How to Determine the Causes of Pododermatitis in Small Animals

Pododermatitis is common in small animal practice and can be frustrating if not properly diagnosed and treated. A useful way to approach pododermatitis is to think that there is a primary underlying disease (e.g., allergy) and often also a secondary infection (e.g., bacteria, yeasts) contributing to the pruritus. In most chronic cases, perpetuating factors (e.g., fibrotic changes, interdigital cysts) prevent resolution of the disease.¹ (Note that the differentiation between cysts and furuncles is under debate and is beyond the scope of this article.) For outcome success, all factors should be identified and corrected.

This article presents the differential diagnoses for diseases affecting the feet, footpads, and nails in dogs and cats and provides tips on how to rank the diseases based on specific clinical signs and presence of other clinical signs. The descriptions are presented in order of common (e.g., allergies) to less frequent (e.g., metabolic, autoimmune) clinical conditions.

History and Physical Examination of Pododermatitis

The history of patients with pododermatitis is extremely useful. Generally, allergic skin diseases start early in life (1 to 3 years of age) and progressively worsen. Knowing whether the problem occurs seasonally or all year is helpful, as is being aware of other clinical signs (e.g., autoimmune diseases wax and wane, and patients tend to be anorexic and lethargic during flares).

The combination of signalment, history, and findings on physical examination is used to formulate the list of differential diagnoses and their ranking. During physical examination, determining whether the footpads and/or nails are affected helps narrow down underlying diseases, as fewer diseases also affect footpads and nails. The type of lesions and their distribution should be noted, as should whether body areas other than the feet are affected. Signs of atopy start with pruritus, and initial lesions may be erythema only. Signs of contact allergy start with a primary papular eruption² (FIGURE 1), and if present, other areas of the body may be affected. In dogs with contact allergy, the erythema and pruritus can be severe (FIGURE 2) and their history is typically of having failed to respond to multiple antipruritic therapies.

FIGURE 1. Ventral interdigital spaces of a dog with contact allergy. Note the papular eruption in the interdigital spaces.

FIGURE 2. Severe erythema on the feet and legs of a dog with contact allergy.

Determining the Cause of Pododermatitis

STEP 1: Assess cytology.

Cytology and skin scraping should be performed for all dogs with pododermatitis as infections are very common and Demodex infestations can be exhibited in different ways. Failure to address infections can complicate the response to treatments and the interpretation of food trials. Infections increase pruritus and thus need to be eliminated before it can be determined whether the underlying disease is a pruritic one. Therefore, among the first diagnostic tests to perform for each evaluation of a patient with pododermatitis is skin cytology, which can indicate presence and kind of bacteria as well as presence of yeasts (e.g., Malassezia).

Yeasts can dramatically increase pruritus and many times lead to treatment failure when dogs with allergies receive antipruritic drugs but no treatment for the yeast infection. Yeasts can affect the interdigital areas and sometimes also the nail bed area, leading to rusty discoloration of the nails. If the infection is caused by bacteria, depending on the depth of the infection, initial treatment can be topical (e.g., chlorhexidine) and possibly systemic if the infection is deep. For patients that have already received multiple courses of systemic antibiotics, a sample should be submitted for culture and sensitivity. Multidrug resistance is rampant among dermatology patients,³ and deep infections require long courses of treatment; therefore, identifying the correct antibiotic is crucial.

After infection has been ruled out and/or controlled, common differentials for pododermatitis with no nail or footpad involvement are demodicosis and allergies.

STEP 2: If no infection is detected, take a deep skin scraping to check for pododemodicosis.

A common cause for pododermatitis is infestation with Demodex mites (pododemodicosis), which can cause pruritus and not just hair loss. The patient can exhibit hyperpigmentation (FIGURE 3), comedones (FIGURE 4), erythema (FIGURE 5), and alopecia (FIGURE 6). Deep pyoderma is common in patients with pododemodicosis, leading to swollen and painful feet (FIGURE 7).

FIGURE 3. Hyperpigmentation and hypotrichosis in a young dog with pododemodicosis. The hyperpigmentation is the result of the coalescing comedones.

FIGURE 4. Close-up of the ventral interdigital spaces of a dog with pododemodicosis with evident comedones.

FIGURE 5. Erythema and hypotrichosis in a dog with pododemodicosis. The patient was very pruritic and was chewing on his feet, leading to a secondary bacterial infection.

