Liver abscess

Most affected cattle show no signs, and abscesses are usually discovered at slaughter. When signs occur they include intermittent fever, poor appetite, pain on palpation, and episodic drops in milk yield in dairy cows. Complications produce more dramatic pictures: peritonitis or sudden death if an abscess ruptures, and caudal vena caval thrombosis leading to lung abscesses, pneumonia, coughing up blood, nosebleeds and endocarditis. Pressure on the portal system can cause an enlarged liver, ascites and diarrhoea. Blood work may show neutrophilia, raised fibrinogen, globulins and acute-phase proteins, and ultrasonography helps, though abscesses on the left side of the liver may be missed.

In cattle, liver abscesses are mostly a sequel of ruminal acidosis. Rapid fermentation of dietary carbohydrate produces lactic acid that inflames and necroses the rumen wall. Fusobacterium necrophorum, a Gram-negative anaerobe that normally lives in the rumen and is more abundant on grain diets, colonises these lesions; bacterial emboli then enter the portal venous blood and lodge in the liver, forming abscesses. Trueperella pyogenes is often found alongside it, and streptococci, staphylococci and Bacteroides occasionally. Early abscesses are pale yellow and spherical, later becoming encapsulated; a liver typically holds several, a few centimetres across. Complications include caudal vena caval thrombosis, which sends emboli to the lungs.

Liver abscesses occur in cattle of all types but matter most economically in grain-finished feedlot cattle, and they are also seen in dairy cows. MSD cites an incidence of 12-32% in US slaughter cattle, and a 2016 US beef quality audit attributed nearly half of all liver condemnations to abscesses, affecting over 20% of fed cattle. High-concentrate rations, abrupt change from roughage to finishing diets and poor feed bunk management raise the risk. Losses come from condemned livers, carcass trimming and slower growth: severely affected feedlot cattle gain 5-15% less per day. Younger animals may show signs of navel vein infection.

MSD names traumatic reticuloperitonitis (hardware disease) as the condition to distinguish from abscesses caused by Fusobacterium necrophorum. Because most affected cattle show no signs, and those that do show only non-specific illness, abscesses are usually confirmed by ultrasonography or found at slaughter.

Liver, rumen wall, hepatic portal vein, caudal vena cava, lungs, heart valves (endocarditis), peritoneum, umbilical vein (calves)

Prevent ruminal acidosis: step up grain gradually, keep adequate roughage, feed several times daily, use dietary buffers. In-feed tylosin or virginiamycin where permitted; a F. necrophorum leukotoxoid vaccine reduces incidence.

Most abscesses resolve into sterile scars without treatment. Rupture, peritonitis or caudal vena caval thrombosis can be fatal. Draining abscesses in dairy cows carries a poor prognosis, so individual treatment is rarely attempted.