Immune mediated skin disease Flashcards

1
Q

What are immune mediated skin disease?

A
  • Immune system fails to tolerate self-antigens
  • Mounts response against normal skin component
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2
Q

What’s the difference between primary + secondary IMSD

A
  • Primary IMSD = No external trigger identified (idiopathic)
  • Secondary IMSD = Exogenous triggering antigen, most commonly drug, bacteria or virus
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3
Q

What clinical assessment should be done with IMSD?

A
  • Consider signalment (particularly breed) & key historical features
  • ID primary lesions
  • Consider lesion distribution
  • Make differential diagnosis list
  • Run tests according to differentials
  • Interpret results in line with clinical findings
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4
Q

What are IMSD lesions?

A
  • Pustules - common
  • Plaques/nodules - common
  • Erythematous macules/patches - common
  • Hypopigmented macules/patches - common
  • Alopecia
  • Vesicles
  • Erosions/ulcers - secondary - loss of blood supply, adhesion, self trauma
  • Crusts - secondary - pus. exudate, blood (dried)
  • Purpura (haemorrhage/bruise)
  • Scale
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5
Q

How can you diagnose IMSD?

A
  • Lesion cytology
  • Skin biopsy & histopathology
  • Haematology, biochemistry, urinalysis
  • Diagnostic imaging = radiography, ultrasonography
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6
Q

What are advantages of cytology?

A
  • Easy, cheap, rapid (in house) results - direct impression / FNA
  • Differentiate sterile from septic (infectious) disease
  • Determine type of inflammation
  • May inform management prior to histopath results
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7
Q

What are benefits of skin biopsy + histopath?

A
  • Definitive diagnosis - rule out differentials, determine skin pathology
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8
Q

Case 1 =
Betty = 7yr FN springer spaniel
* Hx = 10wk non-pruritic progressive crusting dermatosis
- reduced appetite last 3 days
* Physical examination =
- General WNL except pyrexia 40oC and
- mild peripheral lymphadenomegaly
* Lesion morphology =
- Thick, yellow adherent crusts, pus under crusts
* Lesion distribution =
- Multifocal
- Dorsal muzzle, periocular, medial pinnae, footpads

What are differentials for pustules?

A
  • Bacterial infection (pyoderma/folliculitis)
  • Pemphigus foliaceus
  • Superficial pustular drug reaction (rare) - ruled out as not had drugs
  • Superficial pustular dermatophytosis (rare)
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9
Q

Betty’s cytology =

  • Direct impression smear =
  • Needle rupture of intact pustule or
  • Below crust after gentle removal
  • Microscopy =
  • Sterile neutrophilic inflammation and acantholytic keratinocytes +/- eosinophils
  • what does this indicate from the differentials?
A

= Consistent with pemphigus foliaceus

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10
Q

How do acantholytic keratinocytes form with pemphigus foliaceus?

A
  • Auto-antibodies (mainly IgG) target components of desmosomes that link keratinocytes in superficial epidermis
  • Separation of KCs > acantholytic ‘rounded up’ KCs
  • Neutrophilic inflammatory response > superficial pustules with free floating acantholytic KCs
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11
Q

What are signalment + history indications of pemphigus foliaceus?

A
  • Signalment =
  • middle aged (any), predisposed breeds = akita, chow chow, cocker spaniel, dachshund, LR, BBD & SSD (affects many breeds)
  • History = variable pruritus, possible drug-trigger (including topical and oral ectoparaciticides)
  • Often UV exacerbation
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12
Q

Case 2

Bernie
* Signalment = 6 yr FN Basset hound
* History = 4 yr CAD & Malassezia dermatitis
- ASIT, itraconazole (5-10mg/kg), topical chlorhexidine & miconazole
- Acute onset non-pruritic lumps and discharging tracts
* Physical examination = General WNL
* Lesion morphology =
- 3-8 cm (huge) soft nodules (fixed to dermis)
- Overlying skin normal or erythematous and ulcerated, draining serosanguinous fatty fluid
* Lesion distribution = Trunk and proximal limbs

