Conditions of the Canine Foot Pad

Dr Heidi Schroeder, BVSc MMedVet(Med)

Small Animal Physician

Willow Park Small Animal Medicine Specialist Hospital,

Willow Glen, Pretoria

Tel: 012 813 8009

wpsam@absamail.co.za

Foot pad conditions are usually part of generalised skin conditions or systemic conditions that also cause skin lesions and clinical signs elsewhere on or in a patient.The most important differential diagnoses are discussed in this article.

There are not many foot pad conditions and therefore when the footpads are affected, they can aid in the diagnosis of a particular condition. There are also a few conditions that affect the foot pads only.

When a patient is presented with a foot pad condition it is important to take a good history and do a full clinical examination. Consider the age (e.g. genodermatoses, parasites and infectious diseases in young dogs versus auto-immune and metabolic conditions in older dogs).

It is also important to determine whether there are concurrent systemic signs, e.g. necrolytic migratory erythema (NME), whether one or more pads are affected and whether there are signs of skin disease elsewhere on the body. Skin or foot pad biopsies for histopathology are required in many cases to make a final diagnosis.

HOOKWORM DERMATITIS: Hookworm dermatitis is caused by Ancylostoma caninum where infected larvae, present in soil or mud, in poorly kept kennels or highly contaminated environments, penetrate the skin and burrow into the hair follicles of thin skinned areas (axillae/inguinal regions/ventral abdomen), the foot pads and interdigital areas where they continue their life cycle. Young animals living in groups in unhygienic conditions and hunting dogs are highly predisposed.

The thin skinned areas commonly have papules, crusts and excoriations and the foot pads are usually oedematous, thickened and ulcerated. Paronychia and deformed nails may be present in chronic cases. Systemic signs such as diarrhoea, anaemia and weight loss are often present. Diagnosis is made with faecal flotation. Histopathology usually reveals eosinophilic perivascular dermatitis and sometimes larvae can be found. Prognosis is good if the affected dog is dewormed and removed from the contaminated environment.

HARD PAD DISEASE: There are 2 different types of hard pad disease: The first type is a crusting, thickened foot pad and is seen with e.g. pemphigus foliaceous, zinc responsive dermatosis, distemper infections and necrolytic migratory erythema. These foot pads may be painful and cause lameness.

Most commonly these cases will have other accompanying skin lesions and systemic signs, although rare cases of pemphigus foliaceus may present with foot pad lesions only. Biopsies are the most helpful diagnostic procedure. Treatment will depend on the underlying cause.

The second type is a foot pad with excessive fronds of normal appearing keratin. This is most obvious at the margins of the pads and represents overgrowth of the normal keratin mounds of the pads. Inflammation and exudate are not present. Lameness and pain are usually not detected. This condition appears more as if the pads grow abnormally fast and do not desquamate.

PEMPHIGUS FOLIACEUS: Pemphigus foliaceus is the most common of the pemphigus complex. It is characterized by a scaling, crusting and pustular dermatitis that usually affects the face, ear pinnae and foot pads. Some cases may become generalized. The foot pads are usually swollen and hyperkeratotic with scaling, crusting, hardening and fissuring. In severe cases there may be pustule formation, greenish/yellowish discoloration and significant epithelial loss of the foot pads. Cytological examination of the purulent material will reveal large numbers of neutrophils and/or eosinophils and acantholytic keratinocytes which are highly suggestive of pemphigus foliaceus. Bacteria are usually not present on cytology of intact pustules, but may contaminate ruptured lesions. There are usually not systemic signs, but lesions may be painful. The diagnosis is supported by cytology and should in all cases be confirmed by histopathology. This condition is treated with immunosuppressive dosages of prednisolone with or without azathioprine. Topical corticosteroid therapy may be useful for stubborn localised lesions.

fig-3

Pemphigus

foliaceus affecting the footpad

(Photo: Dr Heidi Schroeder)

DEMODICOSIS: Demodicosis is a differential diagnosis for every case of pododermatitis. Usually this is a generalised skin disease that can involve the paws but rarely if may affect the paws only and in very rare cases the foot pads as well. The feet become inflamed and may show hair loss, redness, swelling, crusting and scaling. The foot pads become crusty and thickened.

