Canine pododermatitis does not constitute a single nosological entity, but rather represents a complex and multifactorial cutaneous reaction pattern, resulting from a dynamic interaction between primary causes, predisposing factors, and perpetuating elements. This synthesis report aims to provide a comprehensive, nuanced, and updated analysis of the etiology, pathophysiology, and therapeutic strategies for canine pododermatitis.

This review integrates the most recent scientific data, notably the 2025 guidelines from ISCAID (International Society for Companion Animal Infectious Diseases) on the rational use of antimicrobials, the WAVD (World Association for Veterinary Dermatology) consensus on demodicosis and Malassezia dermatitis, as well as technological advances in fluorescence biomodulation. The analysis also relies on new trends in bacterial resistance observed in Europe and Asia, highlighting the urgency of a rigorous diagnostic approach and therapeutic management that is conservative with antibiotics.

In daily clinical practice, canine pododermatitis remains one of the most frequent reasons for consultation, but also one of the most frustrating for both the veterinarian and the owner. The clinical presentation, although often stereotyped—characterized by interdigital erythema, alopecia, edema, and sero-purulent exudate—masks considerable etiological diversity. This extends from common environmental hypersensitivity to complex autoimmune disorders, including serious systemic metabolic diseases such as hepatocutaneous syndrome.

For the veterinary dermatologist, the challenge lies not only in the symptomatic management of inflammation or pedal pruritus, but in the precise elucidation of the underlying pathogenic cascade. Inadequate management, often limited to repeated empirical antibiotic therapy without etiological investigation, inevitably leads to chronicity. The latter is characterized by irreversible dermal fibrosis, the formation of follicular cysts, the appearance of conformational modifications of the foot, and the emergence of multidrug-resistant bacterial strains, notably methicillin-resistant Staphylococcus pseudintermedius (MRSP) and Gram-negative bacilli such as Pseudomonas aeruginosa or Escherichia coli.

I. Pathophysiology and Functional Anatomy: The Terrain of Disease

1.1 The Interdigital Skin Barrier and Pedal Microclimate

Understanding the pathogenesis begins with the analysis of functional anatomy. The skin of the interdigital spaces presents particularities that intrinsically predispose it to inflammation and infection. Unlike glabrous skin, the interdigital epidermis is exceptionally rich in sebaceous and apocrine glands. This glandular density, associated with the “closed” anatomical configuration of the interdigital space, creates a warm, humid, and lipid-rich microclimate, particularly favorable for microbial proliferation.

This environment constitutes an ideal ecological niche for commensal populations, notably coagulase-positive staphylococci and the lipid-dependent yeast Malassezia pachydermatis. Moreover, the skin barrier at this level is subjected to constant and intense mechanical stress due to locomotion and the animal’s weight. Any alteration of this barrier, whether of allergic, parasitic, or traumatic origin, allows the penetration of allergens and pathogens, triggering a local immune response that is often disproportionate.

1.2 The Concept of Follicular Cyst and Furunculosis: Mechanism of Chronicity

A central pathophysiological mechanism in establishing the chronicity of pododermatitis is the rupture of the hair follicle, leading to furunculosis. This phenomenon is often poorly understood and incorrectly termed a “sebaceous cyst.” Under the effect of initial inflammation (due to allergy or demodicosis) or frictional trauma (poor conformation, overweight), the follicular ostium becomes obstructed by hyperkeratosis. This obstruction leads to cystic dilation of the follicle.

The rupture of the weakened follicular wall then releases the follicle’s contents into the surrounding dermis: free keratin, hair shafts, and bacteria. Keratin, once outside the follicle, is recognized as an endogenous foreign body by the immune system. It triggers a severe pyogranulomatous inflammatory reaction, initially sterile, which rapidly evolves into a deep bacterial infection. Hair fragments act as persistent irritating spines, maintaining inflammation even after apparent bacterial sterilization. It is this foreign body reaction process that explains why antibiotics alone systematically fail to resolve chronic nodular lesions and why surgery or laser may be required.

