Equine proliferative enteropathy (EPE) is an infectious disease caused by the bacterium Lawsonia intracellularis. EPE mainly affects young horses during the fall and winter months. [1]

EPE is characterized by thickening of the lining of the small intestine due to excessive cell growth, which leads to reduced absorption of nutrients. Signs of EPE can include diarrhea, weight loss, colic, and decreased gastrointestinal sounds.

Foals can suffer severe illness as a consequence of diarrhea, which can lead to dehydration, electrolyte imbalances, and edema (fluid swelling) resulting from low protein levels in the blood. [2][3]

Diagnosis of EPE is typically based on clinical signs, response to treatment, and can be confirmed through blood tests, fecal tests, or intestinal biopsy. [3]

Treatment involves administering antibiotics effective against L. intracellularis. Supportive care, including proper nutrition and possibly intravenous fluids, is also important for recovery. [3] Horses that respond well to EPE treatment have a good long-term prognosis. [2]

Equine Proliferative Enteropathy

Equine proliferative enteropathy (EPE) occurs due to infection with Lawsonia intracellularis, a unique bacterium that lives and replicates inside cells in the intestine.

The bacteria infect cells lining the intestine, leading to abnormal cell growth and thickening of the intestinal lining. [4] This thickening disrupts normal nutrient absorption by the gut, resulting in symptoms like weight loss, diarrhea, and colic in horses.

EPE gets its name from the distinctive way the disease affects the horse’s intestines:

  • Proliferative describes the rapid and excessive growth or proliferation of cells in the intestinal lining
  • Enteropathy denotes disease of the intestine

The term enteritis is sometimes used interchangeably with enteropathy, and refers to inflammation of the intestine.


L. intracellularis is capable of infecting various mammals. While it predominantly affects horses, pigs, and rodents, this bacterium has also been identified in a range of domestic and wild animals. [2][4][5]

Lawsonia was first identified in horses in 1982. Infections are reported worldwide, but are best described in North America, Europe, and Australia. [3][6]

EPE tends to follow a seasonal pattern, likely relating to age of the foal. In North America, EPE is most frequent from August to January, peaking in November and December. [7]

Foals aged 3-12 months can show symptoms of Lawsonia infection, but it is foals aged 4-7 months who are most commonly affected. [2]

While isolated cases of EPE are more typical, outbreaks can occur on farms with a high number of susceptible animals. [8]

Lawsonia does not pose a risk to human health. [1]

Clinical Signs

EPE can be challenging to detect in horses because the symptoms are not specific and can be mistaken for other gastrointestinal disorders.

Common signs of EPE in horses include: [2][3][9][10]

  • Soft to watery diarrhea
  • Fever
  • Weight loss
  • Poor/rough hair coat
  • Colic
  • Lethargy
  • Poor appetite
  • Decreased fecal output
  • Black feces
  • Decreased gastrointestinal sounds
  • Potbelly appearance
  • Increased heart rate
  • Increased breathing rate
  • Collapse
  • Unwillingness to rise (recumbency)
  • Unresponsiveness
  • Purple gums
  • Seizures

EPE in foals often leads to dehydration. Signs of dehydration include a prolonged skin tent, sunken eyes, and tacky or dry gums. [9]

Sudden death of foals can also occur in severe cases. [9]

Secondary conditions

Foals with equine proliferative enteropathy have a weakened immune system, making them more susceptible to secondary infections and health complications.

Secondary conditions that can arise in foals as a result of Lawsonia infection include: [2][3][11]

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The primarily mode of transmission of L. intracellularis is through the ingestion of contaminated feces from horses infected with the bacterium. This can occur when horses consume food or water contaminated with the feces. [4][8]

Other environmental sources of Lawsonia infection have been suggested, including: [4]

  • Contact with rodents
  • Contact with pigs
  • Contact with infected feces from other wild or domestic animals

Older horses may contract the infection without showing symptoms and can spread it to susceptible foals by shedding the bacteria in their feces. The bacteria can survive in the environment for 1 – 2 weeks after being passed in feces. [4]

Foals infected with the bacteria can shed it in their feces for 5 – 17 days before showing any symptoms, further contributing to the environmental transmission of EPE. [12]

Disease Progression

After ingesting Lawsonia from the environment, the bacteria targets cells of the ileum, known as enterocytes, which are the cells lining this lower part of the small intestine.

