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==Description==

==Description==

Hepatic abscessation occurs most commonly in cattle and is a common cause of economic losses due to carcass condemnation and reduced production efficiency. The disease is associated with a change from pasture to a high concentrate ration that predisposes to the development of rumenitis.  

Hepatic abscessation occurs most commonly in cattle and is associated with a roughage-deficient or high concentrate diet. The disease is a common cause of economic losses due to reduced production efficiency and carcass condemnation or trimming.  

==Pathogenesis==

==Pathogenesis==

The main causative agent of the disease is ''Fusobacterium necrophorum'', a gram-negative obligate anaerobe and a component of normal rumenal microflora. ''Arcanobacter pyogenes'' has also been implicated in the disease. Damage of the wall of the rumen secondary to rumenal acidosis leads to bacteraemia. Bacterial emboli from the inflamed rumen wall enter the hepatic portal system and are transmitted to the liver, leading to abscess formation.  

The main causative agent of hepatic abscessation is ''Fusobacterium necrophorum'', a gram-negative obligate anaerobe and a component of normal rumenal microflora. ''Arcanobacter pyogenes'', Staphylococci and Streptococci have also been associated with the disease. Damage of the wall of the rumen secondary to rumenal acidosis leads to embolisation of bacteria emboli from the inflamed rumen wall. The bacteria enter the hepatic portal system and are transmitted to the liver, leading to bacterial proliferation and abscess formation. Eventually the abscesses may heal via formation of a fibrous scar.

==Clinical Signs==

==Clinical Signs==

Clinical signs are a rare feature of the disease and abscesses are frequently only observed as incidental findings at slaughter or post mortem. Detailed clinical examination may reveal signs of pyrexia, depression and weight loss. Evidence of abdominal pain may be present such as bruxism, grunting when pressure is applied to the xiphisternum and abduction of the elbows. There may be a history of feeding of a high-concentrate ration, anorexia and reduced milk production.  

Clinical signs are a rare feature of the disease and abscesses are frequently only observed as incidental findings at slaughter or post mortem. Detailed clinical examination may reveal signs of pyrexia, depression and weight loss. Evidence of abdominal pain may be present such as bruxism, grunting and abduction of the elbows. There may be a history of change in diet from pasture to a high-concentrate ration, as well as anorexia and reduced milk production. Clinical signs of caudal vena cava thrombosis may be apparent if abscesses have involved the posterior vena cava, including chronic diarrhoea, emaciation, ascites and distension of subcutaneous abdominal veins.

Rupture of the abscesses is associated with anaphylactic shock and death.

 

Rupture of hepatic abscesses is associated with anaphylactic shock and death. In these cases, the lungs appear markedly oedematous and collapsed at post mortem.