II. Algorithmic and Reasoned Diagnostic Approach

When faced with pododermatitis, the clinical approach must be rigorous, sequential, and exhaustive to avoid diagnostic errors and the unnecessary prescription of symptomatic treatments that mask the primary cause.

2.1 History and Medical History: Initial Clues

The clinical investigation begins with a detailed history. The age of onset of signs is a major discriminating indicator. Pododermatitis occurring in a young dog (less than one year) should immediately orient the clinician toward juvenile demodicosis or early atopic dermatitis. Conversely, the appearance of pedal lesions in an older dog, with no dermatological history, requires consideration of serious metabolic causes such as hepatocutaneous syndrome, neoplasias (squamous cell carcinoma, cutaneous lymphoma), or autoimmune diseases (pemphigus foliaceus).

The seasonality of signs is another key element: an exacerbation in spring or summer suggests environmental atopy (pollens), while non-seasonal pododermatitis may indicate food allergy or a non-allergic cause. The notion of contagion to other animals in the household or to owners (pruritus in humans) points toward a zoonotic parasitic origin, such as sarcoptic mange, or fungal, such as dermatophytosis.

2.2 Dermatological Clinical Examination

The physical examination should not be limited to the extremities alone. The distribution of lesions on the body provides valuable clues about etiology:

• Isolated pododermatitis (unipedal): This presentation suggests a local cause such as a foreign body (foxtail), trauma, neoplasia, or localized opportunistic fungal infection.
• Generalized pododermatitis (quadripedal): Simultaneous involvement of all four paws is strongly suggestive of systemic causes: allergies (food or environmental), autoimmune diseases (pemphigus), metabolic causes, or leishmaniasis.
• Precise location on the foot: Involvement of the paw pads (hyperkeratosis, ulcers, depigmentation) points toward pemphigus, hepatocutaneous syndrome, or leishmaniasis, whereas strictly dorsal interdigital involvement is more classic for atopy or demodicosis.

2.3 Immediate Complementary Examinations

The deep skin scraping and trichogram are non-negotiable imperatives. They must be performed systematically to rule out demodicosis, even in adult dogs receiving apparent antiparasitic prophylaxis (isoxazolines), as therapeutic failures, compliance issues, or severe immune deficits can occur. In chronic forms with fibrosis, mites may be difficult to demonstrate by scraping; skin biopsy then becomes necessary.

2.4 Cutaneous Cytology: The Cornerstone of Infectious Diagnosis

Cytology, performed by direct impression, swab, or fine needle aspiration for nodules, is the most cost-effective and informative examination. It allows objective quantification of the presence of:

• Bacteria: The distinction between cocci (generally Staphylococcus) and rods is crucial. The presence of rods should immediately alert the clinician to a possible Gram-negative infection, potentially Pseudomonas, justifying immediate bacterial culture.
• Yeasts: Detection of Malassezia pachydermatis (yeasts shaped like a “bottle” or “peanut”) is frequent in allergic pododermatitis.
• Inflammatory cells: Characterization of the infiltrate (degenerate neutrophils, eosinophils, macrophages, acantholytic cells) guides diagnosis. The presence of acantholytic cells in sheets strongly suggests pemphigus foliaceus.

III. Etiology: Detailed Classification of Primary Causes

It is fundamental to distinguish primary causes, which initiate the process, from secondary causes (infections) and perpetuating causes (anatomical modifications). Treatment of secondary causes without management of the primary cause inevitably leads to recurrence.

3.1 Allergic Dermatoses: The Predominant Cause

Allergies constitute, by far, the most frequent primary cause of chronic canine pododermatitis.

• Canine Atopic Dermatitis (CAD): Pedal pruritus is a cardinal sign of CAD, often the first to appear. Interdigital erythema, initially ventral then dorsal, and compulsive licking cause a characteristic brownish coloration of the hairs by salivary porphyrins (salivary chromonychia). The ICADA guidelines emphasize the importance of multimodal management, targeting both skin barrier dysfunction and immune dysregulation.
• Food Allergy (Adverse Food Reaction): Clinically indistinguishable from CAD, it can manifest as isolated pododermatitis or associated with digestive disorders (soft stools, borborygmi) and otitis. The elimination diet remains the diagnostic “gold standard.”
• Contact Dermatitis: Often underdiagnosed, it primarily affects glabrous areas in direct contact with the ground (palmar/plantar surface of digits, ventral interdigital spaces) while sparing the dorsal hairy spaces. Frequent allergens include floor cleaning products, fertilizers, cements, or certain plants (Pampas Grass, Tradescantia).

