Serum Hepatitis / Theiler's Disease

Serum hepatitis, commonly known as Theiler's disease, is a devastating form of acute hepatic necrosis in horses characterized by rapid onset, severe liver failure, and high mortality rates. First described by Sir Arnold Theiler in 1918 following administration of equine-origin antiserum, this condition has since been associated with various equine biological products including plasma, serum, tetanus antitoxin, pregnant mare serum gonadotropin, and certain vaccines produced using equine tissue culture. The hallmark of Theiler's disease is massive hepatocellular necrosis that develops four to ten weeks after exposure to the inciting product, though cases without identifiable exposure also occur.

Theiler's disease can affect horses of any age, breed, or sex, though adult horses appear more commonly affected than foals. The condition occurs worldwide wherever equine biological products are used. Incidence varies considerably, with reported rates following biological product administration ranging from less than one percent to over four percent depending on the product and population studied. The apparently random occurrence among horses receiving identical products suggests that host factors, including immune response characteristics and possibly pre-existing subclinical liver disease, influence disease development.

The impact of Theiler's disease on affected horses is severe and often fatal. The acute onset and rapid progression give little time for treatment to be effective. Horses may appear normal one day and develop fulminant hepatic failure over subsequent days. Mortality rates historically ranged from fifty to ninety percent, though improved intensive care has modestly improved survival in recent years. Survivors may recover completely or retain permanent liver damage affecting long-term health and performance. The unpredictable nature of the disease creates challenges for risk assessment when equine biological products are medically indicated.

Understanding Theiler's disease is important for all horse owners and veterinarians because equine biological products, particularly plasma and tetanus antitoxin, are commonly used in equine medicine. Risk-benefit analysis should accompany decisions to administer these products, and owners should be informed about the possibility of Theiler's disease. Early recognition of clinical signs and prompt intensive care offer the best chance for survival. Research continues into the causative agent and potential preventive measures, though definitive answers remain elusive. Maintaining awareness of this condition and monitoring horses following biological product administration enables early intervention when disease develops.

The primary association of Theiler's disease is with administration of equine-origin biological products, though the exact causative mechanism remains incompletely understood despite over a century of investigation. Products implicated include tetanus antitoxin, hyperimmune plasma and serum, pregnant mare serum gonadotropin, botulism antitoxin, and various vaccines produced using equine cell cultures or containing equine serum. The common factor appears to be exposure to equine blood products or tissues from horses other than the recipient. Notably, autologous products (derived from the same horse) have not been associated with disease development.

Recent research has identified equine-origin pegivirus and equine parvovirus-hepatitis as potential causative or contributing agents. Theiler's disease-associated virus (TDAV), an equine parvovirus, has been detected in affected horses and in contaminated biological products. However, the relationship is complex—not all exposed horses develop disease, and some horses with Theiler's disease test negative for known viral candidates. Current understanding suggests that viral infection transmitted through biological products triggers disease in susceptible individuals, possibly through direct hepatocyte damage or immune-mediated mechanisms. Co-infection with multiple agents may increase disease severity.

The pathophysiology involves massive hepatocellular necrosis occurring four to ten weeks after exposure, suggesting an incubation period during which the causative agent replicates or triggers immune responses. The delay between exposure and clinical disease complicates diagnosis, as owners and veterinarians may not connect current illness to product administration weeks earlier. Histopathologically, affected livers show centrilobular to massive hepatocyte necrosis with minimal inflammatory infiltrate, distinguishing Theiler's disease from more inflammatory hepatic conditions. The severity of necrosis determines clinical outcome—horses with massive involvement die rapidly, while those with less extensive damage may survive.

Risk factors for developing Theiler's disease following exposure to equine biological products remain poorly defined. Individual variation in immune response likely plays a role, as only a small percentage of exposed horses develop clinical disease. Pre-existing subclinical liver disease may predispose to clinical manifestation. Some evidence suggests that horses receiving larger volumes of biological products or products from single donors rather than pooled sources may face elevated risk, though this is not consistent across studies. Geographic and temporal clustering of cases suggests batch-specific contamination of biological products. Concurrent illness or stress at the time of product administration might influence susceptibility.