Lawsonia can enter these cells without being detected or destroyed by the immune system. It typically takes about 5 days following ingestion for the bacteria to infect the cells. [2][5][9]

Once intestinal cells are infected by Lawsonia, they begin to divide prematurely. This leads to an overgrowth of cells that are inefficient at absorbing nutrients. This phenomenon is described as “proliferative,” highlighting the rapid proliferation of these intestinal cells. [2][3][10]

EPE can also involve loss of protein from the blood into the intestine. When this occurs, the movement of protein draws water into the intestinal lumen leading to diarrhea and dehydration. Over time, this loss of protein and and poor nutrient absorption leads to weight loss and a failure to thrive. [2]

Risk Factors

Risk factors for EPE are not well understood, but certain factors are believed to make foals more prone to Lawsonia infection.

Stress may predispose foals to developing EPE. Managing stress during critical periods such as weaning, training, and while providing routine preventative care can help maintain a strong immune system. [2][11]

Other potential risk factors for EPE in foals include: [3][8]

  • Overcrowding: High-density living conditions can facilitate the spread of infectious agents.
  • Change in Feed: Dietary changes can disrupt gut health and may make foals more susceptible to infection.
  • Use of Antibiotics: Antibiotic treatment can alter gut flora, potentially increasing vulnerability to Lawsonia.
  • Mixing Animals: Introducing new animals to a group can introduce new pathogens and stress existing animals.
  • Transportation of Animals: The stress and environmental changes associated with transportation can weaken the immune system.

Understanding and managing these risk factors can help prevent the occurrence and spread of EPE in horse populations.


Diagnosing EPE in foals can be challenging due to its nonspecific symptoms, which can resemble other gastrointestinal disorders.

Your veterinarian will make a presumptive diagnosis of EPE based on clinical signs, bloodwork, ultrasound, and ruling out other causes of disease. [4][13]

Sometimes, a presumptive diagnosis is made based on the response to antibiotic treatments. If the horse’s condition improves with antibiotics that are known to be effective against Lawsonia intracellularis, this can further support the diagnosis of EPE.


Blood tests can reveal abnormalities that suggest malabsorption or inflammation in the intestines, indicating a likely diagnosis of EPE.

The most common bloodwork finding in foals with Lawsonia infection is hypoproteinemia (low protein levels in the blood). Typically, there is a decrease in albumin, which is the most abundant protein in the blood. [2][9][13]

Affected horses may also have elevated white blood cell counts, although these counts can also be normal or low, depending on the severity of the disease. [13]

Other bloodwork findings may include: [9][13]

  • Low red blood cells (anemia)
  • Low calcium
  • Low electrolyte levels (i.e. sodium and chloride

Diagnostic Imaging

Ultrasound can be used to visualize the intestines and support a diagnosis of EPE.

In foals infected with Lawsonia, the intestinal wall is often significantly thickened, typically measuring up to 5 mm in thickness.[9][13]

Specific Testing

Specific fecal and blood tests are available to aid in diagnosing Lawsonia infection. Using a combination of blood tests and fecal analysis can lead to a more accurate diagnosis. [2]

PCR (Polymerase Chain Reaction) tests, which can be conducted on fecal or blood samples, are used to detect the presence of Lawsonia bacteria. However, these tests may yield false-negative results, particularly in the early stages of the disease or if treatment has already commenced. [4][13]

Blood tests that detect antibodies against the bacteria are also an option. However, it can be difficult to distinguish between horses that are actively infected and those that have merely been exposed to the bacteria. [4][13]

Unlike other bacterial infections, Lawsonia cannot be cultured for diagnostic purposes. This is because the bacteria grows and multiplies inside of cells and will not grow on standard culture media. [13]

Post-Mortem Examination

Post-mortem examination can be used to diagnose EPE in foals that have died, with the diagnosis based on the appearance of the intestines.