Pododermatitis of atopic origin

3.2 Parasitic Diseases

• Demodicosis due to Demodex canis: The pedal form, or pododemodicosis, may be a chronic sequela of an unresolved juvenile generalized form or appear de novo in adulthood. In adults, it is often associated with underlying immunosuppression (hypothyroidism, Cushing’s syndrome, chemotherapy, long-term corticosteroid therapy). Lesions are typically scaly, alopecic, comedonal, and hyperpigmented (“blue feet”), frequently evolving toward severe deep pyoderma with furunculosis and marked edema.
• Demodicosis due to Demodex injai: This parasite, morphologically longer than D. canis, resides preferentially in sebaceous glands. Although it classically causes dorsal seborrheic dermatitis (“greasy keratoseborrheic state”) in Terriers, it can also induce pedal pruritus and diffuse erythema, often confused with allergy.
• Dermatitis due to Pelodera strongyloides: This saprophytic nematode penetrates skin in contact with damp, soiled bedding (straw). It causes erythematous, alopecic, and extremely pruritic pododermatitis, affecting areas in contact with the ground.
• Hookworm infection: Larvae of Ancylostoma can penetrate percutaneously at the level of interdigital spaces, causing pruritic papular dermatitis and hyperkeratosis of the paw pads.

3.3 Endocrinopathies and Metabolic Diseases

Hypothyroidism and hyperadrenocorticism (Cushing’s Syndrome) do not directly cause inflammatory pododermatitis per se, but strongly predispose to secondary bacterial and fungal infections by altering cutaneous immunity and the epidermal barrier. Dystrophic cutaneous calcinosis, a complication of iatrogenic or spontaneous Cushing’s syndrome, can manifest as hard, whitish, and calcified plaques on the paw pads or in interdigital spaces, surrounded by a foreign body inflammatory reaction.

Superficial necrolytic dermatitis

Also called necrolytic migratory erythema, it is a serious dermatosis associated with severe chronic vacuolar hepatopathy or, more rarely, with a glucagon-secreting pancreatic tumor (glucagonoma). The pathogenesis involves profound deficiency in circulating essential amino acids, leading to necrosis of keratinocytes in the granular layer. Pedal lesions are characteristic and painful: severe hyperkeratosis of paw pads with deep fissures, exudative erythema, and adherent crusts. Histopathology reveals the pathognomonic “Red, White, and Blue” sign (parakeratosis, edema, basal hyperplasia). The ultrasound appearance of the liver in a “honeycomb” (honeycomb pattern) is highly evocative.

Pododermatitis due to superficial necrolytic dermatitis

3.4 Autoimmune and Immune-Mediated Diseases

• Pemphigus Foliaceus: This is the most frequent autoimmune disease in dogs. It targets desmoglein-1, leading to superficial acantholysis. Clinically, it manifests as pustules (rarely intact because fragile), epidermal collarettes, yellowish crusts, and villous hyperkeratosis of paw pads, often painful. Claw involvement is rare, unlike facial and auricular involvement. Recent studies suggest that the presence of concomitant vasculopathic lesions worsens the prognosis.
• Symmetrical Lupoid Onychodystrophy (SLO): This condition, preferentially affecting German Shepherds, Gordon Setters, and Bearded Collies, is unique because it exclusively affects the claws. It often begins with the acute and painful loss of one or two claws (onychomadesis), followed sequentially by involvement of all claws on multiple paws. Regrowth is abnormal, producing brittle, deformed, short, and friable claws (onychodystrophy). It is considered a vasculopathy or interface dermatitis specifically targeting the nail matrix.