FIGURE 6. Alopecia and crusting on a dog with pododemodicosis and secondary deep bacterial infection. This type of presentation can be challenging because feet are painful and bleed easily when scraped, sometimes leading to false-negative deep skin scraping results.

FIGURE 7. Interdigital alopecia and oozing of the skin in a dog with pododemodicosis and secondary bacterial infection.

STEP 3: If infection and pododemodecosis are ruled out, consider allergic disease.

If the history is suggestive of an allergic disease, then the clinician should formulate a plan to rule out a food allergy for nonseasonal cases (by performing an appropriate food trial), rule out a contact allergy (by performing a confinement trial), and/or consider a clinical diagnosis by exclusion of atopic dermatitis. Cases considered to be “resistant atopic dermatitis” can sometimes actually be cases of contact allergy. Practically speaking, ruling out contact allergy is much faster (7 to 10 days of avoidance) than ruling out food allergy (2 to 3 months of a food trial).

Food trial: Two factors are typically evaluated: pruritus and relapse of secondary infection. Thus, successful infection control is essential for proper interpretation of food trial response. Extensively hydrolyzed diets are preferred over partially hydrolyzed diets⁴ and, if feasible, individual amino acid diets are believed to be a valid choice for food trials.

Confinement trial: To rule out a contact allergy, washing the patient, practicing avoidance for 7 to 10 days, and monitoring pruritus and lesions are recommended. Worsening of signs within 24 to 28 hours after reexposure indicates a positive response.

STEP 4: Determine whether the nails and/or footpads are involved.

STEP 5A: If nails are involved, consider the following:

When the nails are also affected, they are often brittle and distorted (onychodystrophy) or sloughing (onychomadesis). Common differentials are dermatophytosis and symmetric lupoid onychodystrophy.

Dermatophytosis

Dermatophytes require keratin to thrive; thus, when the infection is on the feet, common lesions are alopecia and crusting of the haired areas and dystrophy of the nails (FIGURE 8). To obtain a diagnosis, affected nails are clipped and placed on dermatophyte test medium for testing in-house or at an outside laboratory. Usefulness of Wood’s lamp testing is limited as dermatophytes that cause pododermatitis do not fluoresce under this light. Antifungal drugs that accumulate in nails (e.g., itraconazole, terbinafine) are suitable choices for onychomycosis. However, before starting treatment, running a blood chemistry panel is recommended as these drugs are heavily metabolized in the liver.

FIGURE 8. Dystrophic nail resulting from dermatophytosis.

Symmetric Lupoid Onychodystrophy

This clinical syndrome may affect only the nails or may be associated with vasculitis in some patients. The exact cause is not fully understood, but some genetic association in bearded collies has been documented.⁵ Affected dogs are otherwise systemically healthy. Multiple feet may be affected. Before the nails are lost, they first characteristically lift off and are replaced by a small, soft, distorted nail (FIGURE 9). Before the nail separates, the nail bed may swell and the outer nail may separate from the lower nail (FIGURE 10).

FIGURE 9. Nails of patients with symmetric lupoid onychodystrophy. (A) Multiple nails have been lost and replaced by short, soft, distorted, and hemorrhagic nails.

FIGURE 9B. Nails are shorter and softer than regular nails.

FIGURE 10A. (A AND B) Toes of a patient with symmetric lupoid onychodystrophy with clefting in the nail bed area.

FIGURE 10B. (A AND B) Toes of a patient with symmetric lupoid onychodystrophy with clefting in the nail bed area.

FIGURE 10C. Foot of the same patient with a lost nail.

Treatment involves immunomodulation with glucocorticoids, often combined with pentoxifylline. Depending on the severity of the case, a long-term maintenance regimen of glucocorticoids may be needed. For patients that cannot tolerate glucocorticoids, oclacitinib has anecdotally been effective. Cyclosporine and essential fatty acid supplementation can also be used for management.⁶ Essential fatty acids are typically used as adjunctive treatment.⁷ Only rarely, treatment requires more aggressive immunosuppression (e.g., azathioprine, mycophenolate). Although most cases of symmetric lupoid onychodystrophy are idiopathic, some may be aggravated by vaccines⁸; thus, the history should be thorough to determine if a trigger could be identified and possibly avoided in the future. 

