Difference between revisions of "Hepatic Abscessation"

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*with supportive hepatitis
+
{unfinished}}
*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 - Anatomy & Physiology|liver]]
 
*from rumenitis caused by overfeeding with grain
 
**erosion of ruminal epithelium due to acidosis
 
  
=====Clinical Signs=====
+
==Description==
*subclinical
+
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.
*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=====
+
==Pathogenesis==
*large
+
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.
*pale greenish-yellow pus
+
 
*thick fibrous capsule
+
==Clinical Signs==
=====Sequelae=====
+
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.
*variable
+
Rupture of the abscesses is associated with anaphylactic shock and death.
**resorption and healing
+
 
**abscess may extend into the heaptic vein
+
 
***give rise to thrombosis in the caudal vena cava
+
==References==
***possible pulmonary abscesses
+
*Divers, T. J., Peek, S. F. (2008) '''Rebhun's Diseases of Dairy Cattle''' ''Elsevier Health Sciences''
***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 [[Liver - Anatomy & Physiology|livers]] [[Category:Hepatitis, Bacterial]]
 
 
[[Category:To_Do_-_Clinical]]
 
[[Category:To_Do_-_Clinical]]

Revision as of 20:05, 29 September 2010

{unfinished}}

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.

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.

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


References

  • Divers, T. J., Peek, S. F. (2008) Rebhun's Diseases of Dairy Cattle Elsevier Health Sciences