Proceedings of the 33rd World Small Animal Veterinary Congress

www.ivis.org Proceedings of the 33rd World Small Animal Veterinary Congress Dublin, Ireland - 2008 Next WSAVA Congress :

8 Dermatology Int r a c ta b l e p o d o d e r m at i t i s : diagnosis a n d c a s e m a n a g e m e n t Rory Breathnach MVB, PhD, MRCVS University Veterinary Hospital, University College Dublin, Belfield, Dublin, Ireland Podo is a common and frequently debilitating inflammatory disease of the pedal skin of dogs. The clinical history is often characterized by periods of disease exacerbation and remission. While podo may represent simply one component or manifestation of an otherwise more extensive dermatological disease, some dogs have lesions confined solely to the foot. Clinical features Podo has no specific age, sex or breed predispositions although short-coated breeds such as boxers, bulldogs, bull terriers and German shorthaired pointers are over-represented in some surveys. The clinical signs of podo include diffuse erythema and thickening of the skin, particularly in the dorsal interdigital and ventral palmoplantar regions. The primary lesions of podo are often complicated by alopecia, hyperpigmentation, pyoderma and sinus tracts with serosanguinous/seropurulent discharges. Nodules, ulcers, haemorrhagic bullae and swelling of the feet are also reported. Podo is frequently painful and pruritic. Salivary staining of pedal hairs may occur and paronychia is occasionally seen. Severely affected animals may be reluctant to walk or may display systemic ill health including depression and inappetance. Aetiology of podo Aetiological causes of podo are numerous, and are detailed in Table 1. It should be emphasized, however, that for many of the conditions specified in Table 1, affected animals may have cutaneous lesions at sites in addition to the feet. Diagnosis The diagnostic investigation of dogs with podo should include the collation and analysis of a detailed history, an in-depth clinical examination and appropriate laboratory or ancillary tests. History Initial attention should focus on the housing and general environment of the dog. Rough surfaces that can traumatize the skin and unsanitary housing or runs should be excluded as possible underlying causes. The irritant or allergenic potential of the animal s bedding, or various preparations used within the immediate environment, should be considered. The health status of in-contact animals may also be important if environmental or infectious causes are suspected. The duration of disease or any seasonal recurrence could be an important consideration. The response, or lack thereof, to previous medication may heighten the index of suspicion for certain underlying causes. Attention should also focus on any potential iatrogenic component. A detailed dietary history should also be obtained. Other relevant factors in the history include the presence of skin lesions at other body sites and the animal s general health status. Any history of stress could be significant in cases with a suspected psychogenic component. As certain causes of podo are potentially zoonotic to humans, any history of skin disease involving family members or other in-contact people should be ascertained. Clinical examination Attention should focus on precise identification of the lesion pattern or type. Any alteration in the nature or distribution of the lesion(s) is also important and may suggest secondary changes such as microbial infection. However, the clinical appearance of lesions in podo rarely allows for the underlying cause to be identified without confirmation by ancillary diagnostic tests. Laboratory / ancillary tests Table 1 lists the specific laboratory/ancillary tests required to investigate the various aetiological causes of podo. In general, the initial laboratory tests indicated include the examination of skin scrapings/ hair plucks, fungal culture, trichograms and stained smears of exudate or pustular contents to rule out the various infectious causes of disease. Bacterial culture and susceptibility testing are also indicated in cases presenting with (sero)purulent discharges, and in dogs displaying chronic lesions that are non-responsive to treatment. Biopsy specimens for histopathology usually allow confirmation of the diagnosis and may prove invaluable in identifying the underlying aetiology. Biopsy material may also be submitted for bacterial and fungal culture. Immunohistochemical staining of lesional skin biopsies may allow for the demonstration of immunoglobulin (IgG, IgA or IgM) and complement component deposits in the epidermis or at the basement membrane zone. A zinc sulphate faecal flotation test may be performed to rule out hookworm. A trial elimination diet and modified environment are indicated for cases of suspected food hypersensitivity and contact, respectively. Patch testing may sometimes prove beneficial in confirming a diagnosis of 156 WSAVA / FECAVA Programme 2008

