Liver abscesses are seen in all ages and breeds of cattle wherever cattle are raised. They are most common in feedlot and dairy cattle fed rations that predispose to rumenitis. Cattle with liver abscesses have reduced production efficiency. Affected livers are condemned at slaughter, and adhesions to surrounding organs or the diaphragm may necessitate carcass trimming. Liver abscesses can also lead to disease syndromes associated with posterior vena caval thrombosis.
Fusobacterium necrophorum, a gram-negative, obligate anaerobic bacterium, and a component of normal rumen microflora, is the primary etiologic agent. Infection in the liver usually originates from a necrobacillary rumenitis. Two biovars have been implicated. Biovar A (F necrophorum necrophorum), the more virulent, is the predominant biovar in the rumen microflora and is isolated, usually in pure culture, from most cases of liver abscessation. Biovar B (F necrophorum funduliforme) is commonly isolated from microabscesses in the rumen wall but is less commonly isolated from liver abscesses, in which it is always found in mixed culture with biovar A or other bacterial species. Trueperella pyogenes, streptococci, staphylococci, and Bacteroides spp are most frequently recovered from mixed cultures.
Rumenitis is usually the result of rapid intraruminal fermentation of dietary carbohydrate with subsequent production of lactic acid and increased acidity of the ruminal fluid ("grain overload"). Rations with high levels of carbohydrate are the principal cause in both dairy and feedlot cattle, but the texture of the feed and method of feeding can be modifying factors. The incidence of rumenitis in feedlot cattle is significantly higher when the cattle are transferred directly from a roughage ration to a finishing ration, and when there is poor feed bunk management. F necrophorum, alone or with other bacteria, colonizes through the area of superficial necrosis produced by the acid rumen contents. Leukotoxin may facilitate resistance to phagocytosis. Bacterial emboli from the lesions invade the hepatic portal venous system and are transported to the liver, where they can establish infectious foci of necrobacillosis that eventually develop into abscesses.
Other sources of infection in liver abscesses include foreign body penetration from the reticulum, direct extension of infection from omphalophlebitis in neonatal calves, and bacteremic diseases.
Cattle with liver abscesses seldom exhibit clinical signs. Detailed clinical examination may show periodic fever, inappetence, and evidence of pain when pressure is applied to the xiphisternum and posterior rib cage on the right side. Grunting and other signs of pain may occur with movement or when the animal lies down. An episodic drop in milk production occurs in dairy cattle. Clinical signs of omphalophlebitis are commonly present when there is liver abscessation resulting from extension of omphalophlebitis. Acute-phase proteins are increased early in the course of the disease, and serum sialic acid concentrations have been used for antemortem diagnosis. When there are several abscesses or a large abscess, leukocytosis with neutrophilia and increased fibrinogen levels develop, and serum globulin concentrations may increase. Ultrasonography is an aid to diagnosis, but abscesses in the left side of the liver may not be visualized. Feedlot cattle with abscessed livers have reduced feed efficiency, and those with severely abscessed livers gain 5%–15% less per day than cattle without abscesses. Most liver abscesses are occult lesions that regress to a sterile scar. Untoward sequelae include peritonitis after abscess rupture into the peritoneal cavity, and sudden death from an anaphylactic or toxic reaction when there is rupture of an abscess into hepatic blood vessels. Rupture into hepatic veins can also lead to thrombophlebitis of the posterior vena cava with thromboembolic disease, endocarditis, pulmonary thromboembolism, multiple pulmonary abscesses, and chronic suppurative pneumonia. Aneurysms of the pulmonary artery consequent to pulmonary thromboembolism may rupture into airways to result in hemoptysis, epistaxis, and death. Caudal vena caval thrombosis may also lead to portal hypertension with a resulting syndrome of hepatomegaly, ascites, and diarrhea.
The ruminal lesions are characterized by a marked inflammatory reaction and necrosis. Occasionally, abscesses are found in the deeper layers of the rumen wall. Hepatic necrobacillosis lesions of <6 days duration are pale yellow and spherical with irregular outlines; they are characterized by coagulation necrosis of the hepatocytes with a surrounding intense zone of hyperemia and inflammation. Older abscesses have a core that is progressively encapsulated by fibrous connective tissue. Abscesses are usually 4–6 cm in diameter. Affected livers usually have 3–10 abscesses but may have up to 100.
Liver condemnation rates as high as 40% were recorded in a large survey of cattle slaughtered in the USA. Culture is seldom done to confirm the diagnosis. Occasionally, liver abscesses due to F necrophorum must be distinguished from those resulting from traumatic reticuloperitonitis (see Traumatic Reticuloperitonitis Traumatic Reticuloperitonitis Traumatic reticuloperitonitis develops as a consequence of perforation of the reticulum. It is important as a differential diagnosis of other diseases marked by stasis of the GI tract, because... read more ).
Tylosin phosphate fed at 10 g/ton of feed significantly reduces the number of liver abscesses and increases feed efficiency and weight gain but has little, if any, effect on prevalence of ruminal lesions. Virginiamycin fed at 16 g/ton of feed or chlortetracycline fed continually at 70 mg/head/day during the finishing period is also used. With dairy cattle, percutaneous drainage and longterm therapy with procaine penicillin G (22,000 IU/kg) can be attempted, but the prognosis is poor. A vaccine consisting of the leukotoxoid of F necrophorum combined with a bacterin of T pyogenes, given when cattle enter the feedlot, reduces abscess incidence and severity.
The primary control is by managing ruminal acidosis through the method of feeding, diet composition, diligent feed bunk management, and use of buffers in the diet. Fewer ruminal lesions develop when the ratio of concentrate to roughage is decreased and when the transition period from a roughage to a finishing ration is lengthened. Increased roughage in the ration and multiple daily feedings increase the time of mastication and saliva flow; this increases buffer to the rumen and provides a continuous and uniform fermentation that reduces intraruminal acidity, which in turn lowers the number of ruminal lesions and, indirectly, the number of liver abscesses.