The diagnosis can be made by microscopic examination of hair plucks or skin scrapings from the paws, but biopsy and histopathology are required in most cases. Treatment with systemic and topical parasiticides for many weeks to months is usually required for successful management. Secondary bacterial infections are common and should be treated.

CUTANEOUS DRUG REACTIONS: Cutaneous drug reactions are adverse reactions following systemic and topical drug administration. The pathogenesis is complicated involving both immunological and non-immunological reactions. All types of hypersensitivity reactions have been reported. Clinical signs are highly variable. In most cases the clinical signs are mild (urticaria, erythroderma), but can also be very serious and sometimes fatal (erythema multiforme, toxic epidermal necrolysis and drug-induced pemphigus foliaceus).

Cases present with various lesions which may include papules, plaques, erosions and ulcers on various parts of the body, including the foot pads and pad margin. Drugs that have been reported to cause such reactions include antibacterial (sulphonamides, cephalosporins), antifungal (itraconazole, griseofulvin) and antiparasitic drugs (ivermectin, moxidectin), vaccines, topical drugs, hormones and tranquilisers.

There is often a lag period of 5 to 21 days before clinical signs manifest. In most cases discontinuation of the medication and treatment of secondary infections, if present, results in resolution of the skin lesions. Some cases require more aggressive treatment e.g. glucocorticoids and other immunosuppressive drugs. Adverse effects can persist for 1 to 3 weeks after discontinuation of the offending medication.

FOOT PAD HYPERKERATOSIS:

Familial foot pad hyperkeratosis: Familial foot pad hyperkeratosis has been described in Irish setters, Kerry blue terriers and Labrador and Golden retrievers. Other breeds may be affected as well. Symptoms are usually present by 6 months of age. All foot pads are usually affected with crusting, fissures and pronounced compact keratin that in some cases can produce horns. These lesions can result in severe lameness and pain. Histopathology shows moderate to severe hyperplasia with marked papillated and diffuse hyperkeratosis. Treatment is discussed below. Affected dogs should not be bred.

Idiopathic nasodigital hyperkeratosis: This is an idiopathic hyperkeratosis characterised by hyperkeratosis of the foot pads with or without involvement of the nasal planum. Idiopathic nasodigital hyperkeratosis is seen in older dogs and characterised by increased horny tissue on the nose and/or foot pads. The nose/ foot pads appear vegetative with projections of firm, feathered and cracked horny tissue on the nose and/ or foot pads. Sometimes only the margins are affected but in severe cases the entire nose and/or foot pad is involved. Certain breeds, such as the Cocker spaniel, may be predisposed. Histologically, idiopathic nasodigital hyperkeratosis is characterized by epidermal hyperplasia and marked orthokeratotic to parakeratotic hyperkeratosis.

The diagnosis is generally based on history and clinical findings, and, in some cases, histopathology. There is no specific treatment for these conditions. Symptomatic treatment may be considered when the hyperkeratosis is a problem. Excess keratin may be removed with regular filing, scissors or a blade and fast growing nails should be trimmed regularly. Daily foot soaks in 50% propylene glycol may be of benefit. A topical corticosteroid-antibiotic cream may be used for fissured lesions. Owners should be warned of the potential “mess factor” associated with these topical therapies. Secondary bacterial infections should be treated where present. Oral Vitamin A therapy may be of benefit.

fig-12afig-12b

Idiopathic nasodigital hyperkeratosis of the footpads (http://foothillsanimalhospital. blogspot.

