Atopic Dermatitis In Dogs: Comprehensive Veterinary Reference Guide

Quick Q&A

Question: What is atopic dermatitis in dogs and how is it different from other skin allergies?

Answer: Atopic dermatitis in dogs is a chronic, inflammatory, and pruritic skin disease with a genetic predisposition, triggered by environmental allergens such as pollens, dust mites, and moulds. Unlike food allergies which are triggered by dietary proteins, or flea allergy dermatitis which is caused by flea saliva, atopic dermatitis is an immune system hypersensitivity to inhaled or absorbed environmental substances.

Question: Can atopic dermatitis in dogs be cured?

Answer: Atopic dermatitis in dogs is a lifelong condition that cannot be cured but can be effectively managed. With a multimodal treatment approach including allergen avoidance, medical therapy, immunotherapy, and skin barrier support, most dogs achieve good quality of life and acceptable symptom control.

Question: What are the first signs of atopic dermatitis in dogs?

Answer: The earliest signs typically include excessive licking of the paws, rubbing the face on furniture or carpets, and scratching the armpits, groin, or ears. These behaviours often begin between 6 months and 3 years of age and may be seasonal initially before becoming year-round.

1. Introduction to Canine Atopic Dermatitis

Canine atopic dermatitis (CAD) is one of the most common dermatological conditions encountered in small animal veterinary practice worldwide. It is a genetically predisposed, chronic, inflammatory, and pruritic skin disease associated with the production of immunoglobulin E (IgE) antibodies directed against environmental allergens. The condition significantly impacts the quality of life of affected dogs and their owners, requiring long-term, multimodal management strategies.

According to the American Veterinary Medical Association (AVMA) and the American Animal Hospital Association (AAHA), atopic dermatitis affects approximately 10 to 15 percent of the canine population, making it the second most common allergic skin disease after flea allergy dermatitis. The European Medicines Agency (EMA) and the Federation of Veterinarians of Europe (FVE) recognise CAD as a major welfare concern due to the chronic pruritus and secondary skin infections it causes.

The pathophysiology of atopic dermatitis in dogs involves a complex interplay between genetic susceptibility, epidermal barrier dysfunction, immune system dysregulation (specifically a T-helper 2 (Th2) dominant response), and environmental allergen exposure. Unlike acute urticarial reactions, CAD is a chronic relapsing condition that requires a comprehensive diagnostic approach and individually tailored therapy.

The condition typically presents in young adult dogs between 6 months and 3 years of age. Certain breeds are overrepresented, including the West Highland White Terrier, Labrador Retriever, Golden Retriever, German Shepherd Dog, French Bulldog, Boxer, Shih Tzu, and Dalmatian. However, any breed or mixed breed can be affected. There is no sex predilection, although some studies suggest a slight female predisposition.

Clinical signs are primarily driven by pruritus, which is often the owner's chief complaint. The distribution of lesions follows a characteristic pattern involving the face, ears, paws, flexural surfaces of the limbs, and ventral abdomen. Chronic scratching and licking lead to secondary changes including alopecia, erythema, hyperpigmentation, lichenification, and excoriations.

Secondary bacterial and yeast infections (pyoderma and Malassezia dermatitis) are extremely common and often complicate the clinical picture. These infections can amplify pruritus and make the condition more difficult to manage. Recurrent otitis externa is also a frequent comorbidity, with some dogs presenting primarily with ear disease.

The diagnosis of atopic dermatitis in dogs is based on compatible history, clinical signs, and the exclusion of other pruritic skin diseases. There is no single definitive diagnostic test. Intradermal skin testing and serological allergen-specific IgE testing can help identify offending allergens for inclusion in immunotherapy, but they are not diagnostic for the disease itself.

Management of CAD requires a multimodal approach. The International Committee on Allergic Diseases of Animals (ICADA) and the World Association of Veterinary Dermatology (WAVD) have published consensus guidelines for the diagnosis and treatment of CAD. These guidelines emphasise the importance of combining allergen avoidance, topical therapy, systemic anti-pruritic medications, allergen-specific immunotherapy (ASIT), and management of secondary infections.