Importantly, Theiler's disease can occur without identifiable exposure to equine biological products. These idiopathic cases present identically to product-associated cases and likely share common etiology, suggesting that exposure to causative agents can occur through routes other than intentional product administration. Possible alternative transmission routes include blood-contaminated equipment, biting insects, and direct horse-to-horse contact, though these remain speculative. The existence of idiopathic cases means that Theiler's disease should be considered in any horse presenting with acute hepatic necrosis, regardless of recent medical history.

Early warning signs of Theiler's disease develop following a latent period of four to ten weeks after exposure to equine biological products, during which horses appear completely normal. Initial symptoms are often subtle and nonspecific, including mild depression, decreased appetite, and subtle lethargy that owners might attribute to minor illness or environmental factors. Some horses show decreased water intake or mild changes in manure consistency. Because these early signs occur weeks after product administration, the connection is often not recognized. The latent period is followed by rapid deterioration over hours to days as hepatic necrosis reaches critical levels.

As the disease progresses, more recognizable symptoms emerge with alarming speed. Jaundice develops, evidenced by yellow discoloration of mucous membranes, sclera, and unpigmented skin. The degree of jaundice often increases visibly over hours. Progressive weakness and depression become marked. Some horses develop colic signs due to hepatic capsule distension or concurrent gastrointestinal dysfunction. Anorexia is typically complete—affected horses show no interest in food or water. Weight loss may not be prominent due to the acute nature of the disease, though horses appear unthrifty and may develop abdominal distension from ascites.

Behavioral changes reflecting hepatic encephalopathy represent some of the most dramatic symptoms. As the massively damaged liver fails to detoxify ammonia and other neurotoxins, neurological dysfunction develops. Affected horses may appear dull and obtunded or conversely may show agitation, anxiety, and hypersensitivity. Head pressing against walls or fences is characteristic. Aimless wandering, circling, and apparent blindness occur. Some horses become aggressive or show compulsive behaviors including yawning and repetitive licking. Ataxia and incoordination progress to recumbency in severe cases. Seizures may occur terminally.

Physical examination reveals multiple abnormalities reflecting multi-system failure. Mucous membranes appear deeply icteric and may show petechial hemorrhages indicating coagulopathy. Heart and respiratory rates are often elevated. Temperature may be normal, elevated, or subnormal depending on disease stage. Abdominal distension from ascites may be palpable. Dependent edema affects the ventral abdomen and lower limbs. Skin may show evidence of photosensitization on unpigmented areas. Rectal examination may reveal decreased fecal production and potentially a small, firm liver edge if palpable.

Symptom progression in Theiler's disease is typically rapid and devastating. Horses may progress from apparently normal to moribund over as little as twenty-four to seventy-two hours. The acute nature distinguishes Theiler's disease from more slowly progressive hepatopathies like pyrrolizidine alkaloid toxicity. Neurological signs often worsen rapidly, with horses becoming increasingly unresponsive or developing status epilepticus. Hemorrhagic tendencies may manifest as bleeding from gums, venipuncture sites, or body orifices. Horses that survive the initial crisis may stabilize or may continue declining over days.

Emergency symptoms requiring immediate veterinary intervention include any combination of jaundice with neurological abnormalities. Seizures, collapse, or coma indicate critical hepatic encephalopathy and represent medical emergencies. Spontaneous hemorrhage or prolonged bleeding from minor wounds suggests severe coagulopathy. Rapid deterioration in mentation even without obvious jaundice warrants emergency evaluation. Horses that become recumbent and cannot rise face extremely poor prognosis. Any horse that received equine biological products within the previous four to twelve weeks and develops unexplained illness should be evaluated for Theiler's disease. Early intervention offers the best, though still limited, chance for survival.

Diagnosis of Theiler's disease requires integration of clinical presentation, history, and laboratory findings. A thorough history is essential, specifically inquiring about administration of any equine-origin biological products within the preceding four to twelve weeks. Products to ask about include tetanus antitoxin, plasma transfusions, hyperimmune serum products, pregnant mare serum gonadotropin for breeding management, and any vaccines. Documentation of product lot numbers is valuable for epidemiological investigation if disease is confirmed. Physical examination assesses jaundice severity, neurological status, and signs of hemorrhage or other complications.