Dermatology 8 contact allergic, although this technique has certain practical limitations. Atopic is usually diagnosed on the basis of history, clinical signs and the exclusion of all other resembling pruritic dermatoses, with intradermal testing and serological testing for allergen-specific IgE or IgG being frequently employed to help select allergens for incorporation in immunotherapy formulations. For cases of suspected endocrine or systemic disease, appropriate ancillary tests may include one or more of haematology, biochemistry, urinalysis, diagnostic imaging, tissue biopsy and dynamic endocrine testing. Serum immunoglobulin and lymphocyte blastogenesis assays are indicated in dogs in which underlying humoral or cell-mediated immunodeficiency disorders, respectively, are suspected of contributing to the pathogenesis of recurrent microbial pedal skin infections. Based on the results of these initial tests, more in-depth diagnostic methods including specialized staining protocols, polymerase chain reaction or culture techniques may subsequently be indicated to confirm a diagnosis of atypical bacterial, fungal or protozoal infection. Treatment and prognosis The treatment of dogs with pododo is largely influenced by the underlying aetiological cause of disease (see standard texts). For many infectious and parasitic causes of disease, the use of appropriate systemic/topical antimicrobial or antiparastic agents, combined with other control/preventative measures, will usually prove curative. Pedal lesions due to atopic are normally controlled through allergen avoidance (if possible), allergen-specific immunotherapy or appropriate pharmacotherapy. Avoidance of offending drugs, contact allergens/irritants or dietary proteins is usually sufficient for the longer-term control of dogs with drug hypersensitivity, contact or food allergy, respectively, though symptomatic antiinflammatory therapy may be indicated in the shortterm management of these cases. For immune-mediated diseases such as pemphigus complex or discoid lupus erythematosus, immunomodulatory drugs such as prednisolone, cyclosporine or topical tacrolimus are typically required. Hormonal and other metabolic causes of disease are treated using conventional standard of care therapy. Zinc-responsive podo requires the introduction of an appropriately formulated diet, or dietary zinc supplementation as appropriate. Some causes of podo, however, carry a more guarded to poor prognosis due to the severity (e.g. hepatocutaneous syndrome) or genetic basis (e.g. nodular dermatofibrosis, familial hyperkeratosis, lethal acro) of the underlying pathology. For others, the dynamic nature of the disease means that inflammatory lesions (e.g. pyogranulomas) can persist or progress even after the initiating cause has been identified and removed. Once again, longer-term antiinflammatory ± antimicrobial therapy may be indicated to symptomatically control clinical signs in such cases. For some dogs with idiopathic podo, long-term or pulse antibiotic therapy is recommended to control relapsing interdigital pyoderma; however, another subgroup of dogs with idiopathic disease fail to respond to antimicrobial drugs or autogenous vaccines, and instead require glucocorticoids or other immunomodulatory agents to control clinical signs. A surgical procedure, termed a fusion podoplasty, has been recommended for cases of chronic fibrosing interdigital pyoderma that fail to respond adequately to conventional therapy. In this latter procedure, chronically inflamed skin between the digits is surgically removed, and skin/pad flaps sutured together to help reconstruct the pedal surface. Although several weeks to months are required for full tissue healing, the above procedure has resulted in meaningful longer-term benefits for many chronically affected patients. Idiopathic podo Despite the large number of differential diagnoses for podo outlined in Table 1, the results of laboratory and other ancillary investigations in affected dogs frequently prove unrewarding. Animals that fall within this category are classified as having idiopathic podo (IP). Although poorly understood, various theories have been proposed to explain the underlying pathogenesis in idiopathic disease including pedal conformation, trauma, immunosuppression, bacterial infection and furunculosis with dermal granuloma formation. Bacterial infection has been reported to be a significant component of IP. However, bacterial infection invariably occurs secondary to other diseases such as hypersensitivity disorders or immunosuppression. Furthermore, pedal lesions that heal by second intention may be predisposed to mixed dermal infections involving opportunistic bacteria. It has been suggested that bacterial folliculitis may progress to furunculosis, with the subsequent release of follicular contents into the dermis and resultant granuloma formation. Thus, it is possible that bacterial infection and hair follicle-related pathology may contribute to the dynamism frequently encountered in IP dogs. Lymphocytic-plasmacytic podo A sub-population of IP dogs has recently been described in which affected animals are systemically healthy but have persistent inflammation and pruritus confined to the pedal skin. Lesions are characterized clinically by erythema, swelling, pain and alopecia. Although failing WSAVA / FECAVA Programme 2008 157