This comprehensive veterinary reference guide aims to provide an exhaustive overview of atopic dermatitis in dogs, covering pathophysiology, clinical presentation, diagnostic approach, treatment options, and long-term management strategies. It is intended for veterinary professionals, veterinary students, and informed pet owners seeking a deep understanding of this complex condition.

2. Pathophysiology and Immunology

2.1 Genetic Predisposition

The genetic basis of atopic dermatitis in dogs is well established. Breed predispositions strongly suggest a heritable component. Studies have identified multiple candidate genes involved in skin barrier function, immune regulation, and allergen recognition. In West Highland White Terriers, for example, linkage analysis has identified regions on chromosomes 3, 4, and 13 that are associated with CAD.

The condition is considered polygenic, meaning multiple genes contribute to the phenotype. This genetic complexity explains the variability in clinical presentation, severity, and response to treatment among individual dogs. The AVMA recognises that breeding affected dogs is not recommended, as it perpetuates the genetic predisposition.

2.2 Epidermal Barrier Dysfunction

The stratum corneum, the outermost layer of the epidermis, serves as the primary physical barrier against environmental insults. In atopic dogs, this barrier is compromised. Key abnormalities include:

• Reduced ceramide levels in the intercellular lipid matrix
• Altered lipid composition with an increased cholesterol to ceramide ratio
• Abnormal cornification and desquamation
• Increased transepidermal water loss (TEWL)
• Reduced skin hydration

This defective barrier allows increased penetration of allergens, microbes, and irritants, triggering and perpetuating the inflammatory cascade. The Cornell College of Veterinary Medicine emphasises that skin barrier repair is a cornerstone of CAD management.

2.3 Immunological Dysregulation

The immune response in atopic dermatitis in dogs is characterised by a predominance of Th2-type cytokines. When allergens penetrate the compromised skin barrier, they are captured by Langerhans cells and other antigen-presenting cells in the epidermis. These cells process and present allergens to naive T lymphocytes, promoting differentiation into Th2 cells.

Th2 cells produce interleukin-4 (IL-4), IL-5, IL-13, and IL-31. These cytokines drive several key processes:

• IL-4 and IL-13: Promote B cell class switching to IgE production. Allergen-specific IgE binds to high-affinity FcεRI receptors on mast cells and basophils.
• IL-5: Attracts and activates eosinophils.
• IL-31: A key pruritogenic cytokine that directly stimulates sensory neurons in the skin, causing itch. IL-31 is now recognised as a major therapeutic target.

Upon re-exposure to the offending allergen, cross-linking of surface-bound IgE on mast cells triggers degranulation, releasing histamine, tryptase, prostaglandins, and leukotrienes. This immediate hypersensitivity reaction contributes to acute pruritus and erythema.

The late-phase response involves recruitment of eosinophils, neutrophils, and T cells to the skin, leading to chronic inflammation. This phase is associated with the clinical signs of erythema, oedema, and lichenification.

2.4 Role of the Microbiome

The skin microbiome of atopic dogs differs significantly from that of healthy dogs. There is reduced microbial diversity and increased colonisation by Staphylococcus pseudintermedius and Malassezia pachydermatis. These organisms can act as superantigens, further driving inflammation and pruritus.

The dysbiosis is both a consequence of the disease and a contributing factor. Secondary infections exacerbate pruritus and inflammation, creating a vicious cycle. The Canadian Veterinary Medical Association (CVMA) recommends that management of secondary infections be prioritised before or concurrently with anti-allergic therapy.

2.5 Environmental Allergens

The most common environmental allergens involved in CAD include:

• House dust mites: Dermatophagoides farinae and Dermatophagoides pteronyssinus are the most frequently implicated allergens worldwide.
• Pollens: Grasses, weeds, and trees (seasonal variation)
• Moulds: Alternaria, Aspergillus, Cladosporium, Penicillium
• Storage mites: Acarus siro, Tyrophagus putrescentiae
• Epithelial allergens: Dander from other animals (less common)

In North America and Europe, house dust mites are the predominant allergens. In Australia, the AVA notes that pollens and dust mites are both significant triggers, with regional variations depending on climate and vegetation.