Blood chemistry and hematology provide essential diagnostic information with characteristic abnormalities. Liver enzymes are dramatically elevated: gamma-glutamyltransferase (GGT), sorbitol dehydrogenase (SDH), and aspartate aminotransferase (AST) may increase to levels ten to one hundred times normal values. The marked magnitude of enzyme elevation reflects massive hepatocellular necrosis. Bilirubin is severely elevated, explaining clinical jaundice. Bile acids are markedly increased. Albumin decreases as synthetic function fails, while globulins may initially remain normal. Ammonia levels are elevated and correlate with encephalopathy severity. Blood glucose may be critically low due to failed gluconeogenesis. Coagulation parameters including prothrombin time are prolonged, and fibrinogen may be decreased. Complete blood count may be relatively normal or show anemia.

Advanced diagnostics help confirm diagnosis and assess prognosis. Abdominal ultrasound may reveal hepatomegaly acutely, progressing to decreased liver size as necrosis advances. The liver may appear heterogeneous with areas of differing echogenicity. Ascites is frequently present. Liver biopsy, if coagulation status permits, shows the characteristic histopathological finding of massive or submassive centrilobular hepatocellular necrosis with minimal inflammatory infiltrate. This pattern differs from more inflammatory hepatopathies. Testing for specific viral agents including equine parvovirus-hepatitis and equine pegivirus may be available through specialized laboratories and can support the diagnosis. Testing implicated biological products, if available, may identify contamination.

Differential diagnosis includes other causes of acute hepatic failure in horses. Pyrrolizidine alkaloid toxicity causes similar liver failure but typically develops more insidiously and shows characteristic megalocytosis on histopathology rather than acute necrosis. Other hepatotoxins including certain drugs, mycotoxins, and other plant toxins must be considered based on exposure history. Acute cholangiohepatitis shows more inflammatory changes and biliary involvement. Tyzzer's disease causes acute hepatic necrosis in foals but is rare in adults. Hepatic lipidosis presents differently, typically in ponies with metabolic syndrome. Acute hemolytic anemia causes jaundice without primary liver enzyme elevation. The history of equine biological product administration, timing of clinical signs, and characteristic laboratory and histopathological findings usually establish the diagnosis of Theiler's disease.

Emergency treatment for Theiler's disease focuses on aggressive supportive care, as no specific therapy exists to halt hepatocellular necrosis once it has begun. Intravenous fluid therapy is fundamental to support circulation, maintain blood glucose, and facilitate toxin excretion. Balanced electrolyte solutions with dextrose supplementation are typically used; lactate-containing fluids should be avoided as the failing liver cannot metabolize lactate. Hypoglycemia is common and may be severe, requiring concentrated dextrose infusions. Plasma transfusion replaces clotting factors in horses with coagulopathy and provides albumin, though the irony of treating Theiler's disease with plasma is recognized and autologous products are preferred when available.

Medical management addresses hepatic encephalopathy and metabolic derangements. Lactulose administered orally or by nasogastric tube acidifies colonic contents, trapping ammonia and reducing its absorption—this is a cornerstone of encephalopathy management. Oral neomycin or metronidazole reduce ammonia-producing intestinal bacteria. Branched-chain amino acid supplementation may support minimal protein intake while reducing encephalopathy risk. Complete dietary protein restriction is implemented initially. B vitamin supplementation, particularly thiamine, addresses deficiencies. Vitamin K may help support coagulation though benefits are limited when synthetic function is severely impaired.

Anti-inflammatory and hepatoprotective therapies are commonly employed though evidence for efficacy specifically in Theiler's disease is limited. Flunixin meglumine or other non-steroidal anti-inflammatory drugs may reduce inflammation and provide comfort, though hepatic metabolism of these drugs is impaired. S-adenosylmethionine (SAMe) and silymarin (milk thistle extract) are used as hepatoprotectants, theoretically supporting remaining hepatocyte function and reducing oxidative stress. Corticosteroids have been used based on possible immune-mediated components, though their value is uncertain and they carry risks in systemically ill horses. N-acetylcysteine has been investigated as an antioxidant.

Supportive care extends to managing complications and maintaining patient comfort. Photoprotection is necessary if photosensitization develops. Nursing care for recumbent horses includes frequent repositioning, thick padded bedding, bladder monitoring, and prevention of secondary complications. Anti-ulcer therapy with omeprazole or sucralfate protects against stress-induced gastric ulceration. Pain management requires careful drug selection given impaired hepatic metabolism. Monitoring for secondary infections is important as immune function may be compromised. Temperature regulation support may be needed for horses unable to thermoregulate normally.

