South African Equine Veterinary Association Congress 2015 Protea Hotel Stellenbosch
Do horses really get liver disease?
Schott HC*
Professor, Equine Internal Medicine
Department of Large Animal Clinical Sciences
D-202 Veterinary Medical Center
Michigan State University, East Lansing, MI 48824-1314
(517)-353-9710 [email protected]
Although relatively uncommon, a number of liver diseases occur in horses. Causes include
intoxication (most commonly from ingestion of toxic plants), altered metabolic function
(hypertriglyceridemia and hepatic lipidosis), and ascending infection (cholangiohepatitis with or
without cholelithiasis). Although recognized for over a century, serum hepatitis (Theiler‟s
disease) has recently been found to be associated with a viral infection. Presenting complaints for
liver disease are non-specific and often include lethargy, decreased appetite, and weight loss / ill
thrift. Detection of icterus on physical examination can provide an important clue although it is
important to remember that anorectic horses and those grazing pasture may also have moderate
yellowing to mucosal membranes. Additional signs may vary from photosensitization in areas of
non-pigmented skin to bizarre neurological deficits characteristic of hepatic encephalopathy.
Serum biochemical abnormalities, ultrasonographic imaging, and hepatic biopsy are useful in
further determining the cause of liver disease. Unfortunately, due to the large functional reserve of
hepatic tissue, nearly 80% of liver function must be lost before clinical disease becomes apparent.
Consequently, the prognosis for recovery from may be guarded to poor.
Clinical syndromes of hepatic disease:
Hepatotoxicity and photosensitization: Photosensitization syndromes are termed primary when
exogenous photodynamic agents are either ingested or administered to horses. The classic
example is ingestion of Hypericum perforatum (St. John‟s wort) that contains hypericin. Feeding
alfalfa hay has occasionally been associated with primary photosensitization but neither the
photodynamic agent nor the characteristics of the alfalfa (e.g., cutting, stage of maturation, etc.)
are well understood. Use of certain medications (e.g., phenothiazines, thiazides, potentiated
sulfonamides, tetracyclines, and others) can also cause primary photosensitization but these
reactions are uncommon and appear to be idiosyncratic in nature. Secondary photosensitization is
the more commonly recognized syndrome in horses that develops when phylloerythrin, a
photodynamic metabolite of chlorophyll, accumulates with liver disease. Although secondary
photosensitization can be a sign of any type of liver diseases, it is more commonly recognized
with ingestion of hepatotoxic plants. Detection of icterus during physical examination coupled
with finding elevated hepatic enzyme activities, particularly increased -glutamyl transferase
activity, on a serum chemistry profile allows diagnosis of hepatic disease as the primary problem.
A simple yet important clue that ingestion of a hepatotoxic plant by horses at pasture is the cause
of liver disease is detection of photosensitization and elevated hepatic enzyme activities in several
horses within a group. Regardless of the cause, treatment of photosensitization is supportive and
typically consists of topical wound care. Occasionally, systemic anti-inflammatory medications
and antimicrobial agents may be required. Prevention of further skin injury is accomplished by
limiting exposure to ultraviolet light by stabling horses during the day (affected horses can be
turned out at night) or applying sun block to non-pigmented skin.
Grazing pasture containing alsike and red clover is probably the most common cause of secondary
photosensitization of horses in North America. Pyrrolizidine alkaloid-induced hepatotoxicity by
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