3. Clinical Presentation

3.1 Signalment and History

Atopic dermatitis in dogs typically presents in young adults between 6 months and 3 years of age. Onset before 6 months is uncommon, and first presentation after 7 years of age should prompt consideration of other diagnoses such as food allergy, scabies, or cutaneous lymphoma.

A thorough history is essential. Key historical features include:

• Age of onset: Young adult
• Breed: Predisposed breeds as listed above
• Seasonality: Early disease may be seasonal (spring/summer for pollens) but often progresses to year-round
• Response to therapy: Partial response to corticosteroids; good response to ciclosporin or oclacitinib
• Concurrent conditions: Recurrent otitis externa, pyoderma, Malassezia dermatitis
• Environmental changes: Worsening after moving to a new home, new carpet, or changes in bedding
• Dietary history: Lack of response to elimination diet (important for ruling out food allergy)

3.2 Pruritus and Lesion Distribution

Pruritus is the hallmark of CAD. It is often the first and most consistent sign. Owners may report:

• Licking or chewing at the paws (pododermatitis)
• Rubbing the face on carpets, furniture, or grass
• Scratching the axillae, groin, and flanks
• Head shaking or ear scratching (otitis externa)
• Scooting or licking the perianal area

The distribution of lesions is characteristic and typically involves:

• Face: Perioral, periocular, and muzzle erythema. Cheilitis (lip fold inflammation) is common.
• Ears: Pinnal erythema, ceruminous otitis, and proliferative changes in chronic cases
• Paws: Interdigital erythema, salivary staining (brown discolouration from licking), and pododermatitis
• Flexural surfaces: Axillae, inguinal region, medial thighs, and ventral abdomen
• Perineum: Erythema and hyperpigmentation

The dorsum and lateral thorax are typically spared, which helps differentiate CAD from flea allergy dermatitis (where the lumbosacral area is commonly affected).

3.3 Primary and Secondary Lesions

Primary lesions (directly caused by the allergic response):

• Erythema (redness)
• Macules and papules
• Wheals (urticaria, less common)

Secondary lesions (resulting from self-trauma and infection):

• Alopecia (hair loss from scratching/licking)
• Excoriations (linear scratches)
• Scale and crust
• Hyperpigmentation (darkening of the skin)
• Lichenification (thickening and roughening of the skin, with exaggerated skin folds)
• Pyoderma (bacterial infection): Papules, pustules, epidermal collarettes, crusts
• Malassezia dermatitis: Greasy, yellowish scale, erythema, and a characteristic "yeasty" odour
• Salivary staining (brown discolouration on light-coloured fur)

3.4 Clinical Severity Grading

Several validated scoring systems are used in clinical practice and research to assess severity:

• CADESI-4 (Canine Atopic Dermatitis Extent and Severity Index): Evaluates erythema, lichenification, and alopecia/excoriation across 20 body sites. Scores range from 0 to 160.
• PVAS (Pruritus Visual Analog Scale): Owner-reported assessment of pruritus severity on a 0 to 10 scale.
• Owner-assessed quality of life questionnaires

These tools help monitor response to therapy and guide treatment adjustments.

3.5 Regional Variations in Presentation

North America: House dust mite allergy is predominant. Seasonal patterns are common in northern regions with distinct pollen seasons. In the southern United States, year-round disease is more typical due to prolonged allergen exposure.

Europe: Similar pattern to North America, with house dust mites being the most common trigger. In the United Kingdom, the CVMA (British Veterinary Association) notes that grass pollens are a significant seasonal trigger.

Australia: The Australian Veterinary Association (AVA) reports that dust mites and pollens are both common triggers. The warmer climate leads to prolonged allergen seasons. Tick paralysis regions (eastern coast) require careful consideration of ectoparasite control.