Rehabilitation for surviving horses is prolonged and cautious. Even after apparent recovery, liver function may be permanently reduced. Exercise restriction continues for weeks to months after clinical recovery. Serial blood chemistry monitors hepatic enzyme trends and synthetic function. Return to work proceeds very gradually, with repeated monitoring ensuring the liver tolerates increased metabolic demand. Some horses recover fully and return to previous performance levels, while others retain significant hepatic impairment requiring permanent activity modification.

Treatment decisions should acknowledge the grave prognosis associated with Theiler's disease. Historical mortality rates of fifty to ninety percent have improved modestly with modern intensive care, but survival remains uncertain even with aggressive treatment. Factors associated with better outcomes include lower ammonia levels, less severe coagulopathy, maintained blood glucose with support, and absence of severe neurological signs. Horses with recumbent encephalopathy, uncontrolled seizures, refractory hypoglycemia, or severe hemorrhage have extremely poor prognoses. Financial considerations are significant, as intensive care is expensive and prolonged. Honest discussions about realistic expectations help owners make informed decisions about treatment intensity and duration.

Recovery timeline for horses surviving the acute crisis of Theiler's disease varies considerably based on the extent of hepatic necrosis and the adequacy of hepatic regeneration. Horses that survive the initial one to two weeks of critical illness demonstrate that sufficient functional liver tissue remains to support life. Improvement is often gradual, with appetite returning first, followed by resolution of jaundice over weeks, and normalization of neurological function. Liver enzymes decline gradually over weeks to months, though may remain mildly elevated indefinitely. Complete recovery may take three to six months, and some horses never fully normalize hepatic function.

Post-treatment care requires sustained intensive management during the recovery phase and careful long-term monitoring. Dietary management continues with protein restriction gradually liberalized as liver function improves. Multiple small meals of easily digestible feeds support nutrition without overwhelming recovering hepatic capacity. Regular blood chemistry monitoring tracks improvement, initially weekly then monthly as stability is demonstrated. Owners must remain vigilant for any recurrence of symptoms suggesting hepatic decompensation. Activity restriction continues throughout the recovery period, with gradual return to exercise only after liver function normalizes and veterinary clearance is obtained.

Prognosis for horses with Theiler's disease depends primarily on disease severity at presentation and response to initial treatment. Horses presenting with mild to moderate clinical signs, maintained consciousness, and only moderate enzyme elevations have better survival prospects than those with severe encephalopathy, profound hypoglycemia, and massive liver enzyme elevations. Response to treatment within the first forty-eight to seventy-two hours provides prognostic information—horses that stabilize and begin improving have reasonable chances of survival, while those that continue deteriorating despite aggressive care face poor prognoses. Published survival rates range from approximately ten percent in severe cases to fifty percent or higher in horses receiving prompt, intensive treatment.

Long-term soundness and athletic outlook for survivors is generally favorable compared to chronic liver diseases. Because Theiler's disease causes acute necrosis rather than progressive fibrosis, survivors may regenerate substantial functional hepatic tissue if enough hepatocytes remain. Many survivors return to previous levels of athletic performance after complete recovery. However, some horses retain permanent hepatic insufficiency manifesting as exercise intolerance or metabolic limitations. Liver function should be thoroughly assessed before return to intense athletic work. Horses that recover from Theiler's disease should probably not receive equine-origin biological products in the future unless absolutely medically necessary, as the risk of recurrent disease is unknown but presumably elevated.

Management practices for Theiler's disease prevention center on judicious use of equine-origin biological products and awareness of disease risk. Before administering any equine-origin product, veterinarians and owners should weigh medical necessity against Theiler's disease risk. Alternative products should be used when equivalent efficacy is available—for example, tetanus toxoid vaccination provides protection without the serum hepatitis risk associated with tetanus antitoxin. When equine biological products are medically necessary, informed consent should include discussion of Theiler's disease risk. Product lot numbers should be recorded for potential epidemiological investigation if disease occurs.

Product selection and sourcing considerations may influence risk, though evidence is incomplete. Some practitioners prefer pooled products from multiple donors over single-donor products, theorizing that dilution reduces potential viral load, though this is not proven. Commercial products from reputable manufacturers with quality control testing may theoretically carry lower risk than farm-produced products, though Theiler's disease has occurred following both. Products subjected to viral inactivation procedures may be safer, though no process guarantees elimination of all potentially causative agents. Research into improved screening and inactivation methods continues.

