Difference between revisions of "Hepatic Abscessation"
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| − | Hepatic abscessation occurs most commonly in cattle and is associated with a roughage-deficient or high concentrate diet | + | |
| + | ==Description== | ||
| + | Hepatic abscessation occurs most commonly in cattle and is associated with a roughage-deficient or high concentrate diet. The disease is an important cause of economic losses due to reduced production efficiency and carcass condemnation or trimming. | ||
==Pathogenesis== | ==Pathogenesis== | ||
| − | The main causative agent of hepatic abscessation is '' | + | 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 | + | 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 hepatic abscesses is associated with anaphylactic shock and death. In these cases, the lungs appear markedly oedematous and collapsed at post mortem. | Rupture of hepatic abscesses is associated with anaphylactic shock and death. In these cases, the lungs appear markedly oedematous and collapsed at post mortem. | ||
==Diagnosis== | ==Diagnosis== | ||
| − | Ultrasonographic examination of the liver is a valuable diagnostic tool for | + | Ultrasonographic examination of the liver is a valuable diagnostic tool for determing the location and size of the abscesses and for determining a prognosis. Serum biochemistry may reveal a neutrophilic leucocytosis and increased serum globulin and fibrinogen. Other laboratory changes frequently observed include increased GGT, SDH and bilirubin. Occasionally, radiographs may reveal displacement of the diaphragm if the liver abscess is large. |
==Treatment== | ==Treatment== | ||
| − | If hepatic abscesses have been diagnosed and located it is possible to consider antibiotic or surgical therapy. | + | If hepatic abscesses have been diagnosed and located it is possible to consider antibiotic or surgical therapy. Penicillin treatment may be successful in cows with smaller, hypoechoic abscesses but recurrence of disease is common unless treatment is given for 4 weeks or longer. Successful surgical treatment has been described but the prognosis is poor for animals with large, hyperechoic abscesses that have caused clinical signs. |
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==References== | ==References== | ||
*Divers, T. J., Peek, S. F. (2008) '''Rebhun's Diseases of Dairy Cattle''' ''Elsevier Health Sciences'' | *Divers, T. J., Peek, S. F. (2008) '''Rebhun's Diseases of Dairy Cattle''' ''Elsevier Health Sciences'' | ||
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Revision as of 20:51, 29 September 2010
{unfinished}}
Description
Hepatic abscessation occurs most commonly in cattle and is associated with a roughage-deficient or high concentrate diet. The disease is an important cause of economic losses due to reduced production efficiency and carcass condemnation or trimming.
Pathogenesis
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 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 hepatic abscesses is associated with anaphylactic shock and death. In these cases, the lungs appear markedly oedematous and collapsed at post mortem.
Diagnosis
Ultrasonographic examination of the liver is a valuable diagnostic tool for determing the location and size of the abscesses and for determining a prognosis. Serum biochemistry may reveal a neutrophilic leucocytosis and increased serum globulin and fibrinogen. Other laboratory changes frequently observed include increased GGT, SDH and bilirubin. Occasionally, radiographs may reveal displacement of the diaphragm if the liver abscess is large.
Treatment
If hepatic abscesses have been diagnosed and located it is possible to consider antibiotic or surgical therapy. Penicillin treatment may be successful in cows with smaller, hypoechoic abscesses but recurrence of disease is common unless treatment is given for 4 weeks or longer. Successful surgical treatment has been described but the prognosis is poor for animals with large, hyperechoic abscesses that have caused clinical signs.
References
- Divers, T. J., Peek, S. F. (2008) Rebhun's Diseases of Dairy Cattle Elsevier Health Sciences