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ENI > Immune response of the skin > Flashcards

Immune response of the skin Flashcards

1
Q

What are the two types of skin disease?

A

Primary: when the pathogen is the direct cause of symptoms/disease
Secondary: when infection results from underlying disease

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2
Q

What bacteria most commonly causes bacterial pyoderma?

A

Most commonly caused by staphylococcus intermedius

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3
Q

What are the two subclassificationsof bacterial pyoderma?

A

The pyoderma may be deemed superficial (affects epidermis and hair follicles) which is the most common or deep (which affects the dermis and deep tissue)

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4
Q

Describe the immune response to bacteria in the skin

A

Bacteria induce Il-6 and IL-8 production from keratinocytes, this cause neutrophils to migrate in following the IL-8/6 the bacteria are then phagocytosed.

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5
Q

Langerhans cells live in the epidermis, what is their main role?
Macrophages live in the dermis, what is their main role?

A

LH- phagocytosis and exceptional APC

M: kills and phagocytoses pathogens, quite good at APC

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6
Q

What is flea allergy dermatitis (FAD)?

A

An immune mediated disease that causes an itchy skin condition of dogs caused by reaction to the chemicals in flea saliva

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7
Q

In the coombs and Gel classification what is type I hypersensitivity?

A

Aka IgE mediated hypersensitivity

Occurs within 30 mins

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8
Q

How does type I hypersensitivity arise?

A

Low levels of IgE in serum as most of the IgE is bound to high affinity receptors (Called Fc Epsilon RI) found on mast cells and basophils
Degranulation of mast cells via antigen contact with antigen specific IgE bound to that mast cell/basophil
This causes leukocyte stimulation/migration, particularly eosinophils which degranulate in tissue causing inflammation.

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9
Q

What is Coombs and Gel type II hypersensitivity?

A

Aka Antibody dependant cell mediated cytotoxicity

Occurs within 5-10 hours

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10
Q

How does type II hypersensitivity arise?

A

The antibody recognises self-antigen on host cells/tissue or a small molecule attached to the cell/tissue which cases the cell to be opsonised and phagocytosed by the innate immune cells or the cells that engage the antibody produce cell toxins
For example Pemphigus Vulgaris (detected by an immunofluorescence test)

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11
Q

What is Coombs and Gel type III hypersensitivity?

A

When immune complexes, soluble antigen or deposits on vessel walls cause an inflammatory response
Maximum reaction at 4-8h

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12
Q

How does type III hypersensitivity arise?

A

Small amounts of antibody/antigens which escape the normal route of clearance
Because the antigen (can be exogenous i.e. pathogenic or endogenous i.e. Self) is soluble so can disperse and affect many different body systems
Example: Arthus reaction (vasculitis on the skin due to an injected antigen) or discoid lupus

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13
Q

What is Coombs and Gel type IV hypersensitivity?

A

AKA delayed type hypersensitivity reaction- DTH

Occurs within 24-72h

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14
Q

How does type IV hypersensitivity arise?

A

T cells recruit and activate mononuclear cells (eg. Monocytes and tissue macrophages (dendritic cells))
Inflammation at the site of DC/T cell interaction occurs rather than in the draining lymph node
There are three subtypes of type IV hypersensitivity

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15
Q

What are the three subtypes of type IV hypersensitivity? What are their reaction times and appearance?

A

Contact: 48-72h Eczema
Tuberculin: 48-72h Local induration (fibrous mass)
Granuloma: 21-28 days Hardening

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16
Q

What is the histology of the three subtypes of type IV hyersensitivity?

A

Contact: Lymphocytes followed by macrophages, oedema of epidermis and the antigen site is epidermal

Tuberculin: Lymphocytes, monocytes, macrophages and the antigen site is intradermal eg. tuberculin injection

Granuloma: Macrophages, epithelioid and giant cells, fibrosis and it surrounds a persistant antigen or foreign body

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17
Q

Describe the process of tuberculin testing

A

Cows are tested by a single intradermal comparative cervical tuberculin test (SICCT test)
Animals positive for mycobacterium bovis will react to intradermal injection of mycobacterium bovis antigen within around 3 days, this occurs because T cells have already been primed by the previous exposure to the antigen
M. Avium can also give a positive test so both antigens are injected at different sites and a comparison is made with M. Avium acting as a control
The injection sites are clipped (about 2cm radius) in the middle third of the neck separated by about 1.3cm. the skin is folded and the thickness measured with callipers. The animal is then injected (avian in the higher site). In 72 hours the thickness is then re-recorded.

18
Q

What breeds of dog have a genetic tendancy to develop allergic disease eg. atopic dermatitis?

A

west highland and Boston terriers

19
Q

What is the most common flea species?

