Liver abscesses occur 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 decreased 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 caudal vena caval thrombosis.
Etiology and Pathogenesis of Liver Abscesses in Cattle
Fusobacterium necrophorum, a gram-negative, obligate anaerobic bacterium, and a component of normal rumen microflora, is the primary etiologic agent of liver abscesses in cattle. Infection in the liver usually originates from a necrobacillary rumenitis. Two biovars have been implicated. Biovar A (F necrophorum necrophorum), the more virulent of the two, 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; it 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, Streptococcus spp, Staphylococcus spp, and Bacteroides spp are the 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; however, the texture of the feed and method of feeding can be modifying factors. The incidence of rumenitis in feedlot cattle is appreciably 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 acidic rumen contents. 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.
Clinical Findings, Lesions, and Diagnosis of Liver Abscesses in Cattle
Incidental finding at slaughter
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 caudal rib cage on the right side. Grunting and other clinical signs of pain may occur with movement or when the animal lies down. An episodic drop in milk production occurs in dairy cattle. In younger animals, clinical signs of omphalophlebitis are commonly present. 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 the abscess is large, leukocytosis with neutrophilia and increased fibrinogen levels develops, and serum globulin concentrations may increase. Ultrasonography is an aid to diagnosis; however, abscesses in the left side of the liver may not be visualized.
Feedlot cattle with abscessed livers have decreased feed efficiency, and those with severely abscessed livers gain 5%–15% less per day than cattle without abscesses. Liver abscesses can represent sizable financial loss if the liver and surrounding tissues are condemned. Most liver abscesses are occult lesions that regress to a sterile scar, but sequelae can include peritonitis or sudden death after abscess rupture into the peritoneal cavity or hepatic blood vessels. Rupture into hepatic veins can also lead to thrombophlebitis of the caudal vena cava with thromboembolic disease, endocarditis, pulmonary thromboembolism, multiple pulmonary abscesses, and chronic suppurative pneumonia. Aneurysms of the pulmonary artery subsequent to pulmonary thromboembolism may rupture into airways, resulting in hemoptysis, epistaxis, and death. Caudal vena caval thrombosis may also lead to portal hypertension with a resulting syndrome of hepatomegaly, ascites, and diarrhea.
Ruminal lesions associated with liver abscesses are characterized by a marked inflammatory reaction and necrosis. Occasionally, abscesses are found in the deeper layers of the rumen wall. Hepatic necrobacillosis lesions lasting < 6 days 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 they may have up to 100.
The incidence of liver abscesses in slaughtered US beef cattle are reported to range from 12-32%.(1 References Liver abscesses are discrete circumscribed focal sites of bacterial infection within the liver parenchyma, generally due to bacterial translocation from the rumen through the portal circulation... read more ) Culture is seldom done to confirm the diagnosis. Occasionally, liver abscesses due to F necrophorum must be distinguished from those resulting from traumatic reticuloperitonitis Traumatic Reticuloperitonitis in Cattle Traumatic reticuloperitonitis of cattle occurs when animals ingest nails, pieces of wire, and other nonmetallic materials that injure the reticular wall. Sharp objects can puncture the reticulum... read more .
Treatment and Control of Liver Abscesses in Cattle
Administering oral antimicrobials in feed
Prevention of rumenitis: increasing dietary fiber and making more gradual feed changes
Tylosin phosphate administration (60–90 mg/head/day) markedly decreases the number of liver abscesses and increases feed efficiency and weight gain; however, it has little, if any, effect on the prevalence of ruminal lesions. Virginiamycin (85–240 mg/head/day during the finishing period) is also used; use of both tylosin and virginiamycin is specified by the Veterinary Feed Directive, and extralabel use is not permitted. With dairy cattle, percutaneous drainage and longterm treatment with procaine penicillin G (22,000 IU/kg, IM, every 12–24 hours) 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, decreases abscess incidence and severity.
The primary control is to manage ruminal acidosis through feeding method, 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 roughage to finishing ration is lengthened. Increasing the amount of roughage in the ration and shifting to multiple daily feedings increases the time of mastication and saliva flow, thereby increasing the buffer to the rumen and providing a continuous and uniform fermentation that decreases intraruminal acidity. The decreased acidity, in turn, lowers the number of ruminal lesions and, indirectly, the number of liver abscesses.
Nagaraja TG, Chengappa MM. Liver abscesses in feedlot cattle: a review. 1998;76(1):287–298.
For More Information
Satué K, Miguel-Pastor L, Chicharro D, Gardón JC. Hepatic enzyme profile in horses. Animals (Basel). 2022;12(7):861. doi: 10.3390/ani12070861. PMID: 35405850; PMCID: PMC8996839.