Introduction

Pododermatitis describes any inflammation of the paw, but the most common problem is chronic interdigital furunculosis. Affected dogs have frequent flares of inflammation and infection. It is very important to manage the underlying causes to reduce or prevent chronic changes. Chronic changes such as hyperplasia or new pad formation make long-term control much harder.

Pododermatitis—A Condition with Primary, Secondary, Predisposing and Perpetuating Causes

Primary Factors

These trigger the initial pedal inflammation. The primary cause may be very subtle and easily missed, especially in chronic cases. Primary causes include:

• Atopic dermatitis
• Adverse food reaction
• Contact allergy
• Foreign bodies/contact irritants (e.g., hair, stone, sand, salt etc.)
• Idiopathic sterile granuloma
• Immunomodulatory-responsive pododermatitis
• Footpad hyperkeratosis and other cornification disorders
• Hypothyroidism
• Hyperadrenocorticism
• Demodex
• Hookworm
• Dermatophytosis (Trichophyton)
• Leishmania

Immunomodulatory-responsive pododermatitis is characterised by severe lymphocytic-plasmacytic pedal inflammation and secondary infection. It responds well to immunosuppressive or immunomodulatory treatment, although it is unclear whether it is always a primary problem or it is a chronic change.

Predisposing Factors

These increase the risk of developing pododermatitis but less commonly cause disease themselves. Predisposing factors include short hairs (which can cause foreign body reactions and chronic inflammation), increased weight bearing (obesity and large breed dogs) and altered weight bearing (limb deformity, osteoarthritis and cruciate disease).

Perpetuating Factors

These prevent resolution, inducing a cycle of inflammation and altered pedal conformation. This is often associated with severe lymphocytic-plasmacytic inflammation. Changes include altered weight bearing (including haired skin), hyperkeratosis and lichenification, scarring and chronic inflammation, conjoined pads, new pad formation, deep tissue pockets, ingrown hairs and sinus tracts.

Secondary Factors

The altered micro-environment and inflammation predispose to secondary infections with organisms such as Staphylococcus pseudintermedius, Streptococcus, E. coli, Klebsiella, Pseudomonas and Malassezia. There can be multiple infections at different depths, especially in chronic cases.

Diagnostic Approach

A detailed history and examination is needed to determine the likely primary, predisposing and perpetuating causes in each case. Both the dorsal and palmer/planter foot surfaces should be inspected, with the interdigital spaces carefully opened out.

Hair plucks, skin scrapes and impression smears should be taken to rule out Demodex, but histopathology may be required in chronic cases. Histopathology can also achieve a definitive diagnosis of chronic pododermatitis. Impression smears should be used to confirm bacterial and/or Malassezia infection, but bacterial culture and sensitivity is mandatory if there is deep infection, and/or multiple antibiotic courses. Samples can be taken from ruptured pustules or draining sinus tracts, but biopsy is often necessary to isolate organisms from deep tissues.

If a foreign body or tumour is suspected, radiographs of the feet possibly with abdominal ultrasound may be appropriate. Haematology, serum biochemistry, thyroid tests and urinalysis should be performed if systemic disease is suspected. Regional lymph nodes are frequently enlarged due to local inflammation, but lymphoma should be ruled out. Fungal culture and faecal analysis can be performed if dermatophytosis or hookworm are suspected. Further investigations may include a diet trial and intradermal or serological allergy testing.

Management of Primary and Predisposing Factors

Management of the primary and predisposing triggers for the pododermatitis is crucial for successful long-term control. In our clinic, the most common primary conditions are atopic dermatitis and adverse food reactions.

Obesity is a common predisposing factor. Pododermatitis is more common in the forelimbs, which bear approximately 60–70% of bodyweight. Excess weight also exacerbates changes in limb conformation and weight-bearing surfaces. Management of pain, altered weight bearing and abnormal conformation could include analgesia and/or corrective surgery. Protective boots (e.g., Ruff Boots®) can be helpful, especially in dogs reluctant to exercise due to pain. Regardless of the cause, chronic inflammation, deep pyoderma, split pads, and non-healing wounds can be very painful. Prompt analgesia and boots should be considered in all cases.

Control of Secondary Infections

Systemic Antimicrobial Therapy

Systemic antibiotics should be selected using culture and sensitivity. Treatment may take 4–6 weeks. Scar tissue can inhibit the penetration of water-soluble antibiotics (e.g., penicillins and cephalosporins) and antibiotics (e.g., clindamycin or fluoroquinolones) with good penetration into scar tissue are beneficial.