Canada: Seasonal disease is common in spring and summer. House dust mites are less prevalent in drier regions but remain significant in humid areas. The CVMA emphasises the importance of ruling out sarcoptic mange in rural and northern communities.

4. Diagnostic Approach

4.1 Diagnostic Criteria

The diagnosis of atopic dermatitis in dogs is based on compatible history, clinical signs, and exclusion of other pruritic diseases. Favrot's criteria are widely used in clinical practice. A dog is considered likely atopic if it meets at least 3 of the following 5 major criteria:

1. Onset of signs before 3 years of age
2. Mostly indoor living
3. Pruritus responsive to corticosteroids
4. Chronic or recurrent yeast infections (Malassezia)
5. Affected front paws (pododermatitis)

Additional supportive criteria include:

• Breed predisposition
• Facial and flexural involvement
• Seasonality (early disease)
• Recurrent otitis externa
• Conjunctivitis
• Positive allergen-specific IgE testing

4.2 Differential Diagnoses

Before a diagnosis of CAD can be made, other causes of pruritus must be ruled out. The key differentials include:

• Flea allergy dermatitis (FAD): Affects the lumbosacral area, tail head, and caudal thighs. Presence of fleas or flea dirt. Responds to rigorous flea control.
• Food allergy (food-induced atopic dermatitis): Non-seasonal pruritus, often with gastrointestinal signs (vomiting, diarrhoea/diarrhoea). Diagnosis requires an 8-week elimination diet with a novel or hydrolysed protein source.
• Sarcoptic mange (scabies): Intense pruritus, often with a positive pinnal-pedal reflex. Highly contagious. Diagnosis via skin scrapings or response to acaricidal therapy.
• Contact dermatitis: Pruritus limited to areas in contact with irritants (e.g., new carpet, plants). Less common.
• Bacterial pyoderma: Primary or secondary. Must be treated before assessing underlying allergic disease.
• Malassezia dermatitis: Often secondary to allergies. Can mimic CAD.
• Cutaneous adverse drug reaction: History of recent medication administration.
• Demodicosis: Localised or generalised. Diagnosis via deep skin scrapings.
• Dermatophytosis (ringworm): Circular areas of alopecia with scale. Wood's lamp examination and fungal culture.

4.3 Step-by-Step Diagnostic Workup

The diagnostic approach recommended by the AAHA and ICADA involves a systematic stepwise process:

Step 1: Thorough History and Physical Examination

• Age, breed, onset, progression, seasonality
• Previous treatments and response
• Diet and environment
• Complete dermatological examination

Step 2: Rule Out Ectoparasites

• Flea combing and flea dirt examination
• Skin scrapings (multiple sites) for Demodex and Sarcoptes
• In some regions, trial acaricidal therapy (e.g., isoxazoline) is warranted even with negative scrapings

Step 3: Rule Out Secondary Infections

• Cytology from skin (impression smears, tape strips) and ears
• Look for bacteria (cocci) and yeast (budding organisms)
• Bacterial culture and sensitivity if deep pyoderma or antibiotic resistance suspected

Step 4: Elimination Diet Trial

• 8-week trial with a novel protein or hydrolysed diet
• Strict adherence (no treats, flavoured medications, or chew toys)
• If pruritus resolves, food challenge to confirm

Step 5: Allergen Testing (if CAD is suspected)

• Intradermal skin testing (IDST) or serological allergen-specific IgE testing
• These tests identify allergens for immunotherapy, not for diagnosis
• IDST is considered the gold standard but requires specialist referral
• Serological testing is more accessible but has higher false-positive rates

Step 6: Additional Diagnostics (as needed)

• Skin biopsy (to rule out neoplasia or autoimmune disease in atypical cases)
• Bacterial culture and sensitivity for recurrent pyoderma
• Thyroid function testing (hypothyroidism can exacerbate skin disease)

4.4 The Role of Allergen Testing

Allergen testing is not diagnostic for CAD. Positive results indicate sensitisation, which may or may not be clinically relevant. The decision to test should be based on the intention to formulate allergen-specific immunotherapy (ASIT).