  • What are differentials for plaques + nodules?
A
  • Immune mediated =
  • Juvenile sterile granulomatous dermatitis and lymphadenitis (juvenile cellulitis)
  • Sterile pyogranulomatous dermatitis and panniculitis
  • Feline plasma cell pododermatitis (not a cat)
  • Canine eosinophilic furunculosis of the face
  • Reactive histiocytosis
  • Canine eosinophilic granuloma
  • Metatarsal fistulation (of GSD)
  • Canine sterile neutrophilic dermatosis (Sweet’s syndrome)
  • Canine acute eosinophilic dermatitis
  • Cutaneous xanthoma
  • Other =
  • Neoplasia
  • Callus
  • Acral lick dermatitis
  • Deep infections: mycobacterial, fungal, protozoal
  • Arthropod/spider bites
  • Foreign body reaction
  • Feline eosinophilic plaque or granuloma - not a cat
  • Calcinosis cutis/circumscripta
  • Sterile pyogranulomatous
  • pododermatitis (interdigital furunculosis/interdigital cysts)
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13
Q

What is seen with eosinophilic furunculosis of the face?

A
  • Signalment = young adults
  • History = rapid onset, intense pruritus
  • Lesion morphology = eroded/ulcerated plaques and nodules
  • Distribution = face
  • Cytology = eosinophilic inflammation
  • Histopathology = eosinophilic folliculitis & furunculosis
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14
Q

What is seen with sterile granulomatous dermatitis + lymphadenitis (juvenile cellulitis)?

A
  • Signalment = puppies (sporadic cases in adults)
  • History = acute onset, non-pruritic (painful), pyrexia, lethargy
  • Lesion morphology = follicular nodules (furuncules) & plaques (often eroded & crusted), diffuse swelling, alopecia (check for Demodex), lymphadenomegaly
  • Distribution = face (muzzle, periocular, pinnae), lymph nodes
  • FNA cytology = sterile pyogranulomatous inflammation
  • Histopath = sterile perifollicular granulomatous- pyogranulomatous inflammation & furunculosis
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15
Q

What can be done to rule out Ddx?

A
  • FNA cytology - deep infections - mycobacterial, fungal, protozoal
  • Skin biopsy + histopath (take extra biopsy + freeze)
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16
Q

On FNA what does sterile pyogranulomatous inflammation
(neutrophils + macrophages) show?

A
  • Sterile nodular panniculitis
  • itraconazole can cause IMSD
17
Q

What are Ddx for hypopigmented / erythematous macules + patches?

A
  • Sterile immune mediated =
  • Cutaneous lupus erythematosus
  • Erythema multiforme
  • Vascular disease (vasculitis / vasculopathy)
    1. Familial (GSD, greyhound)
    2. Proliferative arteritis of nasal philtrum
    3. Proliferative thrombovascular necrosis of the pinnae
  • Mucocutaneous pyoderma
  • Uveodermatologic syndrome
  • Anal furunculosis
  • Subepidermal blistering dermatoses
  • Main non-IM differentials =
  • Erythematous macules/patches, wheals = Type I HSR, particularly urticaria, neoplasia
  • Erosions/ulcers, crusting = Bacterial & fungal infection, neoplasia (SCC, EL)
  • Change in pigmentation = Post inflammatory change, neoplasia (EL)

(epitheliotrophic lymphoma)

18
Q

What is presentation of cutaneous lupus erythematosus?

A
  • Rapid onset = Vesicular CLE (rare)
  • Chronic onset =
  • Facial discoid lupus erythematosus (most common variant)
  • Generalised DLE (rare)
  • Mucocutaneous LE (uncommon)
  • Exfoliative CLE (rare)
19
Q

What is seen with facial discoid lupus erythematosus?