STEP 5B: If footpads are involved, consider the following:

One clinical presentation is pododermatitis with crusting of the footpads, commonly referred to as hyperkeratosis, resulting from the accumulation of pustules and/or abnormal differentiation of the epidermis. Differential diagnoses to consider are pemphigus foliaceus, primary diseases of keratinization, metabolic diseases (e.g., superficial necrolytic dermatitis), nutritional deficiencies, ulcerative disease of the footpads (e.g., vasculitis), and autoimmune disease. It is important to discriminate between pemphigus foliaceus and metabolic disease as pemphigus foliaceus is treated with glucocorticoids, but dogs with metabolic diseases should not receive glucocorticoids as they commonly have diabetes mellitus or prediabetes.

Pemphigus Foliaceus

Pemphigus foliaceus can be exhibited as hyperkeratosis and pododermatitis (FIGURES 11 AND 12).⁹ Crusting on the face and ears is common. Lesions are typically symmetrical, and systemic signs are commonly reported. Cats with pemphigus foliaceus can exhibit hyperkeratosis and paronychia (FIGURE 13). Thus, it is useful to push on the nail bed to extend the nail and collect the material in the nail bed for cytology and identification of acantholytic cells. Collecting a biopsy sample is recommended to confirm the diagnosis as severe infections or dermatophytes can also cause acantholytic cells. After the diagnosis is confirmed, a treatment plan of long-term immunosuppressants needs to be tailored to the specific patient.

FIGURE 11. Hyperkeratosis in a patient with pemphigus foliaceus. Note the layers of pustules most visible at the edges of the pads.

FIGURE 12. Crusting and dry pustules on the foot of a dog with pemphigus foliaceus. On this patient, the lesions are moist and more exudative than those of the patient with symmetric lupoid onychodystrophy shown in FIGURE 11.

FIGURE 13. Nail bed of a cat with pemphigus foliaceus. The material collected from the nail bed area can be used for cytology to look for acantholytic cells.

Primary Diseases of Keratinization

Hyperkeratosis can result from an increased rate of keratinocyte mitosis. Patients with a primary disease of keratinization are young and typically have a crusty nose and/or greasy ears and generalized seborrhea. The signs are evident early in life and are not associated with systemic signs. A classic example is primary seborrhea of cocker spaniels.

Metabolic Diseases

Certain underlying metabolic diseases (e.g., Cushing’s disease, liver disease, glucagonoma, inflammatory bowel disease) can lead to superficial necrolytic dermatitis (also known as hepatocutaneous syndrome or glucagonoma syndrome), which affects older dogs or patients that have received hepatotoxic drugs. Deficiencies of amino acids, zinc, and fatty acids (caused either by decreased absorption or decreased production [amino acids]) lead to epidermal necrosis, which is particularly extreme on the footpads (FIGURE 14).¹⁰ Deep fissures and severe thick crusts are common (FIGURE 15), as are ulceration of the genitalia area and crusting on the commissure of the mouth. Blood work typically reveals hypoalbuminemia, hyperglycemia, and increased liver enzymes. The treatment and prognosis for superficial necrolytic dermatitis depend on the underlying cause, but treatment typically involves nutritional supplementation with amino acids, zinc, and essential fatty acids in conjunction with correction of the underlying disease.

FIGURE 14. Crusting on footpads of a dog with superficial necrolytic dermatitis.

FIGURE 15. Severe crusting, fissures, and ulcers on the footpad of a dog with superficial necrolytic dermatitis. The patient also had a severe secondary bacterial infection that was responsible for the purulent exudate.

Nutritional Deficiencies

Hyperkeratosis can result from nutritional deficiencies in dogs fed imbalanced diets with low zinc and protein; clinical signs can be resolved by feeding a nutritionally balanced diet. Zinc deficiency may also develop in rapidly growing dogs receiving calcium supplementation as calcium interferes with zinc absorption. A separate syndrome, zinc-responsive dermatosis, affects Siberian huskies even when they are fed balanced diets; they are otherwise healthy but require additional supplementation.¹¹ The various hyperkeratosis diseases are ultimately confirmed by skin biopsy.