Pedal involvement in pemphigus foliaceus

3.5 Canine Leishmaniasis

In endemic areas (Mediterranean basin) or in dogs that have traveled, leishmaniasis due to Leishmania infantum must be systematically considered when faced with any pododermatitis. The parasite induces a complex immune response. Besides exfoliative dermatitis (giant scales), it causes spectacular onychogryphosis (abnormally long and curved claws like ram’s horns). This symptom is not simple hypertrophy, but results from chronic inflammation of the nail matrix mediated by the deposition of circulating immune complexes. Paw pad ulcers, nasodigital hyperkeratosis, and necrotizing vasculitis of ear tips are also frequent.

IV. Predisposing and Perpetuating Factors: The Vicious Circle

Recognition of these factors is as crucial as identification of the primary cause. Ignoring perpetuating factors condemns any medical therapy to long-term failure.

4.1 Conformational and Biomechanical Factors

Heavy short-haired breeds (English Bulldog, French Bulldog, Labrador, Boxer, Bull Terrier) are genetically predisposed. Obesity considerably aggravates the problem by increasing pressure on paw pads and causing flattening of interdigital spaces (splayed toes). This flattening increases the surface area of skin-on-skin friction during walking. Moreover, so-called “splayed” paws or those with deep webbing favor moisture retention and maceration.

4.2 “Traumatic Folliculitis” and Interdigital Cysts

Interdigital cysts and furunculosis are often maintained by a simple but devastating mechanical factor: the nature of the hair. In short, stiff-haired breeds, broken hairs act like needles. During walking, constant friction pushes these broken hair shafts backward, into the dermis or through the follicular wall (ingrown hairs). This creates a vicious circle: inflammation -> edema -> increased friction -> follicular rupture -> foreign body reaction -> fibrosis. Cicatricial fibrosis eventually traps follicular debris, forming nidi of chronic infection inaccessible to antibiotics and immune defenses.

V. Advanced Therapeutic Management: 2025 Protocols

Management of canine pododermatitis is inherently multimodal. It must simultaneously:

1. Treat infection (bacterial and fungal).
2. Control inflammation and pruritus to stop self-trauma.
3. Identify and manage the primary cause.
4. Correct perpetuating factors (surgery, weight management).

5.1 Management of Bacterial Infections: New ISCAID 2025 Guidelines

The new ISCAID guidelines, published in 2025, mark a turning point in the approach to pyoderma, emphasizing the drastic reduction of systemic antibiotic use to combat increasing antibiotic resistance.

Surface and Superficial Pyoderma

For infections limited to the surface (intertrigo) or superficial follicles, topical treatment is now the absolute first-line rule. The use of shampoos, foams, or wipes containing chlorhexidine (concentration 2% to 4%) is recommended daily or every other day. Mupirocin ointment is an excellent option for localized focal lesions, particularly against multidrug-resistant staphylococci.

Deep Pyoderma and Furunculosis

Systemic antibiotic therapy often remains necessary for deep forms (furunculosis, cellulitis), but must imperatively be guided by bacterial culture and antibiogram. Empirical antibiotic therapy is strongly discouraged in this context.

• Treatment duration: It is prolonged. Current recommendations advocate treatment of at least 4 to 6 weeks, and especially, continuation of treatment for 2 to 3 weeks after complete clinical resolution of lesions (disappearance of palpable nodules). Premature discontinuation is the primary cause of recurrence.
• Choice of molecules (ISCAID Hierarchy):

• Level 1 (First-line if antibiogram favorable): Cephalexin, Amoxicillin-Clavulanic Acid, Clindamycin, Trimethoprim-Sulfonamides (TMS).
• Level 2 (Reserve molecules): Fluoroquinolones (Enrofloxacin, Marbofloxacin, Pradofloxacin), Doxycycline, Minocycline. To be used only upon proof of resistance to level 1 molecules.

