ENI - Immunology Flashcards
Describe the processes behind bacterial pyoderma
- Staphylococcus intermedia most common
- Can be superficial (epidermis and hair follicles) or deep (dermis/deep dermis)
- Pus in skin
- Bacterial cause
- Pustules not always obvious
- Neutrophils lead to pyogenic efect
- Cytokines recruit neutrophils, engulf bacteria end up with chronic disease
Describe the lymph of the skin
- Afferent lymph deep to epidermis
- Gives rise to cells surveying tissue e.g. T lymphocytes and other dendritic cells
- Allows mobile populations of cells as well as static
Where are mast cells located?
At all points of interface with environment
Describe the actions of Langerhans cells
- Epidermis
- Phagocytose pathogens
- Act as exceptional APCs
- Precursors of dermal dendritic cells
- Migrate into dermis during maturation, become dermal dendritic cell
- Make was as APC to initiate and maintain immune responses
Describe macrophages of the dermis
- Phagocytose and kill pathogens
- Good APCs
What are the different types of hypersensitivity reactions?
- Type I: immediate, IgE
- Type II: IgG
- Type III: IgG/immune complex
- Type IV: T cell
Describe Type I hypersensitivity
- Immediate (30 mins)
- Mast cel degranulation
- IgE mediated
- IgE bound to receptors on mast cells and basophils (Fc Epsilon RI)
- Degranulation via antigen contact with antigen specific IgE on mast cell/basophil
- Leukocyte stimulation/migration
- Esp. eosinophils
Give examples of type I hypersensitivity
- Allergy
- Asthma
Describe type II hypersensitivity
- IgG mediated
- Antibody-dependent cell mediated cytotoxicity
- 5-10h
- Ab recognises self antigen on host cell or tissue
- Or recognises small molecule bound to cell or tissue
- Cell opsonised and phagocytosed by innate immune cells
- Or innate immune cells engage antibody produced cell toxins e.g. NK cell killing
Describe an example of type II hypersensitivity
- Pemphigus vulgaris
- Dogs and cats most common
- Phagocytes destroy epithelium = epidermal lesions
Describe type III hypersensitivity
- Immune complexes, soluble antigen, deposits on vessel wals (e.g. joints, kidney) = inflammatory reaction and destruction of tissue
- Complexes escape normal clearance
- Antigen solube, not attached to organ involved
- May be from exogenous source e.g pathogen
- Or endogenous
- Complexes deposit in tissue to allow receptors on mast cells to bind
Give an example of a localised Type III reaction
- Arthus reaction
- Vasculitis in skin e.g. to injected antigen
Describe tissue destruction in type II hypersentitivity
- Bound to tissue
- Mast cell binds to antigen
- Leads to degranulation
- Vasodilation
- Increased recruitment of neutrophils
- Leads to tissue destruction
- e.g. Discoid lupus (chronic skin condition)
Describe type IV hypersensitivity
- T cell mediated
- Delayed (24-72h)
- Dendritic and primed T cells
- T cells recruit and activate mononuclear cells e.g. monocytes and tissue macrophages
- Inflammation at site of DC/T cell interaction occurs not at draining lymph node
- Accumulation of T cells and bacteria
- Granuloma formation
Compare primary and secondary skin infection
- Primary: pathogen is direct cause
- Secondary: infection results from underlying disease e.g. allergic disease leading pruritus and thus skin damage through which infection can occur
Give examples of immune medaited skin diseases
- Flea allergy dermatitis (FAD) and Atopic dermatitis (AD)
- Pemphigus, discoid lupus-
Describe pemphigus
- Blistering autoimmune disease
- Auto-antibodies to desmoglein
- Antibodies unglue cells (acantholysis), leading to bliserting
- Treated with oral steroids
Describe discoid lupus erythematosus
- Mainly chronic skin condition
- Inflamed skin patches
- Scaling and crusty
- Lighter centre area
- Autoimmune disease - antibodies attacking healthy cells
How is type IV hypersensitivity used in TB testing?
- Single intradermal comparatice cervical tuberculin test
- If positive will react to injection of M bovis antigen as T cells already primed
- Measure skin thickness to establish granuloma formation
- Indicates previous infection
What are atopic dermatitis and flea allergic dermaititis examples of?
- Type I allergic reactions
- Immune mediated, with IgE hypersensitivity
Describe flea allergic dermatitis
- Pruritic condition of dogs and cats
- Most common skin disease
- Reaction to flea saliva peptides
- Produce histamines in response
- Erythema, papules, pustule, crusts
- Sensitised animals intermittently exposed to fleas have increased reaction
- Lessened reaction if constantly exposed
- Mainy Type I, many also show type IV
Describe type I hypersensitivity in FAD
- Mast cells and IgE in skin
- Migration of eosinophils into skin
- Basophils sensitive to allergens in flea saliva
Describe atopic dermatitis
- Pruritic skin disease
- Cause often undiagnosed
- IgE
- Atopy is genetic tendency to develop allergic disease
- WHWT and boston terries more susceptible
- Occurs when in contact with allergen e.g. house dust mite, capet fibres etc
- Th2 response: cytokines, eosinophils and mast cells etc in tissue
- Th1 cytokines in chronic lesions
- Tolerance associated with anti-inflammatory cytokines TGF-beta and IL-10 rather than switch from Th2 to Th1
Outline treatments for FAD and AD
- Anti-inflammatories
- Glucocorticoids often with antibiotics
- Removal of fleas in FAD
- Avoidance of possible allergens
Describe the structure of Gram +ve
- One cell membrane
- Thick cell wall
- Stain able to get stuck
Describe the structure of Gram -ve
- 2 cell membranes
- Thin cell wall
- Stain cannot get in
Describe the structure of acid fast bacteria and explain their stainign properties
- Mycolic acids in cell walls
- Peptidoglycan layer linked to arabinogalactan, furhter linked to high molecular weight mycolic acids
- Resist decolourisation by acid-alcohol, remain stained red colour of first stain in acid fast staining
Describe the structure of mycoplasma and explain their staining properties
- Do have cell membrane but no cell wall
- Hence do not stain Gram +ve
- No distinct structural morphology
Describe the microscopic appearance of Streptococci
- Long chains of cocci
- Gram +ve
- Acid fast
Describe the microscopic appearance of Staphylococci
- Bunches of cocci
- Gram +ve
Describe the microscopic appearance of Diplococci
- Join up as pairs
- Cocci
- Gram -ve
Describe the microscopic appearance of E. coli
- Rod shaped
- Can be motile with flagella
Describe the microscopic appearance of Malassezia
- Yeast appearance
- Snowmen
Describe the microscopic appearance of Actinomyces
- Rod shaped, but clump to appear hyphal
- Gram +ve
- Non-acid fast genera of Actinomycetes
Describe the microscopic appearance of filamentous fungi
Hyphae containing multiple nuclei
Describe the microscopic appearance of Clostridium
- Rod shaped
- Endospores bottle shaped
- Gram +ve
- Endospores stained by malachite green
List some causes of skin disease
- Parasitic
- Bacterial
- Viral
- Fungal
- Neoplastic
- Nutritional
- toxic
- Physical
- Congenital
- Combination of above
How does the keratin layer of skin protect against colonisation?
- Not live cells
- Dry, inhospitable
- pH poor for bacteria
- Shedding also sheds bacteria