Foals that have succumbed to EPE often show severe thickening of the intestinal wall, ulcers on the intestinal lining, and the presence of blood and debris in the intestinal lumen. Despite these characteristic findings, specific testing to detect the bacterium is still recommended for a definitive diagnosis. [9]

Lawsonia is identified through microscopy of the intestinal tissue, using special stains that highlight the bacteria. Additionally, PCR tests can be performed on the intestinal tissue to confirm the diagnosis. [2][8][13]

Differential Diagnoses

Other diseases can present symptoms similar to those of EPE, making it necessary to rule them out as potential causes. These diseases include: [2][3][10][13]

  • Salmonella species
  • Clostridium species
  • Rhodococcus equi
  • Cryptosporidium
  • Cyathostominosis
  • Bacteroides
  • Neorickettsia risticii
  • Rotavirus
  • Inflammatory bowel disease
  • Gastrointestinal ulceration
  • Sand impaction

Historical data from the farm, such as previous cases of illness and management practices, can be instrumental in identifying the likely cause of disease. [11]

Treatment and Prognosis

The primary goal in treating equine proliferative enteropathy is to eradicate the Lawsonia bacteria and provide supportive care to the affected foal. [13]

Treatment is required for foals infected with Lawsonia, as they will not recover without medical intervention. While most cases can be managed on the farm, severely ill foals may require hospitalization. [4][8]

With appropriate treatment, foals have a 90% chance of survival. However, instances of sudden death have been reported. [2]


Lawsonia bacteria is unique because it lives inside the cells. This means that only certain antibiotics will work to clear the infection.

Recommended antibiotics for the treatment of EPE include: [2][4][9][13]

  • Oxytetracycline: 6.6 mg/kg intravenously, twice daily for 3 – 7 days
  • Doxycycline: 10 mg/kg orally, twice daily for 14 days
  • Erythromycin: 15-25 mg/kg orally, three times daily for 3 – 4 weeks
  • Rifampin: 5 mg/kg orally, twice daily for 2 – 3 weeks
  • Chloramphenicol: 44 mg/kg orally, three to four time daily for 2 – 3 weeks

A sequential antibiotic regimen may be used in severe cases to ensure the infection is cleared. For example, oxytetracycline can be administered for 7 days, followed by 14 days of doxycycline. [2]

Other antibiotics are given in combination to improve efficacy, such as the combination of erythromycin and rifampin. [2][13]

Monitoring organ function via bloodwork is crucial during treatment, as some antibiotics can cause kidney damage, especially in dehydrated animals. [13]

Certain antibiotics, like chloramphenicol, are toxic to humans. Special care is required when administering these drugs to horses. [13]

Supportive Care

Supportive care is also recommended for foals recovering from Lawsonia infection. Supportive care may include: [3][9][11][13]

  • Anti-inflammatory medications (e.g., flunixin meglumine)
  • Intravenous fluids
  • Intravenous supplements of sugars and amino acids
  • Anti-ulcer medications (e.g., sucralfate, cimetidine)
  • Diets enriched with vegetable oil, vitamins and minerals
  • Nasogastric tube feeding for additional nutritional support

Additional Treatments

In severely affected foals, additional treatments may be necessary, such as: [2][9][13]

Foals with severe clinical signs, such as recumbency, unresponsiveness, and seizures, have a poor prognosis. In these cases, euthanasia may be the most humane option. [9]


It can take several weeks for foals to return to normal health. The prognosis is less favorable if the foal has concurrent diseases or secondary complications. [2][8]

Foals that make a full recovery go on to have successful racing and competition careers. However, the sale price of foals following Lawsonia may be reduced. [14]


The best strategy to prevent EPE infection involves implementing good biosecurity policies and regularly monitoring your horse’s health. [12]

Early recognition of disease symptoms and prompt isolation of affected horses are key to preventing the spread of the disease. This can be achieved through daily physical examinations, including temperature and weight checks. [4][12]

Implementing robust pest control measures on the farm is also important to prevent exposure to the bacteria. Keep both domestic and wild animals away from feeding areas to minimize fecal contamination. [4][12]

If a farm experiences an outbreak of EPE, it is recommended to test the entire herd to identify infected animals. [12] Sick horses should be isolated until they have fully recovered to limit transmission of Lawsonia bacteria.

