression has been proposed. In Shetland Sheepdogs, inheritance of dermatomyositis has been linked to canine chromosome 35. An immune-mediated or autoimmune basis is possible but it is unclear if immune reaction is the cause of the disease or is in response to pre-existing muscle or skin damage. Lesions could be induced by drugs, vaccines, infection (especially viral), toxins, internal disease, but causal relationship is unproven. Mechanical trauma and sunlight (UV), and reproductive stress (estrus, parturition, and lactation) may worsen the lesions.

3 Vascular lesions and local ischemia appear to play a central role in disease process, explaining the distribution of lesions which occur at pressure points and areas of low sustained circulation (ear and tail tips). A familial basis as been reported in collies, Shetland sheepdogs, Beauceron shepherds; however, the disease has been diagnosed in many other breeds including Australian cattle dog, Welsh corgis, and chow chow. Clinical signs are usually first noticed in dogs less than 6 months, and as early as 7 weeks of age. They wax and wane and vary from minor skin lesions (patchy alopecia, rarely vesicles) to severe ulceration of the skin, with a generalized debilitating myositis affecting the head and distal limbs. Skin lesions are generally characterized by alopecia, erosions and crusting around the eyes, on the bridge of the nose, pinnae, bony prominences (elbows, hocks, digits), and the tail tip. Vesicles and ulceration may be seen. Some dogs also present with onychodystrophy. Pruritus is normally absent unless complicated by another condition such as pyoderma. Many dogs show some degree of skeletal muscle involvement that can vary from subtle atrophy of temporal and masseter muscle to generalized muscular atrophy with megaesophagus and lameness. Young dogs presenting with alopecia and crusting on face, pinnae, and tail tip along with muscle wasting in a predisposed breed (e.g., collie, Shetland sheepdog) is highly suggestive of dermatomyositis. Initial data base may include skin cytological examination to rule out pyoderma and/or Malassezia overgrowth, skin scrapings to rule out demodicosis, and Wood s lamp and fungal culture to rule out dermatophytosis. Serum biochemistry profile may show elevated creatine kinase. CBC and urinalysis results are usually unremarkable. Histopathological evaluation of skin biopsy is characterised by hydropic degeneration in the basal cell layer and cell-poor lymphohistiocytic interface dermatitis. Follicular atrophy may be noted in chronic lesions. Vasculitis is occasionally seen. includes demodicosis, dermatophytosis, bacterial folliculitis, Malassezia dermatitis, discoid lupus erythematosus, and vasculitis, and adult-onset generalized ischemic vasculopathy. The lesions wax and wane and response to therapy is difficult to evaluate. For acute flares, prednisone 1 mg/kg q24h, weaning down to an alternate-day regimen based on a favorable response is recommended. Prednisone can be use in conjunction with pentoxifylline (25 mg/kg q12h) for severe acute flares. Focal lesions can be treated with topical 0.1% tacrolimus. Chronic management includes pentoxifylline (25 mg/kg q12h) alone, Vitamin E IU/12h, oral cyclosporine, topical tacrolimus, and/or oral tetracycline and niacinamide (250 mg q8h PO for dogs < 10 kg or 500 mg q8h PO for dogs > 10 kg of each drug given for a minimum of 3 months, weaning down based on a favourable response). Flares can be minimized by avoidance of sunlight. Affected dogs should be neutered.

