Canine Allergic Dermatitis Study Guide

Overview and Clinical Importance

Canine atopic dermatitis (CAD) is a genetically predisposed, chronic inflammatory and pruritic skin disease with characteristic clinical features, most commonly associated with IgE antibodies directed against environmental allergens. It is one of the most common dermatological conditions encountered in small animal practice, affecting approximately 10-15% of the canine population. CAD significantly impacts the quality of life of affected dogs and their owners, requiring lifelong management in most cases.

Contact dermatitis is a less common hypersensitivity disorder that occurs when the skin directly contacts an irritating substance (irritant contact dermatitis) or an allergen that triggers an immune response (allergic contact dermatitis). Because the canine haircoat provides a protective barrier, contact dermatitis typically affects thinly-haired or glabrous skin areas.

Understanding the pathogenesis, clinical presentation, diagnostic approach, and treatment options for these conditions is essential for the NAVLE and clinical practice. This guide provides comprehensive coverage of both atopic and contact dermatitis in dogs.

Canine Atopic Dermatitis (CAD)

Definition and Epidemiology

Canine atopic dermatitis is defined as a genetically predisposed inflammatory and pruritic allergic skin disease with characteristic clinical features, associated most commonly with IgE antibodies to environmental allergens. The prevalence is estimated at 10-15% of the canine population, though reliable epidemiological data is limited.

Breed Predispositions

While any breed can develop CAD, certain breeds demonstrate strong genetic predisposition. Breed prevalence varies by geographic region due to differences in genetic pools.

Pathogenesis

The pathogenesis of CAD involves complex interactions between genetic predisposition, environmental factors, skin barrier dysfunction, and immune dysregulation.

Key Pathogenic Components

Common Environmental Allergens

Clinical Signs and Lesion Distribution

The hallmark clinical sign of CAD is pruritus, which may manifest as scratching, rubbing, chewing, excessive grooming, licking, scooting, or head shaking. Pruritus may be seasonal (pollen allergies) or non-seasonal (house dust mites, food) and often precedes the development of skin lesions.

Primary Lesions (Acute Disease)

• Erythema - often the first visible sign
• Erythematous macules and papules
• Alesional pruritus (pruritus without visible lesions) - common early in disease

Secondary Lesions (Chronic Disease)

• Self-induced alopecia from licking and scratching
• Excoriations from self-trauma
• Lichenification (thickened, leathery skin) - indicates chronic inflammation
• Hyperpigmentation - post-inflammatory pigment changes
• Salivary staining (rust-colored discoloration from excessive licking)

Classic Lesion Distribution Pattern

The following body regions are most commonly affected in canine atopic dermatitis:

• Face - periocular region, muzzle, lips
• Ears - concave (internal) aspect of pinnae; otitis externa common
• Paws - dorsal and interdigital spaces (foot licking very common)
• Ventrum - axillae, inguinal region, ventral abdomen
• Flexor surfaces - antebrachiocarpal, tarsocrural joints

Secondary Complications

Staphylococcal Pyoderma

Staphylococcus pseudintermedius is the most common bacterial pathogen. Clinical findings include papules, pustules, epidermal collarettes, crusting, and focal areas of alopecia. Diagnosis is confirmed by cytology (cocci with neutrophils).

Malassezia Dermatitis

Malassezia pachydermatis overgrowth commonly occurs in skin folds, ear canals, and areas of lichenification. Clinical findings include greasy seborrhea, erythema, yellowish-brown discoloration, and malodor. Cytology shows characteristic peanut-shaped or footprint-shaped budding yeast (3-5 micrometers).

Otitis Externa

Otitis externa is present in up to 80% of dogs with atopic dermatitis and may be the only clinical sign in some cases. Both bacterial (Staphylococcus, Pseudomonas) and yeast (Malassezia) organisms commonly contribute.

Diagnostic Approach to Canine Atopic Dermatitis

There is no single diagnostic test for canine atopic dermatitis. Diagnosis is based on meeting clinical criteria and systematically ruling out other pruritic skin conditions.