Farms with recurrent infections may conduct routine bloodwork to identify foals with low blood-protein levels, indicating infection. However this approach can be expensive, especially if there are many horses on the farm. [4][12]

Using fecal tests on individual horses is not generally recommended as a screening method due to the high costs involved. Additionally, since healthy horses rarely shed the bacteria, this test does not provide information about disease exposure. [12]

Horses that have recovered from EPE typically develop some immunity to Lawsonia, which decreases their chances of falling ill again from subsequent exposures. [4]


A vaccine against Lawsonia is available for pigs and has been explored for its effectiveness in foals. This vaccine might be recommended on farms that have not previously experienced EPE, to prevent or reduce the disease. [4]

Administered intra-rectally, the vaccine is given in two doses, spaced 30 days apart. It is generally well-tolerated by foals and does not pose a risk of infection. Additionally, vaccinated foals tend to shed less bacteria after being exposed to the disease again. [7][15]

However, it’s important to note that this vaccine is not officially labeled for use in horses. As such, its use should be based on the discretion of the attending veterinarian. [1]


  • Equine proliferative enteropathy (EPE) is an infectious disease caused by the bacterium Lawsonia intracellularis. [1]
  • This condition predominantly affects yearling foals during the fall and winter months. The infection leads to symptoms such as diarrhea, dehydration, and weight loss. [2][3][7]
  • Diagnosis of EPE is based on clinical signs, bloodwork, ultrasound, and specific blood and fecal tests. [2][4][13]
  • Treatment involves a combination of antibiotics and supportive care. With appropriate treatment, affected horses generally recover fully and have a favorable prognosis. [2][13][14]
  • Implementing biosecurity measures, including isolating ill horses and effective pest control on the farm, are practical and cost-effective strategies to prevent EPE. [4][12]

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  1. Page A. and Ruby R., Equine Proliferative Enteropathy Guidelines | AAEP. American Association of Equine Practitioners. Accessed Nov. 14, 2023.
  2. Bacterial Diarrhea in Foals – Digestive System. Merck Veterinary Manual. Accessed Nov. 11, 2023.
  3. Lavoie J.P. et al., Equine Proliferative Enteropathy: A Cause of Weight Loss, Colic, Diarrhoea and Hypoproteinaemia in Foals on Three Breeding Farms in Canada. Equine Veterinary Journal. 2000.View Summary
  4. Pusterla N. and Gebhart C., Lawsonia Intracellularis Infection and Proliferative Enteropathy in Foals. Vet Microbiol. 2013. View Summary
  5. Smith D.G.E. and Lawson G.H.K., Lawsonia Intracellularis: Getting inside the Pathogenesis of Proliferative Enteropathy. Veterinary Microbiology. 2001.
  6. Duhamel G.E. and Wheeldon E.B., Intestinal Adenomatosis in a Foal. Vet Pathol. 1982. View Summary
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  8. Lavoie J.-P. and Hinchcliff K.W., Blackwell’s five-minute veterinary consult: equine. 3rd ed. Wiley-Blackwell. 2019.
  9. Arroyo L.G. et al., Lawsonia Intracellularis-Associated Ulcerative and Necro-Hemorrhagic Enteritis in 5 Weanling Foals. Can Vet J. 2013. View Summary
  10. Bihr T.P., Protein-Losing Enteropathy Caused by Lawsonia Intracellularis in a Weanling Foal. Can Vet J. 2003. View Summary
  11. Crabtree N.E. et al., Pathology in Practice. javma. 2022.
  12. Pusterla N. et al., How to Monitor and Prevent the Occurrence of Lawsonia Intracellularis Infection in Weanling Foals From Farms With Endemic or Sporadic Occurrence of Equine Proliferative Enteropathy. Journal of Equine Veterinary Science. 2020.
  13. Frazer M.L., How to Diagnose and Treat Lawsonia Intracellularis. Equine Veterinary Education. 2019.
  14. Frazer M.L., Sale Price and Race Performance in Horses Previously Diagnosed With Lawsonia Intracellularis Infection. Journal of Equine Veterinary Science. 2020.
  15. Nogradi N. et al., Evaluation of the Field Efficacy of an Avirulent Live Lawsonia Intracellularis Vaccine in Foals. The Veterinary Journal. 2012. View Summary