4 POST-RABIES VACCINE ALOPECIA Localized or generalized ischemic vasculopathy may result from rabies vaccine administration. The causal pathomechanism remains unknown, but it is likely that the formation of rabies antigenantibody complexes that become lodged in vessel walls (a type III hypersensitivity response) is involved. Rabies viral antigen has been demonstrated in vessels and in the epithelium of hair follicles. Rabies vaccine-associated ischemic dermatopathy is usually seen in adult dogs. It is typically seen in small breeds such as miniature poodle, bichon Frisé, Shih Tzu, Lhasa Apso, Maltese, Yorkshire terrier, and Chihuahua. The onset of clinical signs is typically 2 to 3 months after vaccine administration, but occasionally takes longer to develop. It usually consists in a focal alopecic lesion at the site of vaccine-administration, but occasionally can be widespread (see adult-onset generalized ischemic dermatopathy). The local form typically occurs over the shoulders, back or the posterolateral thighs and is characterized by a firm circular patch of erythema and alopecia. Old lesions often have a shiny appearance with mild scaling. Histopathological changes are characterized by nodular perivascular accumulations of lymphocytes, plasma cells, and histiocytes in the deep dermis and panniculus. Macrophages occasionally contain cytoplasmic basophilic material that is believed to be phagocytized vaccine product. The dermal changes also include moderate to severe follicular atrophy, hyalinization of collagen, mild interface dermatitis and mural folliculitis. These changes are often accompanied by cell-poor vasculitis (often quite subtle) of small blood vessels in the panniculus and the deep dermis. This localized form of ischemic dermatopathy does not necessarily require therapy. If inflammation is prominent, short course of glucocorticoids may be used. Pentoxifylline (25 mg/kg q12h) in combination with vitamin E (200 to 800 IU q12h) also can be used if needed. ADULT-ONSET GENERALIZED ISCHEMIC DERMATOPATHY (rabies vaccine-induced or idiopathic) Post-rabies vaccination alopecia associated with concurrent multifocal ischemic dermatopathy can rarely occur. Clinically, it emulates canine dermatomyositis, suggesting that the disease is caused by local ischemia of skin regions that are prone to impaired circulation. The main difference is the older age of onset. A similar clinical manifestation has been reported in Jack Russel terriers with no obvious history of previous vaccination. In rabies vaccine-induced generalized ischemic dermatopathy, multifocal skin lesions develop within a few months after the appearance of the initial skin lesion at the injection site. However, some dogs never develop a lesion at the injection site. Lesions consist in alopecia, crusting, hyperpigmentation, erosions, and ulcers on the pinnal margins, periocular areas, skin overlying boney prominences, tip of the tail, and paw pads. Lingual erosions and ulcers can also bee seen.

5 The dermatohistological changes observed are indistinguishable from those observed in canine dermatomyositis, suggesting a common aetiopathogenesis of immunological damage to the vessels, resulting in ischemic damage to susceptible tissue. In addition, an atrophic, ischemic myopathy paralleling the onset of skin disease can also be seen. The generalized form of ischemic dermatopathy requires systemic therapy. As for dermatomyositis, pentoxifylline (25 mg/kg q12h) or prednisone (1 mg/kg q24h) can be used. Dapsone (1 mg/kg q8h) has also been recommended. Some patients may need a more aggressive immunosuppressive therapy with higher doses of prednisone, cyclophosphamide or azathioprine. ALOPECIA AREATA (Pelade) Alopecia areata is rare in dogs, in contrast to human where it is a relatively common disease. It is believed that the hair bulb melanocyte is a target cell population. Deposition of both immunoglobulin (particularly IgG) and complement around hair follicles, and the presence of circulating IgM and IgG to hair follicle-specific antigens have been documented. However, the pathogenic potential of anti-hair follicle autoantibodies in canine alopecia areata remains unclear. Age of onset is highly variable, ranging from one to 11 years. Dachshunds appear predisposed. Lesions usually consist of spontaneously arising and well-demarcated alopecic patches developing first on the head (muzzle, chin, forehead, peri-ocular, ears) and occasionally on the legs. Facial lesions usually exhibit a bilateral symmetry. In some cases, alopecia can progress to a more generalized distribution. In multicoloured-coated dogs, alopecia usually occurs first in dark brown or black areas (preferentially targeting of pigmented hair). Spontaneous and complete hair regrowth occurred in many dogs. Such regrowth is commonly of white hair, a feature also seen in humans and rodents with alopecia areata. In humans, in the more extensive forms of the disease (alopecia totalis and alopecia universalis), spontaneous remission is rare. Histopathological examination of skin biopsies are required to confirm the diagnosis. The histological hallmark is the so-called swarm of bees consisting of a mild to marked mononuclear cell infiltrate, predominantly composed T-lymphocytes, focusing in (bulbitis) and around (peribulbitis) the anagen hair bulb. As with alopecia areata in humans, T-cells infiltrating the hair bulb epithelium itself are more commonly CD8+, while CD4+ cells predominate in the peribulbar region. includes demodicosis, dermatophytosis, bacterial folliculitis, isthmic mural lymphocytic folliculitis (pseudopelade), ischemic alopecias such as dermatomyositis and rabies vaccineassociated alopecia, and vitiligo. Oral cyclosporine administration appears to be effective in dogs with alopecia areata.