CANINE DISTEMPER: Canine distemper is a multisystemic, often fatal disease, caused by a paramyxovirus virus. It commonly causes gastrointestinal, respiratory and neurological disease, but can also cause vesiculopustular dermatitis and foot pad hyperkeratosis (“hard pad” disease). Classic skin signs such as hyperkeratosis of the foot pads often develop after clinical cure or when the earlier clinical manifestations have cleared.

The foot pad lesions may sometimes be seen in older dogs with an incomplete vaccination history. Since vaccination can prevent distemper, distemper related skin disorders are rare. Diagnosis can be confirmed by histopathology when intra-cytoplasmic and intra-nuclear inclusion bodies can be seen. There is no specific treatment.

CUTANEOUS VASCULITIS: Cutaneous vasculitis involves inflammation of the blood vessel walls and perivascular connective tissue, followed by ischaemia and necrosis. This condition may be primary but is usually secondary to infections (bacteria, rickettsia, fungi), auto-immune disorders (e.g. SLE), chronic diseases (neoplasia, diabetes mellitus) and hypersensitivity disorders. Over 50% of vasculitis cases are idiopathic. With acute vasculitis the face (nose, lips), ear pinnae, digits, foot pads, scrotum and oral mucosa are mainly affected. Skin lesions initially include ecchymotic plaques and haemorrhagic pustules. With time fissures and “punched out” ulcers appear.

These necrotic lesions are painful. Systemic signs such as fever, anorexia, muscle and joint pain and lymphadenopathy are common. Chronic vasculitis typically affects the ear pinnae, tail tip, digits and foot pads where progressive ischaemia results in well circumscribed lesions. Systemic signs are uncommon in chronic vasculitis cases. The diagnosis is supported by histopathology of skin biopsies of the margins of lesions. Although many cases of vasculitis are idiopathic, attempts should be made to identify an underlying cause.

Treatment for idiopathic vasculitis often includes pentoxifylline as a first choice. Other therapies include prednisolone alone or in combination with azathioprine, chlorambucil or cyclosporine. Tetracycline/ niacinamide may be used for milder forms. Topical corticosteroids and 0.1% tacrolimus may be useful for localized lesions.

SYSTEMIC LUPUS ERYTHEMATOSUS (SLE): SLE is an auto-immune condition where multiple circulating auto-antibodies participate in immune-mediated tissue injury directed against the dog’s own body. The most common clinical findings include cyclical fever, polyarthritis, kidney disease and skin disease. Skin lesions are diverse and include erythema, ulcers and crusts of the face (nose, lips), ear pinnae, limbs, axillae and inguinal area. Ulceration and thickening of the foot pads may also occur.

Diagnosis of SLE can be difficult due to the cyclic nature of the disease. Specific diagnostic tests include the antinuclear antibody test (ANA test) and biopsies for histopathology and immunopathology. SLE is treated with immunosuppressive dosages of prednisolone with or without azathioprine or cyclophosamide.

ZINC RESPONSIVE DERMATOSIS: Zinc is very important in ensuring epithelial tissue integrity. Any qualitative or quantitative deficiency in zinc, may therefore cause skin problems. Two types of zinc responsive dermatosis have been described.

Type 1 is a syndrome that has been described in young dogs. It is considered to be a genodermatosis involving a defect in intestinal zinc absorption and possibly zinc metabolism at cellular level. Nordic breeds are predisposed with 75% of cases reported in Siberian Huskies. The age of onset is usually between 6 months and 3 years. This condition mainly affects the face (lips, ear pinnae, bridge of the nose, periorbital area), foot pads and perianal region. Typical skin lesions include erythema, scaling and crusting of all affected areas. Systemic signs, such as pyrexia, are common. Diagnosis is based on history, lesion distribution and histopathology of skin biopsies. Prognosis is good, but recurrences are common. Treatment typically consists of zinc therapy (zinc methionine), low dose prednisolone to help intestinal zinc absorption, antibiotics in cases of secondary bacterial infections and keratomodulating shampoos for the skin lesions.

