Pododermatitis 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 pododermatitis 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

Pododermatitis 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 pododermatitis include diffuse erythema and thickening of the skin, particularly in the dorsal interdigital and ventral palmoplantar regions. The primary lesions of pododermatitis are often complicated by alopecia, hyperpigmentation, pyoderma and sinus tracts with serosanguineous/seropurulent discharges. Nodules, ulcers, haemorrhagic bullae and swelling of the feet are also reported. Pododermatitis 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 inappetence.

Aetiology of Pododermatitis

Aetiological causes of pododermatitis 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 pododermatitis 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 pododermatitis 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 pododermatitis 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 pododermatitis. 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 dermatitis.

A trial elimination diet and modified environment are indicated for cases of suspected food hypersensitivity and contact dermatitis, respectively. Patch testing may sometimes prove beneficial in confirming a diagnosis of contact allergic dermatitis, although this technique has certain practical limitations. Atopic dermatitis 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 pododermatitis 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 antiparasitic agents, combined with other control/preventative measures, will usually prove curative. Pedal lesions due to atopic dermatitis 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 dermatitis or food allergy, respectively, though symptomatic anti-inflammatory therapy may be indicated in the short-term 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 pododermatitis requires the introduction of an appropriately formulated diet, or dietary zinc supplementation as appropriate.

Some causes of pododermatitis, 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 acrodermatitis) 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 anti-inflammatory ± antimicrobial therapy may be indicated to symptomatically control clinical signs in such cases. For some dogs with idiopathic pododermatitis, long-term or pulse antibiotic therapy is recommended to control relapsing interdigital pyoderma; however, another sub-group 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 Pododermatitis

Despite the large number of differential diagnoses for pododermatitis 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 pododermatitis (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 Pododermatitis

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 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 dermo-epidermal 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 pododermatitis, 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 antibiotic-responsive. 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.

Table 1. Diagnostic / ancillary tests recommended to help confirm the aetiology in dogs with pododermatitis.