Nutritional and metabolic health optimization may help horses resist or survive potential exposure, though this is speculative. Maintaining horses in good body condition with healthy liver function reserves may improve outcomes if disease develops. Avoiding concurrent hepatic stressors including other hepatotoxins, excessive medications, and metabolic imbalances is prudent. Ensuring adequate nutrition and hydration supports overall health and potentially immune function.

Vaccination protocols and biological product decisions require risk-benefit analysis on an individual basis. Tetanus antitoxin administration to unvaccinated horses after wounds historically carried Theiler's disease risk; primary tetanus toxoid vaccination eliminates the need for antitoxin in most situations. Plasma transfusions for foals with failure of passive transfer are often medically necessary despite theoretical Theiler's disease risk, as the immediate risk of sepsis outweighs delayed hepatitis risk. Pregnant mare serum gonadotropin use for breeding management should be evaluated against alternative fertility treatments. Discussing Theiler's disease risk as part of informed consent when biological products are recommended enables owners to participate in decision-making.

Monitoring protocols following equine biological product administration may enable early disease detection when treatment is most likely to be beneficial. Owners should be advised to monitor horses for four to twelve weeks following product administration and report any signs of illness, particularly lethargy, appetite loss, or jaundice. Some practitioners recommend baseline liver enzyme measurement before product administration and follow-up testing at four to six weeks, though the cost-effectiveness of this approach is debated. Early detection of enzyme elevations before clinical disease develops may allow supportive measures to begin before critical illness. Awareness among equine veterinarians and owners about Theiler's disease enables appropriate suspicion when compatible clinical signs develop.

Daily management adjustments for horses recovering from Theiler's disease focus on supporting hepatic recovery while preventing complications. Feeding protocols emphasize easily digestible feeds with initially restricted protein that gradually increases as liver function improves. Multiple small meals minimize metabolic burden compared to twice-daily feeding. High-quality grass hay is preferred over higher-protein legume hay during recovery. Grain portions should be moderate, potentially replaced with fat-supplemented feeds to provide calories with less hepatic protein processing. Fresh, clean water must be constantly available. Daily monitoring of appetite and feed consumption helps detect changes that may indicate deterioration or improvement. Body weight and condition scoring track nutritional status through recovery.

Housing and turnout considerations during recovery prioritize rest and reduced stress. Initially, stall rest in a quiet area with minimal disturbance is appropriate. Deep, comfortable bedding encourages rest and prevents pressure sores in weakened horses. Adequate ventilation reduces ammonia accumulation from urine. As horses improve, brief hand-walking provides light exercise without stress. Gradual introduction to limited turnout in a safe, small paddock follows clinical improvement. Full turnout with companions resumes only after substantial recovery, typically weeks to months after the acute illness. Social stress from herd dynamics should be minimized during recovery.

Exercise modifications are essential throughout the extended recovery period. Complete rest is mandatory during acute illness and initial recovery. As clinical status improves and liver enzymes begin declining, short hand-walking sessions begin, typically five to ten minutes once or twice daily. Duration and intensity increase very gradually over weeks based on tolerance and laboratory improvement. Return to ridden work begins only after significant normalization of liver function, often two to three months after acute illness. Initial ridden work should be light, flat work, with gradual progression. Monitoring for exercise intolerance including excessive fatigue, poor recovery, or behavioral changes guides exercise advancement. Some horses return to full work, while others require permanent activity reduction.

Monitoring and ongoing care requirements extend well beyond clinical recovery. Regular veterinary examinations assess overall progress and detect any setbacks. Blood chemistry panels initially are performed weekly during the acute phase, then biweekly, then monthly as recovery progresses. Parameters of interest include liver enzymes, bilirubin, albumin, ammonia, and coagulation times. Owners should maintain daily observation logs recording appetite, attitude, manure production, and any concerning signs. Any recurrence of lethargy, appetite loss, jaundice, or neurological signs warrants immediate veterinary consultation. Long-term annual or biannual monitoring ensures sustained hepatic health.