A
  • Loss of cobblestone surface of nasal planum
  • Hypopigmented macules and patches
  • Erosions, ulcers and crusting of nose
  • Black to blue to pink pigmentary change of nose
  • Hypopigmentation, erosion, crusting of periocular skin and lips
20
Q

What is seen with erythema multiforme complex?

A
  • History =
  • Acute onset, non-pruritic, +/- systemic signs (pyrexia, lethargy, inappetence)
  • Trigger = virus, drug, vaccine, microbial infection, neoplasia, systemic disease, food (can be idiopathic)
  • Lesion morphology = pleomorphic
  • Primary lesion = annular erythematous macule (target lesions rare in animals)
  • Vesicles, bullae, wheals, ulceration, crusts
  • Distribution = Ventral abdomen > generalised, mucosae
21
Q

What is seen with uveodermatologic syndrome?

A
  • Signalment = young to middle aged, Akita predisposed
  • History = acute bilateral uveitis, non-pruritic
  • Lesion morphology = hypopigmented macules > patches, erythematous macules, erosions, ulcers, crusts
  • Distribution = face; nose, lips, periocular skin (occasionally footpads, scrotum, perineum)
22
Q

What can can immune mediated alopecia?

A
  • Sebaceous adenitis
  • Alopecia areata
  • Dermatomyositis
  • Ischaemic dermatopathy
  • Post-injection alopecia
23
Q

What can cause inflammatory alopecia?

A
  • Bacterial folliculitis
  • Demodicosis
  • Dermatophytosis
  • Leishmaniasis
  • Sebaceous adenitis
  • Alopecia areata
  • Dermatomyositis
  • Ischaemic dermatopathy
24
Q

What can cause non-inflammatory alopecia?

A
  • Endocrinopathies
  • Cyclical flank alopecia
  • Telogen/anagen defluxion
  • Paraneoplastic alopecia
  • Post-clipping alopecia
  • Congenital alopecias
  • Follicular dysplasias
  • Pattern alopecia
  • Colour dilution alopecia
  • Post-injection alopecia
25
Q

What is seen with sebaceous adenitis?

A
  • Signalment = standard poodle, Akita, vizsla
  • History = non-pruritic unless SBI
  • Lesion morphology = partial alopecia and poor coat quality, follicular casts and scale
  • Distribution = generalised
  • Cytology = no significant findings unless SBI
  • Histopath = pyogranulomatous inflammation targeting sebaceous glands > destruction of sebaceous glands and hair follicle atrophy
26
Q

What is seen with alopecia areata?

A
  • History = non pruritic, chronic onset
  • Lesion morphology = focal to multifocal, partial to complete patches of alopecia +/- erythema and hyperpigmentation
  • Distribution = head/face
  • Histopath = lymphocytic destruction of hair bulbs
27
Q

What is seen with dermatomyositis / ischaemic dermatopathy?

A
  • Signalment = young collies, SSD, PWD, Beauceron shepherd, Belgian shepherd
  • History = non-pruritic, chronic course +/- myositis
  • Lesion morphology = focal to multifocal alopecia, variable hyperpigmentation, hypopigmentation, scaling, erosion/ulceration & crusting
  • Distribution = face and extremities (dorsal digits, pinnae & tail tips, nails)
  • Histopath = chronic dermal & vascular inflammation > follicular atrophy +/- myositis (include muscle in biopsy)
28
Q

How would you manage IMSD?

A
  1. Removal/treatment of any external triggers =
    - Drugs
    - UV light = sunscreen
    - Confirmed (via blood work/imaging) internal disease including infections
    - Food = perform elimination diet for relapsing disease
  2. Control of inappropriate immune response =
    - Baseline haematology, biochemistry, urinalysis
    - Immunosuppressive/immunomodulatory drugs = topical for mild/localised disease, combination for severe / relapsing disease (generally more effective and better tolerated)
    - Sebaceous adenitits = also need to replace epidermal lipids
29
Q
A