Difference between revisions of "Hepatic Abscessation"

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(Created page with '*with supportive hepatitis *especially common in cattle and sheep =====Causes===== *bacteria involved **''Fusobacterium necrophorum'' 80% + **''Arcanobacterium pyogenes'' **''Str…')
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==Introduction==
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*with supportive hepatitis
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Hepatic abscessation occurs most commonly in cattle and is associated with a roughage-deficient or high concentrate diet. Sudden change in diet to a high grain diet causes ruminal acidosis and rumenitis predisposing to hepatic abscessation. The disease is an important cause of economic losses due to reduced production efficiency and carcass condemnation or trimming.
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*especially common in cattle and sheep
 +
=====Causes=====
 +
*bacteria involved
 +
**''Fusobacterium necrophorum'' 80% +
 +
**''Arcanobacterium pyogenes''
 +
**''Streptococcus''
 +
**''Staphylococcus''
 +
**''Bacteroides''
 +
*spread from umbilicus in young animals
 +
**omphalophlebitis (navel ill)
 +
**usually mixed bacteria
 +
***''Actinomyces pyogenes''
 +
***''Staphylococci'' (predominates)
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*haematogenously from other pyaemic source
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**eg metritis or mastitis
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**bacteria invade ruminal wall and enter portal circulation to [[Liver - Anatomy & Physiology|liver]]
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*from rumenitis caused by overfeeding with grain
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**erosion of ruminal epithelium due to acidosis
  
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==Pathogenesis==
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=====Clinical Signs=====
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The main causative agent of hepatic abscessation is ''[[Fusobacterium necrophorum]]'', a gram-negative obligate anaerobe and a component of normal rumenal microflora. ''[[Arcanobacter pyogenes]]'', [[:Category:Staphylococcus species|Staphylococci]] and [[:Category:Streptococcus species|Streptococci]] have also been associated with the disease. Damage of the wall of the rumen secondary to rumenal acidosis leads to bacterial emboli from the inflamed rumenal 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.
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*subclinical
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*detected at exploratory laparotomy or sluaghter
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*weight loss (most important)
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*decreased weight gain or milk yields
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*sporadic fever and anorexia
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NB: animals can appear in good health as long as abscesses do not rupture
  
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==Clinical Signs==
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=====Gross=====
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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 including pyrexia, depression and weight loss. Evidence of abdominal pain may be present including signs 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.
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*large
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*pale greenish-yellow pus
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*thick fibrous capsule
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=====Sequelae=====
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*variable
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**resorption and healing
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**abscess may extend into the heaptic vein
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***give rise to thrombosis in the caudal vena cava
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***possible pulmonary abscesses
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***endocarditis
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**fibrous adhesion to adjacent viscera
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***if the abscess is near the surface
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**epistaxis, sudden death
  
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Rupture of hepatic abscesses is associated with anaphylactic shock and death. In these cases, the lungs appear markedly oedematous and collapsed at post mortem.
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NB: in many cases, abscesses are incidental findings at slaughter and result in condemnation of the affected [[Liver - Anatomy & Physiology|livers]] [[Category:Hepatitis, Bacterial]]
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==Diagnosis==
 
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Ultrasonographic examination of the liver is a valuable diagnostic tool for determining the location and size of the abscesses and 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.
 
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==Treatment==
 
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If hepatic abscesses have been diagnosed and located it is possible to consider antibiotic or surgical therapy. Systemically administered 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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==Prevention==
 
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The main aim of prevention of hepatic abscessation is to control rumenal acidosis by feeding a diet that is adequate in roughage. Multiple daily feedings may aid in increasing mastication and saliva production, increasing buffer to the rumen and reducing intrarumenal acidity.
 
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==Literature Search==
 
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[[File:CABI logo.jpg|left|90px]]
 
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Use these links to find recent scientific publications via CAB Abstracts (log in required unless accessing from a subscribing organisation).
 
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<br><br><br>
 
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[http://www.cabdirect.org/search.html?q=%28title%3A%28hepatic%29+OR+title%3A%28liver%29%29+AND+title%3A%28absces*%29&fq=sc%3A%22ve%22 Hepatic abscessation publications]
 
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==References==
 
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*Divers, T. J., Peek, S. F. (2008) '''Rebhun's Diseases of Dairy Cattle''' ''Elsevier Health Sciences''
 
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{{review}}
 
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[[Category:Liver Diseases - Cattle]][[Category:Liver - Inflammatory Pathology]]
 
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[[Category:Brian Aldridge reviewing]]
 

Revision as of 14:02, 7 June 2010

  • with supportive hepatitis
  • especially common in cattle and sheep
Causes
  • bacteria involved
    • Fusobacterium necrophorum 80% +
    • Arcanobacterium pyogenes
    • Streptococcus
    • Staphylococcus
    • Bacteroides
  • spread from umbilicus in young animals
    • omphalophlebitis (navel ill)
    • usually mixed bacteria
      • Actinomyces pyogenes
      • Staphylococci (predominates)
  • haematogenously from other pyaemic source
    • eg metritis or mastitis
    • bacteria invade ruminal wall and enter portal circulation to liver
  • from rumenitis caused by overfeeding with grain
    • erosion of ruminal epithelium due to acidosis
Clinical Signs
  • subclinical
  • detected at exploratory laparotomy or sluaghter
  • weight loss (most important)
  • decreased weight gain or milk yields
  • sporadic fever and anorexia

NB: animals can appear in good health as long as abscesses do not rupture

Gross
  • large
  • pale greenish-yellow pus
  • thick fibrous capsule
Sequelae
  • variable
    • resorption and healing
    • abscess may extend into the heaptic vein
      • give rise to thrombosis in the caudal vena cava
      • possible pulmonary abscesses
      • endocarditis
    • fibrous adhesion to adjacent viscera
      • if the abscess is near the surface
    • epistaxis, sudden death

NB: in many cases, abscesses are incidental findings at slaughter and result in condemnation of the affected livers

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