Intradermal Skin Testing (IDST):

• Performed by veterinary dermatologists
• Requires sedation and clipping of a lateral thorax area
• Injections of small volumes of allergen extracts intradermally
• Positive reactions appear as wheals within 15-20 minutes
• Gold standard for ASIT formulation

Serological Testing (ELISA or Immunodot):

• Measures circulating allergen-specific IgE
• Convenient (single blood sample)
• Higher sensitivity but lower specificity than IDST
• Useful when IDST is unavailable or impractical

The EMA and FVE recommend that allergen testing be interpreted in the context of the dog's clinical history and geographic region. For example, a positive test for a pollen that is not present in the dog's environment is likely irrelevant.

5. Treatment and Management

5.1 Overview of Multimodal Therapy

The management of atopic dermatitis in dogs requires a multimodal, individually tailored approach. The ICADA guidelines outline four pillars of therapy:

1. Allergen avoidance and environmental control
2. Skin barrier repair and topical therapy
3. Anti-pruritic and anti-inflammatory medications
4. Allergen-specific immunotherapy (ASIT)

Secondary infections must be treated aggressively before or concurrently with anti-allergic therapy. The goal is to break the itch-scratch cycle and restore skin health.

5.2 Allergen Avoidance and Environmental Control

Complete avoidance of environmental allergens is rarely possible, but reduction of exposure can significantly improve clinical signs.

House Dust Mite Control:

• Use dust-mite-proof covers on dog beds
• Wash bedding weekly in hot water (above 55 degrees C / 130 degrees F)
• Remove carpets, curtains, and upholstered furniture from the dog's environment
• Use high-efficiency particulate air (HEPA) filters
• Maintain low indoor humidity (below 50 percent)
• Vacuum frequently with HEPA-filtered vacuum cleaners

Pollen Avoidance:

• Keep dogs indoors during peak pollen times (early morning and late afternoon)
• Wipe the dog's coat and paws with a damp cloth after outdoor exposure
• Use air conditioning rather than open windows
• Consider a "pollen calendar" for your region

Mould Control:

• Fix leaks and reduce moisture in the home
• Clean mouldy surfaces with appropriate products
• Avoid damp basements and outdoor mouldy areas

The AVMA and AAHA recommend that environmental control measures be implemented as a first-line, low-risk intervention.

5.3 Skin Barrier Repair and Topical Therapy

Restoration of the epidermal barrier is a critical component of CAD management. Topical therapies provide direct relief and reduce the need for systemic medications.

Essential Fatty Acid (EFA) Supplementation:

• Omega-3 and omega-6 fatty acids (e.g., fish oil, evening primrose oil)
• Improve skin barrier function and have anti-inflammatory effects
• May take 8-12 weeks to show benefit
• Often used as an adjunctive therapy

Topical Moisturisers and Barrier Sprays:

• Ceramide-containing products (e.g., Allerderm, DermAllay)
• Phytosphingosine-based sprays (e.g., Douxo)
• Oatmeal-based shampoos and conditioners (colloidal oatmeal)
• Apply after bathing or as needed

Therapeutic Shampooing:

• Frequency: 1-2 times per week initially, then as needed
• Use lukewarm water and leave shampoo on for 10-15 minutes
• Follow with a conditioner or moisturiser
• Shampoos may contain:
  • Chlorhexidine (antibacterial)
  • Miconazole or ketoconazole (antifungal)
  • Oatmeal or phytosphingosine (soothing)
  • Benzoyl peroxide (for greasy skin)

Topical Corticosteroids:

• Hydrocortisone aceponate (Cortavance) is a potent topical steroid with minimal systemic absorption
• Useful for localised lesions (e.g., paw licking, facial erythema)
• Avoid long-term use on large body areas

The CVMA and AVA both endorse topical therapy as a safe and effective component of CAD management, particularly for mild to moderate cases.