Ulcerative Disease of the Footpads

Ulcerative disease of the footpads is a manifestation of vasculitis, which is characterized by ulcerative lesions in the center of each pad (FIGURE 16). Vasculitis can be caused by a variety of triggers (e.g., drugs, vaccines, infections, autoimmune diseases such as systemic lupus erythematosus). Thus, any drug or vaccine that was administered 4 to 6 weeks before development of the vasculitis should be considered as a potential cause. Other areas frequently affected by vasculitis are the tips of the ears (FIGURE 17) and the tip of the tail. Among vaccines, rabies vaccination is known as a trigger of cutaneous vasculitis, particularly in small breed dogs.^12,13 Vasculitis is diagnosed by biopsy. Treatment involves glucocorticoids in combination with pentoxifylline. For dogs that do not tolerate glucocorticoids, oclacitinib can be used as an alternative.¹⁴

FIGURE 16. Ulcerative lesions on the footpads of a dog with vasculitis secondary to Bordetella vaccination.

FIGURE 17. Crusting lesions on the pinna of a dog with vasculitis secondary to rabies vaccination.

Autoimmune Disease

Ulcerative lesions and sloughing of the nails can also result from autoimmune diseases (e.g., pemphigus vulgaris, epidermolysis bullosa, systemic lupus erythematosus) (FIGURE 18), which are rare but can lead to bullous lesions that rapidly ulcerate. In patients with epidermolysis bullosa, the oral cavity and feet are commonly affected (FIGURE 19). Diagnosis is based on results of biopsy of early macular/vesicular lesions. Treatment involves immunosuppressive doses of glucocorticoids in combination with a steroid-sparing agent.

FIGURE 18. Deep ulcerative lesions on the leg of a dog with vasculitis and systemic lupus erythematosus.

FIGURE 19. Bullous ulcerative lesions in the oral cavity of a dog with epidermolysis bullosa.

Clinical Syndromes Associated With Pododermatitis

Feline Plasma Cell Pododermatitis

Cats with this felid-specific syndrome exhibit a pathognomonic swelling of their footpads,¹⁵ some with classic purple discoloration of the metacarpal pad and prominent striations (FIGURE 20). Pads can become extremely swollen and painful (FIGURE 21). For most patients, the exact trigger is not known, but it is believed to be an exaggerated immune response to some antigenic stimulation. Diagnosis is made by biopsy of the pads, and the most common initial treatment is oral doxycycline. Some patients may require additional immunomodulation, and glucocorticoids with or without cyclosporine are a common option. When swelling is extreme, surgical removal of some of the tissue, followed by medical management, may be needed.

FIGURE 20. Swollen metacarpal pad of a cat with plasma cell pododermatitis. Note the purple discoloration and the striations.

FIGURE 21. Severely swollen metacarpal pad of a cat with plasma cell pododermatitis. Patient was very painful and non–weight bearing.

Interdigital Cysts in Short-Coated Large-Breed Dogs

This syndrome involves a primary disease (e.g., allergy, hypothyroidism) and predisposing causes (e.g., conformational issue combined with obesity). Pyoderma is initially superficial (folliculitis) and rapidly progresses to a deeper infection (furunculosis). Staphylococcus species, which are abundant in the hair follicles, are pushed deep into the dermis of the interdigital spaces. In patients with furunculosis, the hair follicle ruptures, releasing bacteria and keratin into the dermis, which triggers a severe inflammatory response and formation of a capsule to sequester the free hairs and bacteria. The cysts act as a common cause for reinfection and relapse, thus requiring long-term treatment.¹⁶ In chronic cases, the foot may undergo extreme swelling and remodeling (FIGURE 22). Treatment goals are to identify and correct the primary disease, effectively treat the deep infection, and surgically remove the cysts after size reduction. Treatment involves long courses of systemic antibiotics in combination with either systemic or topical steroids to decrease inflammation and fibrosis.

FIGURE 22A. Ventral aspect of the feet of a mastiff with chronic deep pyoderma on all 4 feet. Because of the severe secondary changes, this dog was initially very lame and reluctant to walk. (A AND B) The feet before initiation of treatment.

FIGURE 22B. Ventral aspect of the feet of a mastiff with chronic deep pyoderma on all 4 feet. Because of the severe secondary changes, this dog was initially very lame and reluctant to walk. (A AND B) The feet before initiation of treatment.

FIGURE 22C. (C AND D) The same feet after 6 months of systemic antibiotics and topical steroids.

FIGURE 22D. (C AND D) The same feet after 6 months of systemic antibiotics and topical steroids.

Summary

Many diseases can cause pododermatitis, and establishing a correct diagnosis through a systematic step-by-step approach is essential. The most common diseases should be ruled out first and the treatable ones treated. After the basics are covered, the combination of all clinical signs can help rank differential diagnoses, and a skin biopsy may be needed for a final diagnosis.