Type 2 is a syndrome seen in large breed puppies on poorly balanced diets (excessive cereal, phytate or calcium) or in adult dogs with intestinal malabsorption. Dermatological signs are identical to those seen with type 1 and systemic signs, in particular pyrexia, are common. Diagnosis is based on history, clinical signs and histopathology of skin biopsies. The prognosis is excellent in general. Zinc should be given in conjunction with a balanced diet for 3 to 4 weeks and can then be stopped. In cases of malabsorption the supplementation may be lifelong unless the cause of the malabsorption can be diagnosed and treated successfully.

fig-15a

A: Zn-responsive dermatitis affecting the feet and elbow

(http://dermvettacoma.com/zinc-responsive-dermatosis/)

fig-15b

B: Zn-responsive dermatitis affecting footpads

(http://www.siberianhuskyhealthfoundation.com/images/Untitled-1.jpg)

NECROLYTIC MIGRATORY ERYTHEMA (NME) aka Superficial Necrolytic Dermatitis, Hepatocutaneous Syndrome, Metabolic Dermatosis, Metabolic Epidermal Necrolysis: NME is a rare, ulcerative, crusting condition that affects the mucocutaneous junctions (muzzle, lips, nose, eyelids, anus, genitalia) and pressure points (elbows, feet). Hyperkeratosis and fissuring of the foot pads commonly occurs. All foot pads are usually involved and the interdigital spaces and nail folds are also typically inflamed and crusted. The paws often become very painful resulting in lameness and reluctance to walk. Secondary infections with bacteria, fungi or yeasts are common. The disease is generally seen in middle aged to older dogs and may wax and wane. Foot pad and skin lesions are common early manifestations of this condition and precede or accompany chronic liver disease (e.g. cirrhosis, drug-induced hepatitis (phenobarbital) and chronic active hepatitis) or very rarely glucagon-secreting pancreatic tumours (glucagonomas). The lesions are thought to be manifestations of nutritional abnormalities related to amino acids, essential fatty acids or zinc. Systemic signs usually occur later and may include weight loss, lethargy, anorexia, icterus, polyuria and polydipsia. Concurrent diabetes mellitus is relatively common (especially later in the course of the disease). Histopathologic findings of skin biopsies are classic and highly characteristic.

These include a superficial perivascular to lichenoid dermatitis, parakeratotic hyperkeratosis, and a marked intra- and intercellular oedema limited to the upper half of the dermis. These histologic findings appear as a red, white and blue colouring band within epidermis. Once a diagnosis of NME has been made, hepatic ultrasonography should be performed. Hepatic ultrasound usually reveals a hyperechoic network surrounding hypoechoic areas of parenchyma, likened to a Swiss-cheese or honeycomb appearance. This pattern is considered pathognomonic in the dog for NME. There is no effective treatment and the prognosis is guarded. Corticosteroids should not be used as many of these patients are diabetic or prediabetic. Temporary improvement may be achieved with nutritional support. Amino acid supplementation either with intravenous amino acid preparations or with oral supplementation e.g. egg yolks (1 egg yolk per 5 kg body mass), essential fatty acids and zinc can be given. A low fibre, highly digestible diet is recommended. Treatment of the underlying liver disease would be the best option. Drugs such as colchicine and milk thistle are often used. Where a glucagonoma can be surgically removed, the skin lesions start to resolve a week after surgery and completely resolve within 45 days.

fig-13a

Necrolytic migratory erythema of the footpads (http:// www.dermatologyforanimals. com/faq-38/)

FOOT PAD FOREIGN BODIES: Foot pad foreign bodies are very common and easily missed. The entry wound may be very small and the foreign body not visible to the naked eye. Glass and other sharp hard objects are usually the cause. Well localised discomfort is usually present and the patient often presents with lameness. The treatment is general anaesthetic and surgical excision or removal.