Recent Data on Resistance (2024-2025)

Recent epidemiological studies conducted in Europe and China have highlighted worrying trends. High resistance of Escherichia coli (often involved in chronic deep pododermatitis) to amoxicillin has been observed (up to 62% resistance). Conversely, sensitivity to Trimethoprim-Sulfonamide (TMS) remains relatively stable, making it a more rational empirical option (while awaiting culture) than penicillins for suspected Gram-negatives. Resistance to amoxicillin-clavulanic acid shows a downward trend in certain regions, suggesting preserved efficacy if used judiciously.

Type of Infection	Recommended Therapeutic Approach (ISCAID 2025 Consensus)	Average Treatment Duration	Preferred Molecules
Surface / Intertrigo	Topical alone (Chlorhexidine 4%, Mupirocin)	2-3 weeks	Local antiseptics
Superficial	Priority topical +/- Short systemic	3 weeks (1 wk after healing)	Cephalexin, Clindamycin
Deep (Furunculosis)	Systemic (according to antibiogram) + Adjuvant topical	4-8 weeks + (2-3 wks after healing)	According to culture (often Fluoroquinolones, TMS)
MRSA / MRSP	Aggressive topical + Targeted systemic (if possible)	Variable	Chloramphenicol, Doxycycline

5.2 Management of Fungal Infections (Malassezia)

Malassezia dermatitis frequently complicates allergies, causing intense pruritus, a rancid odor, and brownish exudate.

• Topical treatment: Often sufficient. Shampoos containing 2% miconazole and 2% chlorhexidine.
• Systemic treatment: In case of topical failure, severe involvement, or conformation making local care difficult.

• Itraconazole: 5 mg/kg/day or pulsed protocol (2 consecutive days per week).
• Ketoconazole: 5-10 mg/kg/day (beware of hepatotoxicity).
• Terbinafine: 30 mg/kg/day.

5.3 Inflammation and Pruritus Management Strategies

Rapid control of pruritus is essential to break the “pruritus-scratching-inflammation” cycle.

• Glucocorticoids (Prednisolone/Methylprednisolone): Remain the fastest and most effective tool to reduce severe edema and inflammatory fibrosis of interdigital cysts in the acute phase. Anti-inflammatory dose (0.5-1 mg/kg/day) in short course.
• Oclacitinib (JAK Inhibitor): Very effective for controlling allergic pruritus with rapid onset of action (similar to steroids). Comparative studies (Little et al., 2015) have shown that oclacitinib acts faster than cyclosporine and with fewer gastrointestinal side effects. It is ideal for therapeutic diagnosis of atopy.
• Lokivetmab (Anti-IL31 Monoclonal Antibody): Specifically targets interleukin-31, a key mediator of atopic pruritus. It is a safe option, without metabolic or immunosuppressive side effects, usable in young dogs or those with comorbidities.
• Cyclosporine: Effective for chronic cases of atopy and certain autoimmune diseases, but its onset of action is slow (4 to 6 weeks for maximum effect), which limits its utility in the acute phase.

5.4 Innovative Therapies: Fluorescence Biomodulation (Phovia)

Fluorescence Biomodulation (FLE – Fluorescent Light Energy) represents a major non-invasive technological advance for managing deep pyoderma and interdigital furunculosis.

• Mechanism: The Phovia system is based on the application of a gel containing specific chromophores, illuminated by a blue LED lamp. The chromophores absorb blue photons and re-emit light energy by fluorescence at different wavelengths (green, yellow, red) in the visible spectrum. This energy penetrates to different depths of the dermis, stimulating cellular mitochondria, promoting ATP production, reducing inflammation and stimulating tissue regeneration, while having a direct bactericidal effect.
• Clinical Efficacy: Prospective randomized clinical studies (Marchegiani et al., 2021, 2022) have demonstrated that adding FLE to standard antibiotic treatment significantly accelerates clinical healing (reduction of treatment time necessary for resolution) and improves the quality of healing of deep lesions. A protocol of one weekly application proved statistically as effective as two applications per week, which greatly facilitates owner compliance.

5.5 Surgical Options: The Last Resort

In cases of chronic fibrosing pododermatitis refractory to all optimal medical management (and only after strict control of primary causes), surgery can be considered as a salvage procedure.

