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→Clinical signs
==Clinical signs==
==Clinical signs==
Clinical outcome depends on susceptibility of pigs and virulence of strain. Pigs are susceptible after maternal antibody waned (after 3 months) and before protective immunity acquired (3 years).
Clinical outcome depends on susceptibility of pigs and virulence of the strain. Pigs are susceptible after maternal antibody has waned (after 3 months) and before protective immunity acquired (3 years).
Changes in diet, extremes of temperature and fatigue are thought to predispose to infection
Changes in diet, extremes of temperature and fatigue are thought to predispose to infection.
3 forms of disease occur:
3 forms of disease occur:
*Hyperacute
*Hyperacute
Acute:
Acute:
Anorexia and pyrexia are the two most common clinical signs of the acute form in young pigs. Affected animals still die but normally afte day in which time they become dyspnoic.
Anorexia and pyrexia are the two most common clinical signs of the acute form in young pigs. Affected animals still die but normally after a day during which time they become dyspnoic.
Older pigs tend to show pyrexia, anorexia and polydypsia.
Older pigs tend to be pyrexic, anorexic and polydypsic.
Pigs show, pink/purple raised areas or extensive diamond-shaped plaques over skin within 24-48 hours of developing clinical signs. If pregnant sows are infcted at this time they may abort.
Pigs show, pink/purple raised areas or extensive diamond-shaped plaques over the skin within 24-48 hours of developing clinical signs. If pregnant sows are infected at this time they may abort.
Chronic:
Chronic:
Affected animals can completely recover, lesions may resolve within a week, or become necrotic and slough. Ear tips may also be lost.
Affected animals can completely recover, lesions may resolve within a week, or become necrotic and slough. Ear tips may also be lost.
The bacteria localises in joints causing destruction of the synovial membrane lining, hyperaemia, villus formation and lymphocyte and plasma cell infiltration resulting in '''chronic serofibrinous polyarthritis.
The bacteria localises in joints causing destruction of the synovial membrane lining, hyperaemia, villus formation and lymphocyte and plasma cell infiltration resulting in '''chronic serofibrinous polyarthritis.
Initially joints are hot and swollen leading to stiffness, lameness, and non-weight bearing on affected limbs.
Initially joints are hot and swollen leading to stiffness, lameness, non-weight bearing on affected limbs and eventual ankylosis.
Discospondylitis can also occur.
Discospondylitis can also occur.
Additionally valvular lesions may develop in the heart causing chronic valvular endocarditis, vegetatic thrombosis of mitral valves and asymptomatic or congestive heart failure sometimes resulting in sudden death following stress.
Additionally valvular lesions may develop in the heart causing chronic valvular [[Endocarditis| endocarditis]], vegetative thrombosis of mitral valves and asymptomatic or congestive heart failure sometimes resulting in sudden death following stress.
==Pathology==
==Pathology==