FRANK J. MILNE STATE-OF-THE-ART LECTURE


episode rather than being caused by primary hepatic disease. In 2005, Dr. Rachel Gardner reported41 on the surgical and postmortem examinations of horses with RDDLC that demonstrated how positioning of the colon in horses with RDDLC sometimes results in compression of the bile duct causing extrahepatic bile duct obstruction and a subsequent elevation in serum GGT activity and direct bilirubin. The use of GGT as a diagnostic test for RDDLC would result in many false negatives. However, the presence of high GGT activity in a horse with examination find- ings consistent with a colon displacement is support- ive of RDDLC, and in those circumstances was found to have a specificity of 98%. Horses not re- sponding to medical therapy and exhibiting contin- ual abdominal pain with examination findings suggestive of a RDDLC should not have surgery delayed because of elevations in serum GGT or bil- irubin concentration unless historic or ultrasono- graphic evidence are suggestive of a primary hepatic disease.41 Gastric outflow obstruction in suckling foals is


caused by duodenal and pyloric ulcer disease and commonly follows an episode of diarrhea 1–4 weeks earlier. CH can occur in these foals if the obstruc- tion is at or distal to the opening of the bile duct; this is reported to occur in 28% of cases.64 Surgical correction by gastrojejunostomy or gastroduodenos- tomy and often an additional jejunojejunostomy will resolve both intestinal and bile obstruction in most cases. Antimicrobial therapy is required in these cases because feed material and bacteria can be found in the bile duct. Initial reports suggested that having CH decreased prognosis in these cases but a recent report did not confirm that.64 If the obstruction is at the opening of the common bile duct, a hepaticojejunoscopy as first described by Orsini and Donawick42 will be needed in addition to the intestinal bypass surgery. Even with success- ful corrections of obstructions just distal to the hepa- topancreatic ampulla, continued bile reflux into the stomach may cause chronic gastric ulcers and less- than-favorable growth in some affected foals. It may be difficult to determine the extent of CH in the foals prior to surgery because GGT is often only mod- estly increased. With hepatic duct obstruction, GGT and direct bilirubin are more markedly elevated. Barium studies may show barium entering the biliary tree if the obstruction is distal to the opening. An additional and recently reported cause of cholangiohepatitis occurred in a suckling foal asso- ciated with Bartonella henselea infection of the liver.65 This 31


⁄2 -month-old foal was treated with minocycline and seemed to recover.


2. Infectious Causes of Nonobstructive Liver Disease and Failure


Tyzzer’s Disease There are several infectious diseases of foals that may result in liver failure, Tyzzer’s disease (Clos-


74 2015  Vol. 61  AAEP PROCEEDINGS


tridium piliforme) being the most reported and best described.66 Listeria monocytogenes has been re- ported as causing similar findings to Tyzzer’s dis- ease and, on very rare occasions, Actinobacillus spp., Equine herpesvirus-1, Streptococcus zooepidemicus, or Leptospira spp. may cause liver failure in young foals.36,67 All ofthesehaveaconcurrentbacteremia/ septicemia. In adult horses, other than previously discussed bacterial cholangitis, infectious causes of severe liver disease or failure include viral hepatitis and infectious necrotic hepatitis (Black disease or Clostridium noyvi).68 Tyzzer’s disease, a cause of acute and generally


fatal hepatitis and bacteremia in 5–36-day-old foals is caused by Clostridium piliforme. Clostridium pl- liforme is thought to be common in the environment but given that it is difficult to culture, little is known regarding the epidemiology and pathogenesis of the disease. Dr. Swerczek, at the University of Ken- tucky who first reported the disease in the United States in foals in 1973, has recently authored an excellent retrospective study on 148 cases of the disease.66 The average age of foals at death in that study was 20 days and there was not believed to be a breed or sex predisposition. Relative risk of dis- ease seems to be greater in the later months of the foaling season and one could speculate that, similar to Rhodococcus equi, shedding by both mares and healthy foals increase environmental contamination as the foaling season progresses. Foals normally consume freshly deposited feces from their dam from day2to3566 and the mare’s feces may serve as the source of infection for the foal.66 Affected foals are generally well fleshed at the time of illness, and an increase in protein and carbohydrate diets fed to the mare and foal has been suggested as possibly affect- ing the intestinal microbiome, permitting overgrowth of the C. piliforme bacteria and predisposing the foal to clinical disease.66 The disease is generally sporadic both on and between farms and of low overall inci- dence, likely less than 0.1% of foals per year. Mul- tiple cases have been reported on some farms and increased environmental contamination and bacte- rial colonization of the mares leading to increased fecal-oral transmission is possible.66 One of the more interesting Tyzzer’s case scenarios was de- scribed to me by Dr. Tennant: A draft mare with twins had one foal that died from confirmed Tyzzer’s disease after being admitted to the hospital and while the mare and other live foal were waiting to go home, the second foal developed fever and hepatitis and was treated successfully with antibiotics for suspected Tyzzer’s disease. Affected foals, espe- cially younger ones, are often found dead in the pasture without prior clinical signs being observed. Clinical signs are acute in onset and include signs of both septic shock and liver failure, including fever, weakness, tachycardia, icterus, recumbency, sei- zure, and coma. Laboratory findings are also sug- gestive of septic shock and liver failure, including leukopenia, toxic changes in neutrophils, hypoglyce-


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