5.4 Systemic Anti-Pruritic Medications

When topical therapy and environmental control are insufficient, systemic medications are required. The choice of medication depends on severity, comorbidities, cost, and owner preference.

5.4.1 Glucocorticoids

• Mechanism: Broad anti-inflammatory and immunosuppressive effects
• Examples: Prednisolone, prednisone, methylprednisolone, triamcinolone
• Efficacy: Highly effective for acute flares
• Dosing: Short courses (3-7 days) at anti-inflammatory doses (0.5-1 mg/kg/day prednisolone equivalent), then taper
• Adverse effects: Polyuria, polydipsia, polyphagia, panting, behavioural changes, gastrointestinal ulceration, hepatopathy, iatrogenic hyperadrenocorticism with long-term use
• Recommendation: Use only for short-term flare management. Avoid long-term daily use. Alternate-day therapy may reduce adverse effects.

The AAHA and AVMA caution against long-term corticosteroid use due to significant adverse effects. They are a third-line option after safer medications.

5.4.2 Oclacitinib (Apoquel)

• Mechanism: Janus kinase (JAK) inhibitor, specifically JAK1. Blocks signalling of multiple pruritogenic cytokines including IL-31, IL-4, IL-13, and IL-2.
• Efficacy: Rapid onset (within 24 hours), highly effective for pruritus
• Dosing: 0.4-0.6 mg/kg twice daily for 14 days, then once daily for maintenance
• Adverse effects: Vomiting, diarrhoea/diarrhoea, anorexia, lethargy. Increased risk of demodicosis, papillomas, and urinary tract infections. Not recommended in dogs with serious infections or neoplasia.
• Safety: Generally well-tolerated. Long-term safety data are favourable.
• Approval: Approved by the EMA, FDA, and Australian Pesticides and Veterinary Medicines Authority (APVMA)

Oclacitinib is considered a first-line systemic therapy for CAD by the ICADA guidelines.

5.4.3 Ciclosporin (Atopica)

• Mechanism: Calcineurin inhibitor. Suppresses T-cell activation and cytokine production.
• Efficacy: Good efficacy, slower onset (4-6 weeks for full effect)
• Dosing: 5 mg/kg once daily. May be reduced after clinical improvement.
• Adverse effects: Vomiting, diarrhoea/diarrhoea, gingival hyperplasia, hirsutism, papillomatosis. Rarely, hepatotoxicity or nephrotoxicity.
• Drug interactions: Ketoconazole increases ciclosporin levels (can be used to reduce dose and cost)
• Approval: Approved for CAD in many countries

Ciclosporin is also a first-line therapy, particularly for dogs that do not tolerate oclacitinib or have concurrent conditions.

5.4.4 Lokivetmab (Cytopoint)

• Mechanism: Caninised monoclonal antibody against IL-31. Neutralises the key pruritogenic cytokine.
• Efficacy: Rapid onset (1-3 days), highly effective for pruritus
• Dosing: Subcutaneous injection every 4-8 weeks based on response
• Adverse effects: Very low. Mild injection site reactions in some dogs.
• Safety: Excellent safety profile. No known drug interactions.
• Approval: Approved in the US, Europe, Canada, and Australia

Lokivetmab is considered a first-line therapy, especially for dogs with concurrent disease that precludes other medications.

5.4.5 Antihistamines

• Mechanism: H1 receptor antagonists
• Efficacy: Variable and generally poor as monotherapy. May be useful as adjunctive therapy in some dogs.
• Examples: Cetirizine (0.5-1 mg/kg twice daily), loratadine (0.25 mg/kg once daily), chlorpheniramine (0.2-0.4 mg/kg two to three times daily)
• Adverse effects: Sedation (especially first-generation antihistamines), anticholinergic effects
• Recommendation: Trial for 2 weeks; if no response, discontinue.

The FVE and CVMA note that antihistamines are rarely effective in canine atopic dermatitis, unlike in human atopic dermatitis.

