theiler's disease in horses

Theiler’s disease, or equine serum hepatitis, is an infrequent but sometimes life-threatening liver disease of adult horses. Sir Arnold Theiler first described the disease in the early 1900s as a form of highly fatal acute liver failure that occurred four to 12 weeks after administration of equine antiserum, which was used as part of a vaccination strategy for African horse sickness. Since then, many additional cases of serum hepatitis have been reported, and a variety of blood products of equine origin have been associated with the disease.

In North America, the majority of recent cases have been associated with the administration of tetanus antitoxin, although commercial plasma products also have been incriminated. The number of horses that become ill following administration of a specific lot of incriminated blood product is estimated at 1 to 2%, although more horses might have subclinical disease.

An infectious agent, such as a virus, has long been suspected to cause this condition, and a new equine parvovirus was recently discovered in a horse with a fatal case of serum hepatitis. The parvovirus was present in the diseased horse and in the biologic product that it had received nine weeks earlier. Inoculation of experimental horses with the commercial product resulted in transmission of this newly discovered virus and in liver disease. Variation in individual immune responses to the virus could explain the low percentage of clinically affected horses.

An identical disease, both in terms of clinical signs and pathologic findings, is sporadically seen in adult horses without recent administration of an equine origin biologic. These “nonbiologic” cases tend to mostly occur between June and November and can occur in small outbreaks that span a few weeks. Nonbiologic cases seem to occur most commonly on broodmare farms. The seasonal incidence of the nonbiologic cases suggests the possibility of insect transmission of parvovirus in these cases.

Clinically affected horses with Theiler’s disease frequently have both neurologic signs (hepatic encephalopathy with associated head pressing, stumbling, blindness, etc.) and jaundice (yellow gums and eyes). Once the neurologic signs are noted, there is a rapid progression to death in approximately 70% of the cases. Horses that receive supportive therapy and survive for five days after the onset of fulminant disease generally recover with no long-term effects.

Another recently discovered virus that causes liver disease in horses is nonprimate hepacivirus (NPHV), which is genetically the closest homolog of human hepatitis C virus discovered to date. Experimental horse infections consistently result in biochemical and histopathologic evidence of hepatitis, but the disease is mild and clinical signs are either absent or very mild in recently infected horses. Nonprimate hepacivirus and equine parvovirus are present in some healthy horses, indicating that horses can become healthy carriers of these viruses.

The USDA Center for Veterinary Biologics has issued a notice that all licensed equine blood products have to test free of equine parvovirus and NPHV. This should improve horse health by eliminating most of the blood product-associated cases of hepatitis. Nonbiologic associated cases will likely continue to occur until natural means of virus transmission are determined and necessary control methods implemented.

CONTACT: Thomas J. Divers, DVM, Dipl. ACVIM, ACVECC; Joy E. Tomlinson, DVM, Dipl. ACVIM; and Gerlinde R. Van de Walle, DVM, PhD—tjd1@cornell.edu—607/253-3100—Cornell University College of Veterinary Medicine, Ithaca, New York


This is an excerpt from Equine Disease Quarterly, funded by underwriters at Lloyd’s, London.