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Y4 SA - Dermatology > Overview of canine atopic dermatitis > Flashcards

Overview of canine atopic dermatitis Flashcards

1
Q

Define canine atopic dermatitis

A

Genetically predisposed inflammatory & pruritic allergic skin disease with characteristic clinical features, associated with IgE antibodies most commonly to environmental allergens

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2
Q

Which allergens might cause CAD?

A

Allergens include house dust mites, pollens and mould spores in the environment and food allergens fed to the dog

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3
Q

10-30% of cases have NO detectable allergen-specific IgE for environmental allergens, this is termed…?

A

Atopic like dermatitis

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4
Q

Describe the 4 main features in the pathogenesis of CAD

A
  1. Cutaneous inflammation and pruritis
  2. Defective skin barrier function
  3. Microbial colonisation
  4. Other flare factors
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5
Q

Which hypersensitivities are involved in CAD?

A

Type 1 = Immediate reactions
Type 4 = delayed reactions

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6
Q

Describe type 1 hypersensitivity reactions

A
  • IgE bound to mast cells
  • Allergen bound by IgE causes mast cell degranulation
  • Products of mast cell degranulation cause tissue inflammation and pruritis
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7
Q

Describe type 4 hypersensitivity reactions

A
  • TH2 bias
  • Allergen peptides presented to T-cells by langerhans cells
  • Induce clonal expansion
  • T-cells produce pro-inflammatory cytokines which cause tissue inflammation and pruritis
  • T-cells produce cytokines that direct B-cells to produce IgE
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8
Q

What are the presenting signs of CAD?

A

Most common clinical signs are pruritus, recurrent pyoderma, recurrent otitis, seborrhoea, alopecia and occasionally urticaria

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9
Q

Describe the defective barrier seen in CAD

A
  • Leaky skin – water gets out – microbes and allergens can penetrate more easily
  • Increased transepidermal water loss (TEWL)
  • Wide intercellular spaces between corneocytes
  • Disorganised & fragmented lipid matrix
  • Decreased levels of certain proteins and lipids in some breeds
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10
Q

Dogs with cAD show increased carriage of which bacteria?

A

Staphylococcus spp

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11
Q

How does microbial colonisation affect CAD

A
  • Increased binding sites (due to inflammation)
  • Reduced lipids and other proteins (barrier function)
  • Damage to skin surface (self trauma)
  • Dysbiosis: changed patterns of bacterial colonisation on the skin - imbalance
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12
Q

What are Atopic flares?

A

VERY common to see secondary staphylococcal pyoderma and otitis and Malassezia dermatitis in cases of CAD
Bacteria and yeast induce further inflammation and pruritus that is often not alleviated by specific anti-pruritics (e.g., lokivetmab or oclacitinib)

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13
Q

Describe the ‘vicious cycle’ of CAD

A

Inflammation -> Skin thickening -> increased antigen penetration and presentation -> reduced barrier -> secondary infection ->

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14
Q

What are the common causes of flares in CAD?

A
  • Bacteria and yeast 2˚ infection
  • Increase in allergen through seasonal changes or changes in environment
  • Fleas, scabies or other ectoparasite infestation
  • Reduction of therapy by owner / vet
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15
Q

Clinical diagnosis of CAD is based on which factors?

A

Compatible history
Clinical signs
Exclusion of differential diagnoses
There are no pathognomonic signs!

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16
Q

Describe some typical features of a history that indicate CAD

A
  1. Pruritus seasonal or perennial or both
    - Main clinical sign
    - Pruritus precedes skin lesions
    - 75% of dogs develop signs <3 years (up to 6 years)
    - Food allergy more commonly starts <1 year
  2. Certain breeds predisposed, but may occur in any breed or cross
    - certain breeds may have certain distribution
    - may have affected relatives
    - no sex predilection
  3. History is key: cannot rely on clinical signs
17
Q

What are the main clinical signs of CAD?