8 Dermatology Aetiology Diagnostic/ancillary tests recommended Cold agglutinin disease Biopsy, serological testing for coldreacting autoantibodies Infectious diseases Endocrine diseases Bacterial Cytology, culture and biopsy. PCR for some atypical Mycobacteria spp. Hypothyroidism Biopsy, thyroid function tests, scintigraphy of thyroid gland Dermatophytosis Malassezia Wood s lamp (certain species), KOH of skin scrapings/hair plucks, culture Cytology, culture on Sabouraud s agar or modified Dixon s agar, biopsy Hyperadrenocorticism Hepatocutaneous syndrome ACTH stimulation and dexamethasone suppression tests, ultrasound Skin biopsy, serum biochemistry, ultrasound and FNA/biopsy of liver Intermediate/deep mycoses Demodicosis Biopsy, culture of lesional tissue samples Skin scrapings, biopsy Environmental causes Irritant contact History, clinical signs, avoidance of suspect irritant Neotrombicula infestation Pelodera Hookworm Leishmaniosis Hypersensitive diseases Atopic Food hypersensitivity Contact allergic Drug hypersensitivity Bacterial hypersensitivity Fungal hypersensitivity Autoimmune diseases Pemphigus complex Bullous pemphigoid Systemic lupus erythematosus Visual inspection, microscopy Skin scrapings, biopsy. Modified Baermann technique on litter Faecal flotation test Biopsy. PCR for leishmanial DNA in lesional tissue History, clinical signs and exclusion of resembling pruritic dermatoses Food trial using a novel protein source History, avoidance of suspect allergen, patch testing History, skin biopsy, basophil degranulation test possible Biopsy, intradermal skin testing using staphylococcal extract(s) Biopsy, intradermal skin testing using fungal extract(s) Trauma Frost bite Foreign body History, clinical signs History, clinical signs Surgical exploration of site, biopsy Hyperkeratotic, nodular and pigmentary dermatoses Zinc-responsive dermatosis Digital hyperkeratosis Sterile (pyo)granuloma Nodular dermatofibrosis Biopsy, dietary or breed history. Serum/hair zinc concentrations variable Biopsy, exclusion of other causes of hyperkeratosis Biopsy Biopsy ± ultrasound and biopsy of kidney lesions Psychogenic/ neurological History, clinical signs, biopsy, Acral lick exclusion of other causes Acral mutilation syndrome History, biopsy of affected nerve tissue Table 1. Diagnostic / ancillary tests recommended to help confirm the aetiology in dogs with podo Discoid lupus erythematosus 158 WSAVA / FECAVA Programme 2008

Dermatology 8 to identify the underlying aetiology, lesional biopsies provided evidence of perivascular lymphoplasmacytic infiltrates in all cases investigated. These mononuclear cell infiltrates were predominantly present in the superficial dermis, mid-dermis and beneath the dermoepidermal junction. Additional inflammatory cells (mast cells, eosinophils, macrophages) were only observed in small numbers in individual sections. Epidermal lesions commonly present included hyperkeratosis, epidermal hyperplasia, spongiosis and focal mononuclear cell exocytosis. The interpretation of lymphoplasmacytic infiltrates in skin biopsies is a subject of debate, with some veterinary dermatopathologists viewing them as a common non-specific finding at glabrous and mucocutaneous skin sites. However, the presence of large numbers of lymphocytes and plasma cells within a lesion typically suggests antigenic stimulation and immune reactivity. Although most chronic non-specific dermatitides in the dog contain some lymphoid cells within the inflammatory infiltrate, these cells do not usually dominate the histological appearance of the lesion. Lymphoplasmacytic infiltrates have previously been reported in both antibiotic-responsive and immunomodulatory-responsive dermatoses in the dog. As recurrent interdigital pyoderma is a common cause of relapsing podo, it is initially advisable to employ a combined approach of culture, cytology, biopsy and response to antimicrobial therapy to try and determine which of these cases are truly antibioticresponsive. However, when faced with negative results and/or a poor clinical response, immunomodulatory therapy using prednisolone (2 mg/kg PO q24h) or cyclosporine (5 mg/kg PO q24h) is typically required to obtain lesion resolution. Although tapering of the dose is usually possible for longer-term management, cessation of therapy often results in a relapse of clinical signs in affected individuals. WSAVA / FECAVA Programme 2008 159