Tyzzer Disease
Tyzzer disease is caused by Clostridium piliforme (previously Bacillus piliformis) and results in acute necrotizing hepatitis, myocarditis, and colitis in foals 8–42 days old. (Also see the Tyzzer Disease chapter.) It has been reported in two calves: a 1-week-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 in epithelium and smooth muscle cells of the ileum and cecum. Clinical signs included hypophagia, generalized weakness, depression, and decreased fecal passage. Tyzzer disease in foals is routinely fatal.
Cholangiohepatitis
Cholangiohepatitis is a severe inflammation of the bile passages and adjacent liver, which sporadically causes hepatic failure in horses and ruminants. It occurs secondary to duodenitis ("anterior enteritis"), intestinal obstruction, impending but not yet fulminant diarrhea, cholelithiasis, neoplasia, and parasitism in horses. The fungal toxin sporidesmin from Pithomyces chartarum may cause cholangiohepatitis in sheep and cattle.
Etiology of Cholangiohepatitis in Large Animals
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. Ascarid parasite migration through the liver may predispose some animals to cholangiohepatitis. 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.
Clinical Findings of Cholangiohepatitis in Large Animals
Depending on the severity of infection and virulence of the organism, clinical signs of cholangiohepatitis may be acute with severe toxemia, subacute, or chronic. Acute cholangiohepatitis may occasionally result in septicemia and death. Animals with subacute or chronic cholangiohepatitis show signs of weight loss, anorexia, intermittent or persistent fever, or colic. Icterus, photosensitivity, and clinical signs of hyperammonemic hepatic encephalopathy vary. SDH, AST, GGT, AP, conjugated bilirubin, and total bile acid concentrations are usually increased. Peripheral WBC counts vary depending on the extent of inflammation, endotoxemia, and chronicity.
Lesions
In acute cases of cholangiohepatitis, the liver is swollen, soft, and pale. Suppurative foci may be visible beneath the capsule or on a cut surface. Lesions in other systems may reflect septicemia and jaundice. Microscopically, neutrophils are present in the portal triads and degenerate parenchyma. Purulent exudate is evident in the ducts. In subacute or chronic cholangiohepatitis, bile duct proliferation is more pronounced. Areas of atrophy, regenerative hyperplasia, and periportal fibrosis may be evident.
Diagnosis of Cholangiohepatitis in Large Animals
Clinical signs of fever, icterus, colic, and eventual diarrhea
Increases in plasma biliary enzyme activities, followed chronologically by increases in hepatocellular enzyme activities
Ultrasonographic examination and biopsy of the liver
Liver biopsy can be performed to confirm the diagnosis, especially to obtain a liver sample for aerobic and anaerobic culture and sensitivity testing. Differential diagnoses include other causes of acute to chronic hepatic disease (eg, Theiler disease, pyrrolizidine alkaloid toxicosis), weight loss, colic, or sepsis. If neurologic signs are present, differentials for cerebral diseases must be considered. Because cholangiohepatitis is sometimes associated with cholelithiasis in horses, the presence of one or more calculi must be investigated; ultrasonographic evaluation of the liver may prove valuable in this case.
Treatment of Cholangiohepatitis in Large Animals
Appropriate antimicrobial treatment for several weeks
Pain management, nasogastric decompression, and fluid treatment adjunctively
Treatment based on culture and sensitivity results from liver tissue often gives favorable results. Treatment consists of longterm (4–6 weeks) antimicrobial administration, supportive care with intravenous fluids, and management of hepatic encephalopathy, if present. Initially, broad-spectrum antimicrobials should be administered. Trimethoprim-sulfa, enrofloxacin, or a combination of penicillin and an aminoglycoside may be used. Ampicillin or a cephalosporin can be used instead of penicillin. Ceftiofur sodium has an enterohepatic cycle and broader spectrum and may prove valuable in treatment. In addition to penicillins, metronidazole can be used in horses to treat anaerobic bacteria. Antimicrobial treatment should be altered pending results from culture of tissue obtained by liver biopsy. The prognosis is good if fibrosis is not severe, but poor if severe periportal or bridging fibrosis is present.
Equine Rhinopneumonitis
Equine rhinopneumonitis due to equine herpesvirus 1 is a sporadic cause of interstitial pneumonia, hepatic disease, and typically 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 in the chapter "Clostridial Diseases" for clinical findings, lesions, and control.
Bacillary Hemoglobinuria
Clostridium novyi type D (C haemolyticum) is the anaerobic organism that causes bacillary hemoglobinuria in cattle, other ruminants, and, rarely, horses. Clostridial spores are deposited in the liver after ingestion; if fluke damage to the liver occurs subsequently, the resultant necrosis creates an anaerobic environment and allows Clostridium to proliferate. See Bacillary Hemoglobinuria in the chapter "Clostridial Diseases" for clinical findings, diagnosis, and control.
Hepatic Abscesses
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, Trueperella pyogenes, or 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 (except foals suffering from Rhodococcus equi abdominal infections). 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, clinical signs of hepatic abscesses may be similar to those observed with other abdominal abscesses and include intermittent colic, intermittent fever, and weight loss. Often, liver abscesses are subclinical in cattle. Ultrasonographic evaluation of the liver may prove diagnostic. The prognosis is generally poor because of the lack of response to antimicrobial treatment or because of incomplete resolution. (Also see Liver Abscesses in Cattle.)