Dogs with a staphylococcal hypersensitivity or recurrent infections may benefit from Staphage Lysate (SPL®). This could induce tolerance to staphylococcal proteins and/or enhance anti-staphylococcal immunity.

Some cases of Malassezia overgrowth require systemic antifungal therapy, especially with Malassezia hypersensitivity. Options include itraconazole, ketoconazole or terbinafine. Allergen-specific immunotherapy with Malassezia extracts can be beneficial.

Topical Antimicrobial/Antifungal Therapy

Daily cleaning of the paws is ideal, but the frequency can be reduced for maintenance. Owners should be shown how to spread the digits and thoroughly clean deep pockets or sinus tracts. Chlorhexidine is a highly effective antimicrobial but requires a 5–10 minute contact time. Chlorhexidine wipes are easier to use but have no residual activity and are not effective against Pseudomonas. Hypochlorous acid is a safe and potent antimicrobial but has no residual effect.

Topical antibiotics are often highly effective, but penetration can be variable, and they are less suitable for deep infections. Useful antibiotics include fusidic acid, silver sulfadiazine (which can be combined with gentamicin or marbofloxacin), neomycin or polymyxin B. Many products also contain a steroid (see below).

Anti-Inflammatory Treatment

Anti-inflammatory therapy should be initiated early to limit the development of chronic inflammation and other perpetuating factors. The correct diagnosis is important since immunosuppressive treatment may exacerbate demodicosis and bacterial infections. Both systemic and topical therapies are often required.

Systemic Anti-Inflammatory Treatment

Glucocorticoids are frequently used to reduce inflammation associated with pododermatitis, although they will cause adverse effects and patients on long-term therapy need regular monitoring of blood pressure and urinalysis. Prednisolone or methylprednisolone at 1–2 mg/kg PO every 24 hours is generally used, but dexamethasone at 0.1–0.25 mg/kg every 24 hours can be useful in more severe cases. However, the longer duration of activity makes it less suitable for long-term every-other-day usage, and dogs should be switched to prednisolone/methylprednisolone or twice-weekly therapy as soon as possible. Longer-term control usually requires 0.4–1 mg/kg prednisolone every 48 hours (or the equivalent).

Ciclosporin at 5–10 mg/kg every 24 hours is also beneficial. Long-term maintenance requires 1.5–4.5 mg/kg every 48 hours. Regular urinalysis is advised.

Oclacitinib is licensed for controlling pruritus in dogs with allergic dermatitis. However, chronic pedal inflammation in dogs with allergic skin disease does not respond as well to oclacitinib as to glucocorticoids or ciclosporin.

Topical Anti-Inflammatory Treatment

Topical treatment is most commonly used with systemic therapy to improve clinical remission, although it can be used alone in mild cases and to maintain remission. Once- or twice-daily therapy is used initially, tapering the frequency as the inflammation reduces.

Deep pockets of inflammation and scar tissue limit the efficacy of topical hydrocortisone aceponate. Nevertheless, it is useful for maintenance once the initial inflammation is controlled. More penetrating steroids such as fluocinolone or betamethasone acid are usually required. However, long-term use of these products can lead to local and systemic adverse effects. A 0.1% tacrolimus is also beneficial and well tolerated.

Cytotoxic Drugs

Where inflammation cannot be fully controlled and/or there are concerns over adverse effects, glucocorticoids can be combined with cytotoxic drugs such as azathioprine, chlorambucil, mycophenolate or methotrexate. All of these have the potential to cause bone marrow suppression and other side effects so regular haematology and serum biochemistry are mandatory.

End-Stage Disease and Surgery

Surgery may be required in cases refractory to medical treatment. Fusion podoplasty has been used but is associated with post-operative pain, wound dehiscence and infections.

Laser podoplasty offers minimal post-operative pain and a much-reduced recovery period (patients usually weight bear immediately after the procedure). A CO₂ laser is used to remove all the abnormal tissue and to resurface the foot. Lasers cut, ablate and coagulate tissues, resulting in less haemorrhage, pain and wound dehiscence, and destroy any bacteria, reducing the risk of post-operative infection. Treated tissues take 3–4 weeks to granulate and heal. Post-operative treatment in most cases simply requires daily cleaning and topical antimicrobials. Light bandages with daily changes are advisable for the first 7–10 days, but these are not usually necessary once there is a healthy granulation bed. Boots can be used to protect the foot outdoors until fully healed. Recurrence is less likely following laser podoplasty, as hair follicles, follicular cysts and sinus tracts are ablated and replaced with scar tissue.