Liver inflammation, known as hepatitis, presents a significant health concern for horses. The equine liver possesses a remarkable reserve capacity, meaning that signs of disease frequently remain hidden until the damage is extensive, making early detection difficult. This silent progression necessitates a thorough understanding of the factors that cause liver injury, the resulting clinical classifications, and the diagnostic tools available to veterinarians.
Understanding the Equine Liver and Hepatitis
The liver is the largest internal organ in the horse and performs numerous metabolic functions necessary for survival. Its primary roles include detoxifying the blood, metabolizing fats, carbohydrates, and proteins, and producing bile for digestion. Because the liver can continue to function even when 60% to 80% of its tissue is damaged, clinical signs typically indicate advanced disease.
Hepatitis is defined as inflammation of the liver parenchyma, the functional tissue of the organ. When inflammation leads to severe dysfunction, visible signs often appear. Jaundice (icterus) is a yellowing of the mucous membranes caused by the liver’s inability to process bilirubin. Advanced liver failure can lead to hepatic encephalopathy, causing neurological signs like lethargy, head pressing, or aimless wandering as toxins accumulate and affect the brain. Photosensitization, where unpigmented skin reacts severely to sunlight, is also a consequence of compromised liver function.
Diverse Etiology of Liver Inflammation
The factors that trigger liver inflammation are varied, ranging from ingested toxins to infectious pathogens. Plant-based toxins represent a frequent cause of chronic liver damage, particularly Pyrrolizidine alkaloids (PAs) found in weeds like Senecio (ragwort) or Crotalaria (rattlebox). These alkaloids are metabolized in the liver into toxic pyrroles that inhibit cell division, leading to the formation of abnormally large liver cells called megalocytes.
Toxicity from PAs is cumulative, often resulting in clinical disease months after the horse consumed the contaminated feed or pasture. Other toxic agents include mycotoxins, produced by fungi that can contaminate hay and grains, or exposure to heavy metals. Infectious causes include bacterial infections, such as ascending cholangiohepatitis, where inflammation moves up the bile ducts from the intestine.
Viral agents, such as Equine Herpesvirus and the recently identified Equine Hepacivirus (EqHV), can also cause liver disease. Metabolic disturbances can overwhelm the liver, notably hyperlipemia, a condition predominantly seen in ponies, miniature horses, and donkeys. In hyperlipemia, excessive fat mobilization leads to lipid accumulation in the liver, causing severe dysfunction.
Key Clinical Presentations and Classifications
The classification of equine hepatitis often depends on the clinical presentation or the underlying cause, leading to distinct disease syndromes. One severe and rapidly progressing form is Theiler’s Disease, now frequently associated with the viral agent Equine Parvovirus-Hepatitis (EqPV-H). This syndrome, sometimes called serum-associated hepatitis, historically followed the administration of equine-origin biological products, such as tetanus antitoxin or plasma.
Theiler’s Disease is characterized by fulminant hepatic necrosis, meaning a massive, sudden death of liver cells, typically occurring four to ten weeks after exposure. While EqPV-H is the likely cause, the virus can also spread horizontally, causing outbreaks in horses with no history of receiving biologics. Horses that survive the initial acute crisis may progress to Chronic Active Hepatitis, which involves persistent inflammation and progressive liver scarring (fibrosis).
Chronic Active Hepatitis is diagnosed based on the persistent presence of inflammation and damage seen on a liver biopsy over an extended period. This progressive scarring eventually compromises the liver’s structure and function. In many cases, however, a definitive cause cannot be identified despite extensive testing, leading to a classification known as Idiopathic Hepatitis. These cases require supportive care but remain a diagnostic puzzle.
Veterinary Methods for Accurate Diagnosis
Confirming liver damage and determining the underlying cause requires a combination of diagnostic techniques, beginning with a serum biochemistry panel. Measuring specific liver enzymes is instrumental in determining if hepatocellular injury or biliary obstruction is occurring. Enzymes like Sorbitol Dehydrogenase (SDH) and Glutamate Dehydrogenase (GLDH) indicate active hepatocellular necrosis, with SDH being specific for acute liver cell damage.
Gamma-Glutamyl Transferase (GGT) and Alkaline Phosphatase (ALP) elevate when there is damage to the bile ducts or cholestasis. In horses, GGT is a reliable indicator of liver disease, and persistently high levels suggest ongoing biliary involvement or chronic disease. Total Serum Bile Acids (SBA) are also measured; the liver typically clears over 90% of these acids from the blood, making an elevation an indicator of reduced liver clearance.
Veterinarians use abdominal ultrasound to visually inspect the liver, which can reveal changes in size, texture, or the presence of masses or abscesses. Ultrasound can also detect dilation or obstruction of the bile ducts, which indicates cholangiohepatitis or cholelithiasis (gallstones). While bloodwork and imaging suggest the presence and severity of the problem, the Liver Biopsy remains the definitive diagnostic tool.
A liver biopsy involves collecting a small tissue sample, often guided by ultrasound, for histopathological examination. Microscopic analysis confirms the presence of hepatitis and determines the chronicity of the disease process, distinguishing acute inflammation from advanced fibrosis. A biopsy can also identify specific cellular changes, like the megalocytes characteristic of Pyrrolizidine alkaloid toxicity, providing a precise etiological diagnosis.