6 ISTHMIC LYMPHOCYTIC MURAL FOLLICULITIS (Pseudopelade) Isthmic lymphocytic mural folliculitis is a very rare immune-mediated disease in dogs. Isthmic lymphocytic mural folliculitis in dogs bears some clinicalpathological resemblance to pseudopelade of Brocq in humans which is characterized by a slowly progressive cicatricial alopecia and to the clinical similarity (pseudo) to alopecia areata (pelade) hence the term pseudopelade. However, since pseudopelade in humans represents the end stage of several diseases and thus is an ill-defined term, it has been suggested to use the descriptive term of isthmic lymphocytic mural folliculitis. Of note, canine isthmic mural folliculitis can also be observed in conjunction with demodicosis, dermatophytosis and sebaceous adenitis. As for alopecia areata, it is unknown whether the occurrence of autoantibodies to keratinocyte proteins is a primary or a secondary event in the pathogenesis of this disease. Recently, a non-infectious, mural, mucinotic, isthmus folliculitis alopecia has been reported in Norwegian puffin dogs (lundehunds). It is characterized by a multifocal or serpiginous alopecia, follicular plugging, dry skin, slight scaling and pruritus. A lymphoplasmacytic, mural, isthmus folliculitis/perifolliculitis with follicular and perifollicular mucin was observed on histopathological examination of skin biopsies. Inflammation did not involve the hair bulb but sometimes extended to the sebaceous glands, resulting in atrophy and absence of glands. Spontaneous remission was rare. Clinically, the disease is characterized by gradually progressing non-pruritic, non-inflammatory focal or multifocal well-demarcated patches of alopecia. Scales and hyperpigmentation may be present. Spontaneous hair regrowth may be observed except for the syndrome observed in lundehunds. The major histological finding is a mild to marked predominantly lymphocytic infiltration targeting the mid hair follicle (isthmus) sections. A perifollicular mononuclear infiltrate is also present around the isthmus. In late stage lesions severe follicular atrophy and variable atrophy of sebaceous glands, and sparse inflammation is seen. In lundehunds, follicular and perifollicular mucin is also observed. includes demodicosis, dermatophytosis, bacterial folliculitis, alopecia areata, ischemic alopecias such as dermatomyositis and rabies vaccine-associated alopecia. Due to the small number of cases that have been described in the scientific literature, there is no established therapy for isthmic mural folliculitis in dogs. Cyclosporine was shown to be effective for this disease. In the mucinotic, isthmus folliculitis of the lundehunds, oral prednisolone reduced pruritus but was not effective in resolving clinical lesions. However, all dogs treated with ciclosporin went into remission. REFERENCES 1. Bergvall K, Shokrai A. Clinical and histological characterization of multifocal, spontaneous, noninfectious alopecia in Norwegian puffin dogs (lundehunds). Vet Dermatol. 2014:25: Frazer MM et al. Sebaceous adenitis in Havanese dogs: a retrospective study of the clinical

7 presentation and incidence Vet Dermatol. 2011:22: Gross TL, Ihrke P., Walder EJ, Affolter VK: Skin diseases of the dog and cat. Clinical and histopathologic diagnosis. 2nd ed. Blackwell Science Gross, T.L. & Kunkle, G.A. The cutaneous histology of dermatomyositis in Collie dogs. Vet Pathol. 1987; 24: Gross, T.L. Olivry T, Tobin D. Morphologic and immunologic characterization of a canine isthmus mural folliculitis resembling pseudopelade of humans. Vet Dermatol. 2000;11: Hargis, A.M. & Mundell, A.C. Familial canine dermatomyositis. Comp on Cont Ed 1992; 14: Hargis, A.M., Prieur, D.J, Haupt, K.H., McDonald, T.L., Moore, M.P. Prospective study of familial canine dermatomyositis. Correlation of the severity of dermatomyositis and circulating immune complex levels. American Journal of Pathology 1986; 123: Lam ATH et al. Oral vitamin A as an adjunct treatment for canine sebaceous adenitis. Vet Dermatol. 2011:22: Lortz J, Favrot C, Mecklenburg l, Nett C, Rüfenacht S, Seewald W, Linek M. A multicentre placebo-controlled clinical trial on the efficacy of oral ciclosporin A in the treatment of canine idiopathic sebaceous adenitis in comparison with conventional topical treatment. Vet Dermatol. 2010;21: Miller WH Jr, et al: Muller & Kirk s Small animal dermatology 7 th ed., St. Louis, 2013, Elsevier Saunders. 11. Morris DO. Ischemic Dermatopathies Vet Clin Small Anim 2013; 43: Parker, W.M. & Foster, R.A. Cutaneous vasculitis in five Jack Russell Terriers. Vet Dermatol.1996;7: Reichler IR. et al. Sebaceous adenitis in the Akita: clinical observations, histopathology and heredity. Vet Dermatol. 2001;12; Vitale CB, Gross TL, Magro CM. Vaccine-induced ischemic dermatopathy in the dog. Vet Dermatol. 1999;10: Wilcock, B.P. & Yager, J.A. Focal cutaneous vasculitis and alopecia at sites of rabies vaccination in dogs. J of the Am Vet Assoc 1986;188:

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