CALCINOSIS CUTIS: Calcinosis cutis is a collective description for a group of conditions that result in pathological calcification in the skin. These include dystrophic calcification (seen with hyperadrenocorticism and diabetes mellitus), metastatic calcification (seen with renal insufficiency) and it may be idiopathic (calcinosis circumscripta). Skin lesions are usually firm, cutaneous or subcutaneous nodules.

There is no typical distribution pattern but foot pads are commonly involved. Several cases of foot pad calcification have been reported in small dogs with renal dysplasia. The lesions usually develop after or at the same time as other signs of renal insufficiency. Diagnosis is based on skin and renal signs, histopathology of skin biopsies and further tests to evaluate the kidneys (serum chemistry, urine examination, ultrasound). The prognosis is guarded in most cases depending on the cause of the renal disease.

fig-14

Calcinosis cutis

(Gross TL. 1997.

Calcinosis circumscripta and renal dysplasia in a dog. From: Veterinary Dermatology 8(1): 27 – 32)

FOOT PAD BURNS: Chemical and thermal superficial foot pad burn wounds may present with varying loss of epidermis and dermis. These wounds are treated with topical silver sulfadiazine cream and bandaged with a non-adherent, semi-occlusive bandage. Initially, daily wound dressing and bandage change is recommended. For superficial burns, re-epithelialization may be complete by seven to nine days. With deeper injuries, healing may take up to 21 days, depending on the size of the wound.

fig-18

Foot showing burns of the footpads (http:// livewagbark.com/wp-content/uploads/2015/0 7/5751084148_5085e13 502_b.jpg)

FOOT PAD FROST BITE: When the environmental temperature drops below 0°C, blood vessels close to the skin start to constrict to preserve core body temperature by diverting blood toward the core and away from the cooler parts of the body. This can reduce blood flow in some areas of the body, especially the extremities, to critically low levels. The combination of cold temperature and reduced blood flow can allow the tissues to freeze, causing severe tissue injury. The paws, ears and tail are the most common tissues to be affected. If a dog is wet or damp, these areas are more vulnerable to frostbite.

The initial clinical signs associated with frostbite include discoloration (pale, grey, blue), coldness and swelling of the affected area, pain, blisters or skin ulcers and areas of blackened or necrotic skin. As frostbitten tissues thaw, they may become red and very painful due to inflammation. The clinical signs of frostbite may take several days to appear. Severely frostbitten areas will become necrotic, die and slough off. During this time secondary bacterial infection commonly occurs. Diagnosis is usually based on the history and clinical findings. Treatment is symptomatic and may include treatment for shock and pain. Antibiotics are used to prevent secondary bacterial skin infections.

The prognosis for frostbite depends on the extent of the injuries. Mild cases of frostbite usually resolve with little permanent damage while more severe frostbite may result in permanent disfiguration or alteration of the affected tissues. Amputation of a severely affected body part may even be required.

fig-19

Foot showing frostbite (http://www.famouschihuahua.com/ chihuahua-health-concerns/winter-paw-care/)

FOOT PAD TRAUMA: Foot pad trauma is one of the most common causes of foot pad lesions. Examples are lacerations as a result of sharp trauma or blisters, abrasions and erosions which are frequently found in dogs who accompany their owners jogging on hard surfaces, on hot tar or who obsessively play tug-of-war. Superficial and full thickness injuries to foot pads generally heal in a similar fashion when compared to other skin surfaces, however they heal more slowly and with more complications.

Injured foot pads are exposed to contaminated surfaces, self-trauma and excessive motion and tension and are difficult to prepare aseptically. As a result, contamination of foot pad wounds is more common. Most superficial pad lacerations heal without complications, regardless whether they are repaired or not, if bandaged appropriately. Full thickness pad lacerations should be repaired with a two-layer technique and bandaged to relieve motion and pressure on the repair.