5.5 Allergen-Specific Immunotherapy (ASIT)

ASIT, also known as hyposensitisation or allergy shots, is the only disease-modifying therapy for CAD. It involves administering gradually increasing doses of the offending allergens to induce immunological tolerance.

Mechanism:

• Shift from Th2 to Th1 immune response
• Induction of regulatory T cells (Tregs)
• Production of IgG blocking antibodies
• Reduced mast cell and basophil reactivity

Formulation:

• Based on IDST or serological testing results
• Individualised for each dog
• May be subcutaneous injections or sublingual drops

Protocol:

• Induction phase: Increasing doses over 2-4 months
• Maintenance phase: Stable dose every 2-4 weeks
• Response time: 3-12 months
• Success rate: 60-80 percent show significant improvement

Adverse effects:

• Local reactions (swelling, pruritus at injection site)
• Systemic reactions (urticaria, angioedema, anaphylaxis) are rare
• Owners should be trained to recognise and respond to adverse reactions

Duration:

• Long-term therapy, often lifelong
• Some dogs may maintain improvement after discontinuation

The AVMA, AAHA, and EMA all recommend ASIT as a safe and effective long-term treatment for CAD. It is the only therapy that addresses the underlying immune dysregulation.

5.6 Management of Secondary Infections

Secondary bacterial and yeast infections are a major cause of pruritus amplification in CAD. They must be treated aggressively.

Bacterial Pyoderma:

• Superficial pyoderma: Topical chlorhexidine or benzoyl peroxide shampoos, mousses, or wipes
• Deep pyoderma: Systemic antibiotics based on culture and sensitivity
• Common antibiotics: Cephalexin, cefpodoxime, clindamycin, amoxicillin-clavulanate
• Duration: Minimum 3-4 weeks, continue for 7-10 days beyond clinical resolution
• Methicillin-resistant Staphylococcus pseudintermedius (MRSP) is an emerging concern. Culture and sensitivity are essential.

Malassezia Dermatitis:

• Topical antifungal therapy: Chlorhexidine with miconazole or ketoconazole shampoos
• Systemic therapy: Ketoconazole (5-10 mg/kg once daily with food) or itraconazole (5 mg/kg once daily)
• Duration: 2-4 weeks

Otitis Externa:

• Clean ears with appropriate ceruminolytic solution
• Topical therapy based on cytology (antibacterial, antifungal, anti-inflammatory)
• Chronic cases may require systemic therapy

The CVMA emphasises that recurrent infections are a sign of poorly controlled underlying allergic disease. Effective CAD management reduces infection frequency.

5.7 Novel and Emerging Therapies

JAK Inhibitors:

• Oclacitinib is the only approved JAK inhibitor for CAD in dogs
• Other JAK inhibitors (e.g., upadacitinib) are being investigated

IL-31 Blockade:

• Lokivetmab is the only approved monoclonal antibody for CAD
• Other anti-cytokine therapies (e.g., anti-IL-4, anti-IL-13) are in development

Probiotics:

• Oral probiotics may modulate the gut-skin axis and reduce inflammation
• Evidence is preliminary but promising

Stem Cell Therapy:

• Mesenchymal stem cells have immunomodulatory properties
• Early studies show potential for reducing pruritus and inflammation

Dietary Interventions:

• Novel protein and hydrolysed diets are primarily for food allergy diagnosis
• Some diets with enhanced skin barrier support (e.g., added EFAs, ceramides) may benefit CAD

The AVA notes that while these therapies are promising, they are not yet standard of care and should be used under specialist guidance.

6. Long-Term Management and Monitoring

6.1 Establishing a Treatment Plan

A successful long-term management plan for atopic dermatitis in dogs requires:

1. Realistic owner expectations: Explain that CAD is a lifelong condition requiring ongoing management, not cure.
2. Individualised therapy: Tailor the plan to the dog's severity, comorbidities, and owner's resources.
3. Multimodal approach: Combine environmental control, topical therapy, systemic medications, and immunotherapy as needed.
4. Regular monitoring: Schedule recheck examinations every 1-3 months initially, then every 3-6 months once stable.
5. Flare management plan: Provide clear instructions for managing acute exacerbations.