Stepwise Diagnostic Workup

Step 1: Rule Out Flea Allergy Dermatitis

• Perform flea combing to identify fleas or flea feces
• Note lesion distribution: FAD classically affects dorso-lumbar area, tail base, caudomedial thighs
• Institute strict flea control trial for minimum 8-12 weeks

Step 2: Rule Out Other Ectoparasites

• Sarcoptes: Multiple superficial skin scrapings; positive pinnal-pedal reflex supports diagnosis; trial treatment if suspicious
• Demodex: Deep skin scrapings with skin squeeze, trichography, tape impressions

Step 3: Identify and Treat Secondary Infections

• Perform cytology on all affected skin lesions and ear canals
• Treat pyoderma with appropriate systemic antibiotics
• Treat Malassezia with topical and/or systemic antifungals

Step 4: Rule Out Cutaneous Adverse Food Reaction

• Essential for ALL dogs with non-seasonal (perennial) pruritus
• Strict elimination diet trial for minimum 8 weeks
• Novel protein diet or hydrolyzed protein diet
• Dietary provocation required to confirm diagnosis

Favrot's Criteria for Clinical Diagnosis

Favrot's criteria are evidence-based clinical criteria developed to assist with the diagnosis of canine atopic dermatitis. Apply AFTER ruling out other causes of pruritus.

Interpretation: If 5 of 8 criteria are met, sensitivity is 85% and specificity is 79%. These criteria should NOT be used as the sole diagnostic test.

Allergy Testing

Important: Allergy testing (intradermal testing or serology) is NOT used to diagnose atopic dermatitis. These tests identify allergens for allergen-specific immunotherapy (ASIT) AFTER clinical diagnosis.

Treatment of Canine Atopic Dermatitis

Treatment of CAD requires a multimodal approach addressing inflammation, secondary infections, skin barrier dysfunction, and underlying immune dysregulation.

Pharmacological Treatment Options

Allergen-Specific Immunotherapy (ASIT)

ASIT is the only disease-modifying treatment for canine atopic dermatitis with the potential to induce long-term tolerance. Success rate is approximately 60-70% (greater than or equal to 50% improvement). Response may take 6-12 months. Continue for minimum 12 months before assessing failure.

Contact Dermatitis

Contact dermatitis is relatively uncommon in dogs due to the protective haircoat. Two types exist: Irritant contact dermatitis (direct chemical damage, non-immune) and Allergic contact dermatitis (Type IV hypersensitivity, requires sensitization).

Common Causes

• Irritants: Harsh shampoos, cleaning chemicals, herbicides, fertilizers
• Allergens: Plants (Wandering Jew), metals (nickel), rubber, fabric dyes, topical medications (neomycin)

Clinical Signs

Lesions localized to areas of skin contact, typically affecting thinly-haired regions: ventral abdomen/chest, axillae, inguinal region, interdigital spaces, chin/muzzle.

Diagnosis and Treatment

Diagnosis based on history, distribution pattern, withdrawal trial (removal of suspected agent), and provocation/rechallenge. Patch testing available but requires expertise. Treatment: Avoidance is primary and most effective. Symptomatic therapy (topical/systemic glucocorticoids) for acute management. Prognosis good if offending substance identified and avoided.

Canine Atopic Dermatitis

• Prevalence 10-15%; onset typically 6 months to 3 years
• Classic distribution: face, ears, ventrum, axillae, paws; dorso-lumbar and ear margins SPARED
• Diagnosis: Favrot's criteria + exclusion of differentials (fleas, mites, infections, food allergy)
• Allergy testing NOT for diagnosis - used to identify allergens for immunotherapy
• ASIT is only disease-modifying treatment with 60-70% success rate

Contact Dermatitis

• Uncommon; affects sparsely-haired contact areas
• Diagnosis: withdrawal/provocation testing, patch testing
• Treatment: avoidance is key; good prognosis if trigger identified