• CO2 Laser Surgery: Allows precise excision of cysts, diseased follicles, and fibrosed tissues with excellent hemostasis and sterilization of the operative site. It is the technique of choice for focal nodular lesions.
• Fusion Podoplasty: This heavy intervention consists of excising all diseased interdigital tissues and suturing the digits together (fusion of paw pads). Although effective for eliminating chronic pain and recurrent infections, it presents a high rate of post-operative complications: wound dehiscence (very frequent), necrosis, and long and painful convalescence. Moreover, follow-up studies (Papazoglou et al., 2011) show that some dogs retain residual mechanical lameness or long-term gait discomfort. This surgery should only be offered in ultimate cases (“end-stage pododermatitis”).

VI. Specific Treatments According to Etiology

Adapting the protocol to the precise etiology is the key to success.

6.1 Symmetrical Lupoid Onychodystrophy (SLO)

Treatment of SLO is essentially medical and must often be maintained for life.

• Basic protocol (Gentle Immunomodulation): The combination of Tetracycline (or Doxycycline) and Niacinamide (Vitamin B3) is the historical treatment of choice. Recommended dosages are 250 mg of each (for dogs <20kg) to 500 mg of each (dogs > 20kg), three times daily. This protocol is often associated with massive supplementation in Essential Fatty Acids (Omega-3), notably EPA (Eicosapentaenoic Acid), at high doses (400 mg/10kg).
• Refractory cases: If response is insufficient after 2-3 months, more powerful immunosuppressants such as Prednisolone, Azathioprine, or Pentoxifylline (to improve microcirculation) can be added.
• Surgery: Claw removal (onychectomy) is very rarely necessary, except in case of uncontrollable pain on a specific claw. Spontaneous onychomadesis is part of the natural evolution of the disease.

6.2 Hepatocutaneous Syndrome (SND)

The prognosis is poor, with median survival often short. Management is palliative and essentially nutritional, aimed at correcting hypoaminoacidemia.

• Amino acid infusion: Intravenous administration of crystalline amino acid solutions (Aminosyn 10% type) is the cornerstone of treatment. The protocol involves slow infusions (over 8-10h) repeated every 2 to 3 weeks to fill the catabolic deficit and reduce cutaneous lesions.
• Oral nutritional management: A diet rich in high-quality proteins is imperative. Adding raw egg yolks (3 to 6 per day depending on dog size) is a simple and effective method to provide amino acids. Supplementation with Zinc (Zinc Methionine) and essential fatty acids is also recommended.
• Advanced therapies: In rare cases of identified glucagonoma, surgical excision or use of somatostatin analogues (Octreotide) to inhibit glucagon secretion has shown promising results but remains costly.

6.3 Canine Leishmaniasis

Treatment is based on the synergistic combination of a leishmanicidal and a leishmaniostatic agent.

• Standard Protocol: Meglumine antimoniate (Glucantime) by SC injection for 4 weeks + Allopurinol per os long-term (6 to 12 months minimum).
• Alternative: Miltefosine per os + Allopurinol (useful in case of renal insufficiency limiting the use of antimonials).
• Immune complex management: Allopurinol helps reduce parasite load and thus the formation of immune complexes responsible for onychogryphosis and glomerulonephritis. Monitoring renal function is a priority over managing cutaneous signs.

Conclusion

The management of canine pododermatitis requires the clinical veterinarian to question traditional practices. It is never a simple “paw infection” to be treated with an antibiotic injection, but a complex alarm signal reflecting local or systemic dysfunction. The key to therapeutic success lies in abandoning reflex antibiotic therapy in favor of a complete investigative approach (cytology, scrapings, biopsy) and multimodal therapy.

Integration of new ISCAID guidelines, favoring topical therapy, and adoption of adjuvant technologies such as fluorescence biomodulation, now allow management of cases previously considered hopeless. Faced with the global emergence of bacterial resistance, the veterinary dermatologist must be the guardian of responsible, precise, and evidence-based medicine, where each prescription is justified by diagnostic proof.

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