[Princess Doreen]

From on-line Merck Vet Manual -

Cholangiohepatitis is a severe inflammation of the bile passages and adjacent liver, which sporadically causes hepatic failure in horses and ruminants. It is occasionally associated with cholelithiasis in horses.

Etiology:

Bacteremia due to an organism (eg, Salmonella ) eliminated in the bile, an ascending infection of the biliary tract after intestinal disturbance, or ileus are 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 cholangiohepatis in some animals. Gram-negative organisms, including Salmonella sp , Escherichia coli , Pseudomonas sp , and Actinobacillus equuli are frequently isolated from the liver. Clostridium sp , Pasteurella sp , and Streptococcus sp are less frequently recovered.

Clinical Findings:

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 hepatic encephalopathy are variable. SDH, AST, GGT, bilirubin, 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.

Lesions: 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.

Diagnosis:

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:

Treatment based on culture and sensitivity results from liver tissue often gives favorable results. Therapy should be continued for 4-6 wk or longer. Liver enzyme (GGT) levels and biopsies should be repeated to monitor response to therapy. If no organism is cultured, broad-spectrum antimicrobial therapy 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. Prognosis is good if fibrosis is not severe.