Tyzzer's disease, due to Clostridium piliforme, causes an acute necrotizing hepatitis, myocarditis, and colitis in foals 8–42 days old. (See alsotyzzer's disease, see Tyzzer Disease.) If has been reported in 2 calves—a 1-wk-old Jersey bull calf with enteritis and multifocal necrotizing hepatitis and a second calf with concurrent cryptosporidiosis and coronaviral enteritis. In the latter animal, C piliforme was identified in hepatocytes and epithelium and smooth muscle cells of the ileum and cecum. Clinical signs included hypophagia, generalized weakness, dullness, and decreased fecal passage.
Cholangiohepatitis is a severe inflammation of the bile passages and adjacent liver, which sporadically causes hepatic failure in horses and ruminants. It occasionally occurs secondary to cholelithiasis, duodenitis, intestinal obstruction, neoplasia, parasitism, and certain toxins in horses. The fungal toxin sporidesmin from Pithomyces chartarum may cause cholangiohepatitis in sheep and cattle.
Bacteremia due to an organism (eg, Salmonella spp) eliminated in the bile, an ascending infection of the biliary tract after intestinal disturbance, or ileus is thought to be related to the development of cholangiohepatitis. In foals, duodenal ulceration and duodenitis may result in bile stasis, hepatic duct obstruction, and cholangiohepatitis. Parasite migration through the liver may predispose to cholangiohepatitis in some animals. Gram-negative organisms, including Salmonella spp, Escherichia coli, Pseudomonas spp, and Actinobacillus equuli are frequently isolated from the liver. Clostridium spp, Pasteurella spp, and Streptococcus spp are less frequently recovered.
Depending on the severity of infection and virulence of the organism, clinical signs may be acute with severe toxemia, subacute, or chronic. Most typically, cholangiohepatitis is a subacute or chronic disease process with affected animals showing signs of weight loss, anorexia, intermittent or persistent fever, or colic. Icterus, photosensitivity, and signs of hyperammonemic hepatic encephalopathy are variable. SDH, AST, GGT, conjugated bil-irubin, and total bile acid concentrations are usually increased. Peripheral WBC counts are variable, depending on the degree of inflammation and endotoxemia present. Acute, suppurative cholangiohepatitis may occasionally result in severe septicemia and death.
In acute cases, the liver is swollen, soft, and pale. Suppurative foci may be visible beneath the capsule or on cut surface. Lesions in other systems may reflect septicemia and jaundice. Microscopically in acute cases, neutrophils are present in the portal triads and degenerate parenchyma. Purulent exudate is evident in the ducts. In subacute or chronic cholangiohepatitis, the inflammation is more proliferative and bile duct proliferation more pronounced. Areas of atrophy, regenerative hyperplasia, and periportal fibrosis may be evident.
Liver biopsy should be performed to confirm the diagnosis and to obtain a liver sample for aerobic and anaerobic culture and sensitivity. Differential diagnoses include other causes of acute to chronic hepatic disease, weight loss, colic, or sepsis. If neurologic signs are present, cerebral diseases must be considered. Because cholangiohepatitis is frequently associated with cholelithiasis in horses, the presence of one or more calculi must be ruled out.
Treatment based on culture and sensitivity results from liver tissue often gives favorable results. Therapy consists of longterm (≥4–6 wk) antimicrobial administration, supportive therapy with IV fluids, and management of hepatoencephalopathy, if present. Initially, broad-spectrum antimicrobials effective against gram-negative, gram-positive, and anaerobic organisms should be administered. A combination of penicillin with either a trimethoprim-sulfa or an aminoglycoside or enrofloxacin may be used. Ampicillin or a cephalosporin can be used instead of penicillin. Metronidazole can be used in horses to treat anaerobic bacteria. Antimicrobial therapy can be altered pending results of culture of tissue obtained by liver biopsy. Prognosis is good if fibrosis is not severe, but it is poor if severe periportal or bridging fibrosis is present.
Equine rhinopneumonitis due to equine herpesvirus 1 is a sporadic cause of interstitial pneumonia, hepatic disease, and often death in newborn foals. see Acute Bronchointerstitial Pneumonia in Foals for clinical findings, diagnosis, and treatment.
Infectious Necrotic Hepatitis
Infectious necrotic hepatitis, caused by Clostridium novyi type B, affects primarily sheep but also cattle, horses, and pigs. see Infectious Necrotic Hepatitis for clinical findings, lesions, and control.
(Red water disease, Icterohemoglobinuria)
Clostridium novyi type D (C haemolyticum) is the anaerobic organism that causes bacillary hemoglobinuria in cattle, other ruminants, and rarely horses. see Bacillary Hemoglobinuria for clinical findings, diagnosis, and control.
Hepatic abscesses are generally polymicrobial infections; anaerobes are common. The primary etiologic agent of liver abscesses in cattle is Fusobacterium necrophorum. In goats, most abscesses are due to Corynebacterium pseudotuberculosis, Arcanobacterium pyogenes, and Escherichia coli. Organisms less frequently isolated include Proteus sp, Mannheimia haemolytica, Staphylococcus epidermidis, S aureus, Rhodococcus equi, Erysipelothrix rhusiopathiae, and the yeast Candida krusei. In horses, hepatic abscesses often contain Streptococcus spp (S equi equi, S equi zooepidemicus), C pseudotuberculosis, or enterobacteria after ascending cholangiohepatitis or intestinal disease, and anaerobes. In pigs, hepatic abscesses develop after migration of ascarids into the bile ducts.
The liver is particularly susceptible to abscess formation because it receives blood from the hepatic artery, the portal system, and the umbilical vein in the fetus and the newborn. Hepatic abscesses are most prevalent in ruminants and uncommon in horses. Abscesses are associated with rumenitis (rumenitis-liver abscess complex), bacteremia, septic portal vein thrombosis, and parasite migration or extension from intestinal disease. They can also occur as sequelae of abdominal surgery. In neonates and young animals, abscesses may develop secondary to ascarid migration, bacterial septicemia, or ascending infection of the umbilical vein. In horses and cattle, signs may be similar to those seen with other abdominal abscesses and include intermittent colic, intermittent fever, and weight loss. Often, liver abscesses are subclinical in cattle. Prognosis is generally poor because of lack of response to antimicrobial therapy or incomplete resolution. (See alsoliver abscesses in cattle, see Liver Abscesses in Cattle.)
Last full review/revision March 2012 by Susan D. Semrad, VMD, PhD, DACVIM; Clive C. Gay, DVM, MVSc, DVSc (Hons), FACVSc, DACIM (Hons)