A

Ctenocephalides felis

20
Q

Describe the immune response/hypersensitivity in FAD

A

Type I: causes increased mast cells and IgE i and also causes migration of eosinophils into the skin
Basophils are also sensitive to allergens in flea saliva (flease feed on blood allowing contact to basophils)
Type IV: many animals also show this type of HS so allergen exposure tests are measured after
20mins and 2-3 days too

21
Q

What is the treatment for hypersensitivity?

A

Allergen desensitisation
Anti-inflammatories
Glucocorticoids
Removal of the allergen from the environment

22
Q

What are the dermal responses to damage?

A

Erythema
Oedema
Thickening
Alopecia

23
Q

What is Erythema?

A

Damage causes release of pro-inflammatory mediators (e.g. histamine) which cause vasodilation of the dermal vessels which appears as erythema.
It is very common in infectious and allergic processes and occasionally neoplastic processes.

24
Q

What is Oedema?

A

Mediated by histamine and other cytokines which case increased vascular permeability and increase leakage of urticarial lesions.
It will pit on pressure and appears classically with type one hypersensitivity but can occur for other reasons

25
Q

What causes Thickening of the skin?

A

Associated with longer standing allergic reactions (due to the cellular infiltrate) and chronic inflammatory conditions (due to increased collagen or other connective tissue)
It can sometimes appear as nodular so may need to differentiate with a FNA

26
Q

What is Alopecia?

A

Can be partial or complete and is caused by either a failure of hair to grow properly which can be caused by endcrinopathy or hair follicle dysplasia or a damage to the hair follicles or shafts which is associated with follicular infection, trauma, parasites, neoplasia, nutrition and auto-immune disease.

27
Q

What are the epidermal responses to damage?

A 
Hyperkeratosis 
Follicular hyperkeratosis 
Acanthosis 
Lichenification 
Vesicles and pustules
Hyper/hypopigmentation
Crusting
28
Q

What is Hyperkeratosis?

A

Is an increased depth of the cornified layer and is recognised by:
Scaling, which indicates abnormality of keratinisation also known as seborrhoea. Scaling can either by greasy (oleosa) or dry (sicca) and is either primary (usually inherited) or secondary.
Scaling can lead to crusting which is a form of dried exudate which is always secondary.

29
Q

What does scaling indicate?

A

Scaling is a non-specific sign of increased turnover of the epidermis or an imbalance between turnover and desquamation, it is a feature of many different skin diseases

30
Q

What is Follicular hyperkeratosis ?

A

Keratinaceous plugs in the hair follicle infundibula are called Comedones and are common in demodicosis and endcrinopathy.
They sometimes appear as a keratinaceous collar around the emerging hair and these are called follicular casts, this is a specific feature of idiopathic sebaceous adenitis

31
Q

What is Acanthosis?

A

Is an increase in the depth of the epidermis
Repeated blunt grade trauma cause a release of cytokines from keratinocytes which causes increased division of basal and epidermal cells

32
Q

What cytokines stimulate epidermal growth and where do they come from?

A

From keratinocytes
PDGF: Activates dermal fibroblasts, neutrophils and macrophages
TGF-Alpha: stimulates keratinocyte and fibroblast division

From Fibroblasts:
TGF-Beta
FGF
KGF
IGF-1: all stimulate epidermal and basal cell division

From platelets and macrophages:
EGF:stimulate epidermal and basal cell division

33
Q

What is Lichenification?

A

Thickening and hardening of the skin characterised by exaggeration of the superficial skin markings, non specific finding of many diseases with chronic inflammation or friction

34
Q

What are vesicles?

A

Vesicles are filled with a clear fluid (like a blister), they are short lived as the epidermis of domestic animals is thin and fragile

35
Q

What follows vesicles?

A

The following stage of an erosion is seen (basal layer of epidermis breached) or an ulcer (dermis exposed)

36
Q

What causes vesicles and erosions?

A

They usually occur due to viruses (e.g. Foot and mouth, feline orthopox virus and orf) or autoimmune diseases due to autoantibodies attacking the inter-cellular proteins and causing separation of keratinocytes

37
Q

What are pustules?

A

Are small circumscribed elevations of the epidermis that is filled with pus

38
Q

What causes pustules?

A

Usually associated with infection eg. bacterial pyoderma although sometime can be seen with sterile autoimmune diseases

39
Q

What causes hyper and hypopigmentation?

A

Melanocytes in the basal layer of the dermis provide pigmentation, but also havea role in local modulation of cutaneous inflammation

Hyperpigmentation is non-specific but commonly post inflammatory, associated with some endocrine disorders
Hypopigmentation is a feature of diseases that affect the basal epidermis and dermo-epidermal junction, so often either autoimmune or neoplasia but can be seen post-inflammatory

40
Q

What is crusting?

A

Formed when dried exudate, serum, pus, blood, cells and scale adhere to the skins surface

41
Q

What causes crusting?

A

Caused by exudative and ulcerative diseases: can be caused by physical damage, infections, autoimmune and ulcerating neoplasms

ENI (33 decks)

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