Lymphocytic-Plasmacytic Enteritis in Horses

Lymphocytic-Plasmacytic Enteritis/Enterocolitis (LPE) is a rare form of infiltrative bowel disease that can affect horses of any age, breed and sex. Histopathologic lesions of LPE are characterized by abnormal infiltration of lymphocytes and plasma cells into the lamina propria of the intestinal wall. Weight loss is the most common clinical sign of LPE and the definitive diagnosis of LPE is difficult without performing an intestinal biopsy. LPE generally has a limited response to treatment, and the long-term prognosis for the affected horse is poor.

Introduction and Discussion to LPE in Horses

Lymphocytic-Plasmacytic Enteritis/Enterocolitis (LPE) is a rare form of infiltrative intestinal disease in horses. LPE is classified within the idiopathic bowel disease group (Schumacher, 2009).

LPE presents with vague clinical signs such as weight loss, colic and diarrhea. A large number of more commonly occurring equine diseases present with similar clinical signs including cyathostomiasis, gastric ulceration, dental disease, colonic ulceration, infectious colitis, sand colitis, intestinal lymphoma, other infiltrative bowel diseases and protein-losing nephropathy. To make a diagnosis of LPE, an extensive work-up is required to first rule out many of these other diseases.

Obtaining a definitive diagnosis of LPE in live horses is uncommon because the disease is rare and also because the work-up is very expensive. For these reasons there is limited information available on the true response of LPE to treatment.

Kemper et al (2000) made an attempt to define the pathogenesis of LPE by examining hospital records from three specialist equine veterinary hospitals over a 15-year period. Through this research, Kemper et al were only able to identified 14 horses that had been definitively diagnosed with LPE in this time, and most of these horses were diagnosed post-mortem.

Pathophysiology of LPE in Horses

On histopathology, LPE predominantly affects the small intestine, but lesions can frequently extend to the large intestine.

While the abnormal infiltrate of lymphocytes and plasma cells is suggestive of LPE, it has also been reported with a variety of other etiologies associated with inflammatory bowel diseases.This infiltration can lead to varying degrees of villous blunting, fusion or atrophy.  Mucosal or submucosal edema may also be present (Schumacher, 2009). These changes lead to malabsorption of nutrients and weight loss.

Hypoproteinemia is often diagnosed in horses with LPE (Kemper, 2000), although hypoproteinemia is more commonly seen in other forms of infiltrative enteritis such as granulomatous enteritis. Hypoproteinemia is caused malabsorption of protein, exudation of lymph through dilated lymphatics and intestinal mucosal ulceration.

Kemper et al (2000) reported that the gross appearance of the intestine on necropsy was normal in 10 out of 13 horses in their study. Four out of 13 horses had mesenteric lymphadenopathy. Dilated lymphatics, mucosal ulceration and muscular hypertrophy were also identified in some horses.

Some researchers have considered that LPE might be a possible precursor to the development of intestinal lymphosarcoma (Schumacher 2009).

LPE has not been found to be associated with intestinal parasitism. LPE has been reported to occur in horses with Cushing’s disease and in pregnant mares.

Presentation of LPE in Horses

Horses of many different breeds have been affected by LPE; there appears to be no strong evidence, at this stage, for a genetic or familial predisposition to the disease.

Unlike many of the other inflammatory bowel diseases, which tend to affect young horses, LPE can affect horses of any age. Kemper et al (2000) reported a median age of 12 years, from their group of 14 horses.

The most common presenting clinical sign of LPE is progressive weight loss. Diarrhea has been reported to occur in approximately 50% of cases, while lethargy, colic, and ventral edema are less frequent clinical signs.

The body temperature, heart rate and respiratory rate tend to be within the normal range in horses with LPE unless there is a secondary process such as peritonitis, or concurrent disease.

Diagnosis of Lymphocytic-Plasmacytic Enteritis in Horses

Definitive diagnosis of LPE is difficult and is often based on biopsy of the intestinal tract. As the small intestine is most frequently affected, biopsy in this area is ideal – which requires either an exploratory laparotomy or, if available, a laparoscopic procedure.

Rectal biopsies are occasionally diagnostic, however lymphocytic-plasmacytic rectal wall infiltrations are sometimes found in normal horses, and therefore interpretation of the histopathology results requires an experienced pathologist.

Blood work. On hematology, the white cell count and red cell counts of horses with LPE tend to lie within the normal range, unless the disease is severe and peritonitis has occurred.

Serum Amyloid A and Fibrinogen concentrations are occasionally elevated (Kemper, 2000).

Hypoproteinemia and hypoalbuminemia are relatively common findings in horses with LPE (Kemper, 2000), although not as common as seen with diseases such as infectious colitis, ulcerative colitis and granulomatous enteritis.

Malabsorption of nutrients can be confirmed by performing either an Oral Glucose Tolerance Test or D-xylose absorption tests – these tests are frequently abnormal in LPE-affected horses. In Kemper’s study, these tests were abnormal in 9 out of 12 horses.

Urinalysis is usually normal, but it is an important test to perform to help rule out protein loss through the kidneys.

Peritoneal fluid analysis is usually normal but may show some non-specific evidence of inflammation.

Rectal examination may detect abnormalities such as the presence of mesenteric lymphadenopathy, or thickening of the small intestine.

Abdominal ultrasound may also reveal diffuse thickening of the small intestine – this was seen in 10 out of 13 horses from the Kemper study.

Treatment of LPE in Horses

Successful treatment has not been definitively proven in horses with LPE.  Corticosteroids are usually administered, and may improve or resolve diarrhea, but generally not the weight loss. There apparently have been some rare reports of resolution of LPE with corticosteroids (Schumacher, 2009).

In the Kemper study, the two horses that were diagnosed with LPE ante mortem both showed marked progression of disease by the time postmortem occurred, despite treatment.

Medications used to treat human and small animal versions of LPE are sometimes administered to horses with LPE.To date, none of these treatment approaches have shown convincing efficacy, however with time, and more efficient diagnosis of the infiltrative bowel disease, more information should become available.

In general, LPE has not been found to be particularly responsive to treatment, and affected horses have a guarded to poor prognosis.


At this stage, until more is known about the etiology of the disease, little can be done to prevent it. There is not strong evidence of a genetic cause for LPE, but it might be worth careful consideration before breeding a horse that has been diagnosed with the disease.


  • Kemper, D.L. et al (2000) Equine lymphocytic-plasmacytic enterocolitis: a retrospective study of 14 cases. Equine vet. J., Suppl. 32:108-112.
  • Schumacher, J. (2009) Infiltrative Bowel Diseases. In: Current Therapy in Equine Medicine 6, ed. N.E. Robinson. Saunders, St Louis, Missouri p. 441.
  • Schumacher, J. (2000) Chronic Idiopathic Inflammatory Bowel Disease of the Horse. J. Vet. Intern. Med. 14:258-265.

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