CANINE PAPILLOMA VIRUS: Papilloma viruses (Papovavirus family) exhibit a marked tropism for squamous epithelium, are species specific and potentially contagious. This virus can cause a variety of clinical entities in dogs from warts in the oral cavity and on the skin, cutaneous horns on the foot pads to cutaneous inverted papillomas. Diagnosis is made clinically due to the characteristic lesions but may be confirmed by histopathology. There is no specific treatment. Many virus induced lesions may regress spontaneously after a few months. Treatment that may be attempted for papilloma virus infections include interferon and a vaccine created from surgically excised tissue.

Papilloma viruses have also been implicated as one of the causes of a condition called Canine Foot Pad Papilloma. This condition has primarily been reported in active and retired racing Greyhounds but may affect any breed. The foot pad lesions are firm, well demarcated, circumscribed hyperkeratotic lesions that have a central core of keratin which is often conical. The gross appearance is that of scar tissue. These lesions cause pain and local inflammation and have been called corns. Corns can appear on multiple foot pads and cause lameness. Other proposed causes are foreign bodies and repetitive mechanical trauma from pressure and abrasions.

fig-9a

A: Canine papilloma virus (http://www.askavetquestion. com/answer_np.php?id=4717-wart-on-dogs-foot)

fig-9b

B: Canine papilloma virus (http://www.allwidewallpapers.com/extra-pad-on-dogs-paw/ZXh0cmEtcGFkLW9uLWRvZ3MtcGF3/

fig-17

Corn in foot pad (From: Fawcett A, Phillips A. 2012. Clinical snapshot: A Corn in a Whippet. Compendium for continuing education; September 2012: 34: 9)

VITILIGO: Vitiligo is a condition associated with an acquired loss of pigment in the skin due to selective melanocyte destruction. The pathogenesis is not clear but an auto-immune mechanism is most likely. Vitiligo is sometimes associated with other auto-immune conditions such as juvenile diabetes mellitus. Dermatological signs include achromic macules at mucocutaneous junctions (nose, eyelids, lips and anus) and depigmentation (without inflammation) of the foot pads, nails and coat.

Diagnosis is usually made on clinical findings with or without histopathology. Histopathology shows relatively normal skin which is devoid of melanocytes. There is no specific treatment as the condition is merely cosmetic. Topical 0.1% tacrolimus has occasional success. Spontaneous remission sometimes occurs.

ICHTHYOSIS: Ichthyosis is a congenital disorder resulting from a defect in one or more steps of stratum corneum differentiation. Epidermolytic and non-epidermolytic forms have been described.

Breed specific forms have been identified. Breeds affected include Golden and Labrador retrievers, Cairn and Norfolk terriers, Jack Russell terriers, Rottweilers and American bulldogs.

Dermatological signs vary with the form and breed affected and vary from a mild exfoliative dermatosis to generalised thick, large scales adherent to the skin. Foot pad involvement does not occur in all cases, but where it does, it is characterised by extreme hyperkeratosis and exaggerated thickening of the digital, carpal and tarsal foot pads. Severe cases usually present at the age of 2 months, but milder cases may only present in young adulthood.

Diagnosis is made by histopathology of skin biopsies. Treatment is symptomatic and includes moisturising agents, keratomodulating shampoos to correct excessive scale production and improve skin hydration and essential fatty acid supplementation to limit water loss.

PRACTICAL TIPS

• In a generalised skin condition, where the foot pads are also affected, take samples and biopsies from areas other than the footpads, where possible.

• Foot pad wounds bleed profusely and can be slow to heal.

• It is easy to miss representative lesions when taking biopsies of foot pads.

• Histopathological interpretation of foot pad skin is challenging.

• Foreign bodies should be ruled out as a cause at an early stage, especially in patients who present with lameness and where only one foot pad is affected.

• Consider pain management in all cases.

• Aggressive medical treatment is frequently required.

• Topical treatments will always be a beneficial adjunctive therapy, also useful palliatively.

• Foot coverings will help to protect the foot and increase contact time of topical treatments.

• Review diagnosis in cases of poor response to treatment

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