6.2 Monitoring Tools

• CADESI-4 scoring: Objective assessment of skin lesions
• PVAS: Owner-reported pruritus score
• Quality of life questionnaires: For both dog and owner
• Weight and body condition scoring: Monitor for medication-related weight gain
• Blood work: For dogs on long-term ciclosporin (monitor renal and hepatic function) or oclacitinib (monitor for anaemia, neutropenia)
• Cytology: At each recheck to assess for secondary infections

6.3 Managing Flares

Acute flares of pruritus are common and can be triggered by:

• Increased allergen exposure (e.g., spring pollen season)
• Secondary infections
• Stress
• Changes in environment (e.g., moving to a new home)

Flare management protocol:

1. Identify and address triggers: Check for fleas, secondary infections, environmental changes.
2. Increase topical therapy: Bathe with medicated shampoo twice weekly.
3. Short-term rescue therapy: Oclacitinib twice daily for 3-7 days, or a short course of corticosteroids (e.g., prednisolone 0.5-1 mg/kg once daily for 3-5 days).
4. Recheck: If no improvement in 5-7 days, re-evaluate.

6.4 Cost Considerations

The cost of CAD management can be significant. Owners should be informed of potential costs:

• Initial workup: Consultation, skin scrapings, cytology, elimination diet trial, allergen testing (USD 500-1500)
• Monthly medications: Oclacitinib (USD 50-150), ciclosporin (USD 80-200), lokivetmab (USD 60-120 per injection)
• Immunotherapy: Initial formulation (USD 200-500), then USD 30-60 per month
• Topical therapy: Shampoos, conditioners, sprays (USD 20-50 per month)
• Secondary infections: Antibiotics, antifungals, ear medications (variable)

The AAHA recommends discussing costs openly and helping owners prioritise interventions.

6.5 Prognosis

With appropriate management, most dogs with atopic dermatitis achieve good to excellent quality of life. The prognosis depends on:

• Severity of disease: Mild cases are easier to manage
• Owner compliance: Regular therapy and monitoring are essential
• Response to therapy: Some dogs respond better to certain medications
• Secondary infections: Frequent infections indicate poorly controlled disease
• Comorbidities: Hypothyroidism, diabetes, or other conditions complicate management

The AVMA states that with modern therapies, euthanasia due to uncontrolled CAD is rare. Most dogs can be managed successfully with a multimodal approach.

7. Prevention and Breeding Considerations

7.1 Genetic Counselling

Atopic dermatitis in dogs has a strong genetic component. The AVMA, AAHA, and FVE all recommend that affected dogs should not be bred. Breeders should:

• Avoid breeding dogs with a confirmed diagnosis of CAD
• Avoid breeding closely related dogs (siblings, parents) of affected dogs
• Screen breeding stock for allergic disease history
• Consider genetic testing when available (limited at present)

7.2 Early Intervention

Early diagnosis and treatment may slow disease progression and prevent secondary changes. Puppies from predisposed breeds should be monitored closely for early signs of pruritus.

Some evidence suggests that early exposure to environmental allergens may influence the development of tolerance, but this is not well established in dogs. The AVA recommends a balanced approach: avoid excessive allergen exposure but do not keep puppies in sterile environments.

7.3 Nutritional Considerations

While diet is not a primary cause of CAD, certain nutritional strategies may support skin health:

• Essential fatty acids: Omega-3 and omega-6 supplementation from puppyhood
• Probiotics: May support immune system development
• Antioxidants: Vitamin E, vitamin C, and selenium may reduce oxidative stress

The Cornell College of Veterinary Medicine notes that no diet can prevent CAD, but a high-quality diet supports overall health.

8. Owner Education and Quality of Life

8.1 Key Messages for Owners

• Atopic dermatitis is a lifelong condition, not a curable disease.
• Treatment is multimodal and requires commitment.
• Regular veterinary