Immune System & Allergies

Anaphylaxis is an acute, generalised allergic overreaction of the immune system (usually IgE-mediated) with massive histamine release. Within minutes it can threaten circulation and breathing and is a life-threatening emergency. Typical triggers are injections (medicines, vaccines, sera), insect stings or, more rarely, feed components.

Lymphangitis is a painful inflammation of the lymph vessels and surrounding tissue, usually in one hind leg, with marked swelling. Triggers are often bacterial infections via small skin lesions (e.g. with mud fever), more rarely non-infectious/immune-mediated processes. It runs acutely, is very painful and tends to recur.

Purpura haemorrhagica is an immune-mediated, necrotising inflammation of small blood vessels (type III hypersensitivity). It classically appears about two to four weeks after a strangles infection (Streptococcus equi) or, more rarely, after vaccination/other infections, when the immune system damages the vessel walls with cross-reacting complexes. Typical are extensive oedema and pinpoint mucosal bleeding.

In a true feed allergy, the immune system reacts to a feed component, usually with skin or digestive symptoms. In horses, however, it is rare and often overdiagnosed — many supposed allergies are non-immunological intolerances or have other causes. Proof is demanding and best achieved through a controlled elimination diet.

In photosensitisation, the skin overreacts to sunlight because light-active substances (photosensitisers) in the skin release UV energy and damage tissue. Mainly unpigmented, white skin areas are affected. A primary form (photosensitisers directly from plants) is distinguished from a secondary, liver-associated form, in which a damaged liver no longer sufficiently excretes a chlorophyll breakdown product (phylloerythrin).

Pemphigus foliaceus is the most common autoimmune skin disease of the horse. The immune system forms antibodies against connecting proteins of its own epidermal cells, so that skin layers detach and pustules, crusts and scales form. The changes often start on the head, legs or lower abdomen and can spread.

Hereditary, severe defect of the immune defence in the Arabian foal: through a mutation in the DNA-PKcs gene (PRKDC) functional B and T lymphocytes are not formed. SCID is inherited autosomal-recessive; affected foals are practically defenceless against infections after the maternal antibodies from the colostrum are used up. The disease is not curable, affected foals usually die in the first months of life.