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What is type III hypersensitivity mediated by?
IgG antibodies
What is the pathogenesis of type III hypersensitivity?
Soluble antigens + antibody complexes form in tissues or in circulation
Where do the antigen-antibody complexes get dumped in type III hypersensitivity?
They get deposited in renal glomerulus (most common), dermal arteirole’s, joints and small blood vessels in other sites
More detailed pathogenesis of type III hypersensitivity
Complement activation, C5a and C3a, vasodilation, recruitment of neutrophils, inflammation and tissue damage
Briefly explain localized type III hypersensitivity is the tissues
Antibody excess - high concentration of antigen-specific IgG at re-exposure
What are examples where type III can occur at the site of skin?
Subcutaneous allergen immunotherapy, vaccination
What are examples where type III can occur at the site of the lungs?
Hypersensitivity pneumonitis, fungal spores from moldy hay, cattle, horses (recurrent airway obstruction), people (Farmer’s lung)
What are examples where type III can occur at the site of the eye?
Uveitis (canine adenovirus-1)
Briefly describe systemic type III hypersensitivity
Antigen excess leads to high concentration of antigen at re-exposure
Where is the high concentration of systemic type III coming from?
Circulating immune complexes coming from persistent antigen exposure at chronic infection and autoimmune diseases, delayed clearance of immune complexes
What determines clinical signs of systemic type III hypersensitivity?
location (size of immune complexes, charge and glycosylation, blood flow, predilection sites (glomeruli, joints, skin)).
In what species does purpura hemorrhagic occur?
Horses
What are clinical signs of purpura hemorrhagica, and where does it stem from?
Some clinical signs include subcutaneous edema and mucosal hemorrhages, and it stems from streptococcus equi infection. It can also lead to thrombosis and infarcts in mutliple organs
What is the treatment for purpura hemorrhagica?
Corticosteroids