Bit & Bridle

Equine Viral Hepatitis

Other Names

  • Equine hepatitis
  • Equine Parvovirus-Hepatitis (EqPV-H)
  • Theiler’s Disease (viral form)
  • Serum-associated hepatitis (when linked to biological products)

What is Equine Viral Hepatitis?

Equine viral hepatitis refers to acute viral-induced liver failure in horses. It is most commonly associated with equine parvovirus-hepatitis (EqPV-H), a recently characterised parvovirus identified as the primary causative agent in most cases of what has historically been called Theiler’s disease (serum hepatitis) and what was previously labelled “idiopathic acute hepatitis disease” (IAHD) in horses with no known exposure to equine-origin biologicals.

The condition is characterised by sudden, severe destruction of hepatic (liver) tissue, leading to fulminant hepatic failure. The liver, responsible for hundreds of metabolic processes including detoxification, protein synthesis, glucose regulation, bile production, and clotting factor manufacture, essentially collapses in function within a short period. The consequences — jaundice, hepatic encephalopathy, coagulopathy, and rapid deterioration — can be fatal within days.

Equine viral hepatitis is distinct from other hepatic conditions in horses such as chronic liver disease from ragwort toxicity or cholangiohepatitis, which tend to develop gradually. Viral hepatitis is an acute crisis. It is often considered alongside Theiler’s disease, to which it is closely related.

Causes

  • Equine parvovirus-hepatitis (EqPV-H): Identified in 2018, EqPV-H has been detected in the majority of carefully studied Theiler’s disease cases. The virus is present in equine plasma and tissues and is transmitted via equine-origin biological products (antitoxins, hyperimmune plasma). It may also spread through other routes — sexual contact and direct horse-to-horse transmission have been proposed.
  • Equine pegivirus (EPgV): Another recently identified virus found in horses with hepatitis, though its causal role is less clearly established than EqPV-H
  • Administration of equine-origin biologicals: Tetanus antitoxin and hyperimmune plasma — products made from equine serum — are the most strongly implicated vehicles of transmission, with clinical disease typically appearing 4–10 weeks after administration
  • Unknown triggers: A proportion of cases occur with no identifiable exposure, suggesting other routes of transmission or precipitating factors remain to be elucidated

Symptoms and Signs

Signs reflect acute, massive hepatic failure and can develop with alarming speed:

  • Jaundice (icterus): Yellow discolouration of the mucous membranes and sclera — often the first visible sign to owners. Jaundice in a horse is always serious and warrants immediate veterinary attention.
  • Hepatic encephalopathy: As hepatic function fails, ammonia and other toxins accumulate in the blood, causing profound neurological signs — head pressing, aimless circling, apparent blindness, aggression, disorientation, and eventually coma
  • Anorexia and profound depression
  • Photosensitisation: Skin lesions on unpigmented areas caused by circulating photodynamic compounds the liver can no longer process
  • Dark or discoloured urine
  • Colic-like discomfort
  • Coagulopathy: Excessive bleeding from minor wounds due to impaired clotting factor synthesis
  • Rapid deterioration: From apparent normality to recumbency, seizures, and death within 24–72 hours in the most severe cases

Diagnosis

Diagnosis requires a combination of clinical findings, laboratory evidence of hepatic failure, and — where available — viral testing:

  • Serum biochemistry: Markedly elevated GGT, ALP, AST, and serum bilirubin. Hypoglycaemia (low blood glucose) from impaired hepatic gluconeogenesis. Decreased albumin and total protein in subacute cases.
  • Clotting profile: Prolonged clotting times reflect impaired hepatic synthesis of clotting factors
  • Bile acids: Elevated serum bile acids confirm hepatic dysfunction rather than simple hepatocellular damage
  • PCR testing for EqPV-H: Whole blood or tissue samples can be tested for EqPV-H viral DNA, though this testing may not be widely available. Reference laboratories and university equine diagnostic facilities are the usual route.
  • Abdominal ultrasound: Hepatic parenchymal changes, abnormal echogenicity, and in some cases reduced liver size
  • Liver biopsy: Histopathology confirms coagulative or lytic necrosis characteristic of viral hepatitis. Biopsy is performed cautiously given the risk of haemorrhage in horses with coagulopathy.
  • History: A history of tetanus antitoxin or hyperimmune plasma administration 4–10 weeks prior is a strong clinical indicator