A
  • PRURITIS: includes scratching, rubbing, chewing, excessive grooming or licking, scooting, and/or head shaking
  • Primary lesions may also include erythema +/-papules
18
Q

List some secondary lesions seen in CAD

A

Otitis
Lesions due to pruritus
- Alopecia
- Excoriations
- Salivary staining
- Lichenification
- Pustules, epidermal collarettes and crusts
- Hyperpigmentation

19
Q

Describe the distribution of CAD lesions

A
  • Face and chin
  • Periorbital areas
  • Ears – pinnal and meatal skin (but not the pinnal margins)
  • Elbow creases
  • Feet: dorsal interdigital spaces and plantar/palmar surfaces
  • Ventral abdomen (and axillae)
  • Perianal area (anal gland disease only in some)
20
Q

Is a bilaterally symmetrical disease and inside-out disease or an outside-in disease?

A

Inside out e.g. systemic diseases

21
Q

Name an example of an outside-in disease

A

Infections and infestations

22
Q

List the 7 of Favrot’s criteria for CAD

A
  1. Onset of signs under three years of age
  2. Dog living mostly indoors
  3. Glucocorticoid-responsive pruritus
  4. Pruritus sine materia at onset i.e. pruritis without lesions at onset
  5. Affected front feet and/ or ear pinnae
  6. Non-affected ear margins
  7. Non-affected dorso-lumbar area
23
Q

List some DDx for pruritis

A
  • Ectoparasites: sarcoptic mange, cheyletiellosis, flea infestation and hypersensitivity, trombiculiasis, pediculosis, otodectic mange & some cases of demodicosis
  • Allergic skin disease e.g. contact dermatitis
  • Microbial infection (2˚ to another problem): Bacterial pyoderma
  • Malassezia dermatitis (rarely dermatophytosis)
  • Pemphigus foliaceus
  • Epitheliotropic lymphoma
24
Q

How can you exclude ectoparasites as a DDx?

A
  • Flea combing & Wet paper test
  • Scale exam
  • Acetate tape strips
  • Hair plucks
  • Skin scrapes
  • Treatment trials
25
Q

Ectoparasite treatment trials are used for which 2 parasites?

A

Scabies
Fleas

26
Q

How are secondary infections/overgrowths diagnosed?

A

Cytology

27
Q

If your patient is pruritic… The signs and history are consistent, and you have ruled out:
- Parasites
- Microbial infections
- Other possibilities
Have you diagnose CAD?

A

No - you still don’t know if it is food or environmentally triggered

28
Q

How are food allergies diagnosed?

A

Elimination diet is the only way:
- Home cooked
- Commercial hydrolysed diet
- Novel diet = not been exposed to that food before

29
Q

How long should a food trial last?

A

Minimum of 6 weeks

30
Q

How are food trials monitored?

A

Diary
Make the point to the owners to do the food trial properly once

31
Q

Describe hydrolysed protein diets for food trials

A
  • Avoid need to choose novel protein
  • Common proteins (such as chicken/ soy) may not be rendered completely non-allergenic
32
Q

What is the gold standard diet for elimination diets?

A

Home cooked diet trial

33
Q

List the potential problems of home cooked diet trials

A
  • Identifying appropriate ingredients (cross-reactions)
  • Unsuitable for long term use or growing animals
  • Labour intensive
  • Palatability
  • GIT upsets
  • Cost
34
Q

Describe the use of commercial novel protein diets for exclusion diets

A

Nutritionally balanced
Improved compliance from owner

35
Q

List the potential problems of commercial novel protein diets

A
  • Availability of novel ingredients?
  • Hidden or modified allergens or additives?
  • ¾ over the counter venison diets were positive for soy & 1 for beef
  • The word “hypoallergenic” means nothing
36
Q

Why are steroids or oclacitinib used at the start of food trials?

A

Use these for 2-3 weeks at the beginning of food trials to:
- Reduce secondary inflammation and perpetuating disease
- Have a comfortable animal in the early part of the food trial period
Using such therapy may reduce trials to 4-5 weeks in many animals

37
Q

Describe the use of environmental allergen testing

A
  • NOT a diagnostic test (false positives and negatives)
  • Used to identify environmental allergen-specific IgE for use in management where cAD has been confirmed
  • House dust mites, storage mites, pollens (grass, weeds and trees) and fungi +/- Malassezia

Y4 SA - Dermatology (6 decks)

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