Quality of life and use considerations require ongoing evaluation for recovered horses. Many Theiler's disease survivors achieve good quality of life and return to previous activities. Quality of life assessment should consider comfort, appetite, ability to maintain body weight, energy levels, and apparent contentment. Horses that cannot recover adequate liver function to maintain normal metabolism may struggle with exercise intolerance, weight maintenance, or recurrent illness. Decisions about continued management versus euthanasia should prioritize the horse's welfare. Future use of equine biological products in Theiler's disease survivors should be avoided when possible, as susceptibility to recurrent disease is unknown but presumably present. Frank discussions between owners and veterinarians about long-term expectations guide appropriate management and use decisions.

Theiler's disease affects horses of all breeds without documented genetic predisposition. The condition has been reported in Thoroughbreds, Quarter Horses, Warmbloods, Arabians, ponies, draft breeds, and all other breed types. Risk is determined primarily by exposure to equine-origin biological products rather than by hereditary factors. Adult horses appear more commonly affected than foals, possibly reflecting greater likelihood of receiving biological products or age-related susceptibility differences. No sex predilection has been established. Geographic distribution corresponds to areas where equine biological products are commonly used in veterinary practice.

Breed-related use and discipline considerations influence Theiler's disease risk through associated management and medical practices rather than genetic susceptibility. Performance horses that frequently receive plasma for various medical conditions face elevated exposure risk. Breeding farm horses often receive pregnant mare serum gonadotropin and may receive plasma or serum products during reproductive management. Horses in areas with high tetanus incidence may receive antitoxin following wounds if tetanus vaccination status is unknown. Show horses traveling to unfamiliar areas sometimes receive prophylactic biological products. Newborn foals with failure of passive transfer receive plasma transfusions as standard medical care. Racehorses and sport horses receiving intensive medical management may have multiple biological product exposures over their careers.

Genetic testing for Theiler's disease susceptibility is not available because the condition is not hereditary. However, individual variation in immune response and hepatic reserve may influence which exposed horses develop clinical disease. Research into host factors that predispose to disease following exposure continues. Breeders should be aware that horses recovered from Theiler's disease may pass unknown susceptibility factors to offspring, though this remains theoretical. More practically, breeding farms should implement protocols for judicious use of biological products, maintain vaccination programs that reduce the need for antitoxin products, and ensure staff awareness of Theiler's disease signs for early detection following product administration.

Commonly co-occurring conditions with Theiler's disease reflect the systemic effects of acute hepatic failure. Hepatic encephalopathy is the most significant concurrent condition, developing as the failing liver cannot detoxify neurotoxins. Coagulopathy from impaired clotting factor synthesis causes hemorrhagic tendencies. Hypoglycemia results from failed hepatic gluconeogenesis and glycogen storage. Hypoalbuminemia leads to edema and ascites. Electrolyte derangements including hypokalemia complicate management. Gastric ulceration frequently accompanies critical illness. Photosensitization may develop if sufficient liver function remains to process chlorophyll but not excrete phylloerythrin. Secondary infections can occur with compromised immune function. These concurrent conditions require individual management alongside treatment of underlying hepatic failure.

Conditions with similar symptoms requiring differentiation include other causes of acute hepatic necrosis and failure. Pyrrolizidine alkaloid toxicity causes hepatic failure but typically progresses more slowly and shows different histopathology. Other hepatotoxins including medications and mycotoxins can cause acute liver failure with different exposure histories. Tyzzer's disease causes acute hepatic necrosis in foals with distinct bacterial etiology. Acute cholangiohepatitis presents with more inflammatory changes and biliary involvement. Hemolytic anemia causes jaundice without primary liver enzyme elevation. Neurological diseases including rabies and viral encephalitides may mimic hepatic encephalopathy. Accurate diagnosis requires integration of history, clinical findings, laboratory data, and potentially histopathology.

Potential complications of Theiler's disease extend beyond direct hepatic effects. Cerebral edema may develop with severe hepatic encephalopathy, contributing to neurological deterioration. Disseminated intravascular coagulation represents a severe complication of profound coagulopathy. Renal failure may develop from hepatorenal syndrome or hypovolemia. Laminitis can occur secondary to systemic inflammation and metabolic disturbances. Overwhelming sepsis may develop when immune function is compromised. Aspiration pneumonia is a risk in horses with severe neurological compromise. Pressure sores and myopathy affect recumbent horses. Survivors may develop chronic hepatic insufficiency or recurrent disease. Understanding these complications guides monitoring and intervention strategies during Theiler's disease management.