Treatment

There is no specific antiviral treatment. Management is entirely supportive and aims to maintain the horse while the liver attempts to regenerate:

  • Intravenous fluid therapy: Corrects dehydration, maintains blood glucose, and supports blood pressure
  • Glucose supplementation: Critical when hypoglycaemia is present — continuous glucose infusion may be required
  • Hepatic encephalopathy management:
    • Low-protein diet — reduces ammonia load from bacterial protein fermentation in the gut
    • Oral lactulose — promotes ammonia excretion via the faeces
    • Oral neomycin or metronidazole — reduces ammonia-producing gut bacteria
  • Vitamin supplementation: B vitamins, vitamin C, and vitamin E support hepatic recovery
  • Hepatoprotectants: SAMe (S-adenosyl methionine) and milk thistle (silymarin) are used empirically in many treatment protocols, with some biological plausibility though limited controlled evidence
  • Careful sedation: For horses with encephalopathy-associated danger to themselves or handlers — diazepam is preferred over acepromazine or alpha-2 agonists, which undergo significant hepatic metabolism
  • Plasma transfusion: Fresh frozen equine plasma provides albumin and clotting factors; used in horses with severe hypoproteinaemia or coagulopathy

Intensive nursing care, protection from self-injury during encephalopathic episodes, and close monitoring of blood glucose and electrolytes are central to management. Many horses require hospitalisation at an equine referral clinic.

Prevention

  • Vaccinate horses for tetanus using toxoid formulation — this eliminates the need for tetanus antitoxin, the most common vehicle of EqPV-H transmission
  • Avoid the use of equine-origin biological products unless strictly necessary
  • When tetanus antitoxin must be used (unvaccinated horse at immediate risk), inform the owner of the risk and monitor closely for 10 weeks
  • Screen blood donor horses for EqPV-H before collecting plasma for equine-origin biologicals — where testing is available
  • Practise good biosecurity when multiple horses share equipment, particularly needles and syringes

Prognosis

Prognosis is guarded to grave, particularly once hepatic encephalopathy is established. Published case series report mortality rates of 50–90% in symptomatic cases. Horses that survive the acute crisis and receive intensive supportive care can achieve hepatic regeneration, but this requires that sufficient viable liver tissue remains. Early identification — before severe encephalopathy develops — significantly improves the chance of survival. Horses that recover may have permanently reduced hepatic reserve, limiting their long-term athletic potential.

When to Call the Vet

  • Any horse showing jaundice (yellow gums, yellow sclera) — always a veterinary emergency
  • Neurological signs — head pressing, circling, apparent blindness, or unprovoked aggression in a horse that has been unwell
  • Any febrile horse that is dull, off feed, and has received equine-origin biological products within the past 10 weeks
  • A horse with suspected photosensitisation where liver involvement cannot be excluded

Frequently Asked Questions

Is equine viral hepatitis the same as Theiler’s disease?

They overlap significantly. Theiler’s disease is the clinical syndrome of acute hepatic failure in adult horses, often following exposure to equine-origin biological products. Equine parvovirus-hepatitis (EqPV-H) is now believed to be the causative agent in the majority of these cases. So equine viral hepatitis caused by EqPV-H is effectively the same condition as Theiler’s disease, though “viral hepatitis” can also refer to cases caused by other viruses or without a confirmed EqPV-H link. See our dedicated Theiler’s disease guide for a full breakdown.

How is EqPV-H transmitted between horses?

The primary known route is via equine-origin biological products made from pooled horse plasma (tetanus antitoxin, hyperimmune plasma). The virus is present in horse blood and is not killed by standard processing. Possible additional routes include direct horse-to-horse contact (particularly through blood-contaminated equipment), sexual transmission, and potentially via insect vectors, though these are less well established.

Can a horse be infected with EqPV-H without developing hepatitis?

Yes. Seroprevalence studies suggest that a significant proportion of horses have antibodies to EqPV-H, indicating prior infection without clinical disease. Not all infected horses develop acute hepatic failure — other factors such as the infecting dose, the horse’s immune status, and possibly co-infections may determine who develops clinical hepatitis.

How quickly should I act if my horse is jaundiced?

Immediately. Jaundice in a horse is never a normal finding and is always a sign of significant disease. In the context of viral hepatitis, the window between the appearance of jaundice and the development of life-threatening encephalopathy can be very short — hours to days. Do not wait to see if it improves. Contact your vet as soon as jaundice is noticed. See the BEVA emergency guidance for reference.