History:  A 4-month-old Tennessee Walking horse filly was submitted dead to the ADDL for necropsy.  The filly was hypothermic and had a history of diarrhea of a few days duration.  The filly became depressed and began exhibiting neurological signs such as head pressing, mydriasis, and decreased menace response.  Fluid therapy, as well as plasma and flunixin, were administered.  Clinical laboratory abnormalities included hypoproteinemia, azotemia, neutrophilia, lymphocytosis, and several electrolyte imbalances.  The horse was euthanized.

Gross findings:  Segmental areas of jejunal serosa were purple, with prominent serosal and mesenteric veins.  Throughout the jejunum and ileum, intestinal mucosa was markedly thickened, assuming a cerebriform appearance. 

The thorax contained approximately 1-2 liters of clear, straw-colored fluid.  The cranioventral Nematodes consistent with Parascaris equorum were found within the intestine.portions of both cranial lung lobes were wet and heavy, with interlobular septa expanded by edema fluid.  The abdomen contained approximately 1 liter of clear, straw-colored fluid.

Histologic findings:  Ileal mucosa was markedly expanded by hyperplastic crypts which contained numerous mitotic figures and decreased goblet cells.  Several crypts were tortuous and branching.  Many crypts were dilated and filled with necrotic debris and degenerate leukocytes.  Large foci of mucosa were necrotic, characterized by diffuse loss of tissue architecture that extended into underlying submucosa.  Numerous leukocytes, including lymphocytes and neutrophils, expanded lamina propria replacing some intestinal crypts.  Peyer's patches contained decreased numbers of lymphocytes and karyorrhectic lymphocytes.  Submucosa was diffusely expanded by clear edema fluid.  Similar changes were observed within the duodenum and jejunum, and were consistent with proliferative and necrotic enteritis.

  Alveoli and interlobular septa within the lung were expanded by lightly eosinophilic material, consistent with pulmonary edema.  Clear space surrounded arterioles within cerebral white matter, giving adjacent neuropil a lacy appearance.

  Histologic changes in the brain were consistent with edema.

Ancillary findings:    Two potential inhabitants of the gastrointestinal system, E. coli and Aeromonas caviae, were cultured from the intestine.  Salmonella culture was negative.  Fecal flotation found numerous ova consistent with Parascaris equorum.

  A section of jejunum tested positive for Lawsonia intracellularis via PCR.  A Warthin-Starry stain was applied to sections of jejunum and ileum, and numerous intracytoplasmic bacteria were located in the apical portion of enterocytes lining hyperplastic crypts.

Discussion:  Characteristic gross and histopathologic lesions, coupled with positive PCR, were consistent with proliferative enteropathy in this foal.  The causative agent is an obligate intracellular and gram-negative bacteria that is most often associated with proliferative ileitis in swine. 

  Lawsonia- caused proliferative enteritis occurs sporadically in horses, with both individual cases and outbreaks on breeding farms.  Foals from 3-13 months are most commonly affected.  The most common clinical signs include diarrhea, colic, weight loss, and ventral or submandibular edema, all of which can be fairly acute.   Common clinical pathologic abnormalities usually reflect a marked hypoproteinemia due to loss of protein through affected intestine.  Leukocytosis is also a common abnormality.  Antemortem diagnosis of this uncommon equine disease requires exclusion of other, more common, causes of diarrhea and colic in foals.  If proliferative enteritis is suspected after other causes have been excluded, fecal PCR for Lawsonia intracellularis and serology can be used to aid in diagnosis.

  The above cases differ from previous reports of proliferative enteritis as this foal rapidly developed severe neurological signs such as head pressing.  Because of previous farm history and recent diagnoses on the same farm, Lawsonia intracellularis was the likely cause of diarrhea in this foal.  Indeed, Lawsonia was confirmed histologically and via PCR.  Clinical pathology and gross lesions were consistent with severe hypoproteinemia; thus, cerebral edema was suspected as the underlying mechanism for manifestation of neurologic signs.  Histopathologic examination of the brain supported this hypothesis as lesions suggested cerebral edema.  No other cause of neurologic disease was observed.

-by Dr. Grant Burcham, ADDL Graduate Student

References

1. Brown CC, Baker DC, Barker IK: 2007.  Alimentary system.  In Jubb, Kennedy, and Palmer's Pathology of Domestic Animals, ed. Maxie MG, 5^th ed.  Philadelphia PA, Vol 2, pp 201-203.

2. Lavoie JP et al: 2000.  Equine proliferative enteropathy: a cause of weight loss, colic, diarrhea, and hypoproteinemia in foals on three breeding farms in Canada.  Equine Vet J 32(5): 418-25.

3. McGurrin MK et al: 2007.  An outbreak of Lawsonia intracellularis infection in a standard-bred herd in Ontario.  Can Vet J 48(9): 927-30.

4. Radostits OM, Gay CC, Hinchcliff KW, Constable PD: 2007.  Diseases associated with viruses and Chlamydia.  In: Veterinary Medicine: A textbook of the diseases of cattle, horses, sheep, pigs, and goats.  10^th ed.  Philadelphia PA. Elsevier Saunders.  p 1305.

5. Williams NM et al: 1996.  Proliferative enteropathy in a foal caused by Lawsonia intracellularis-like bacterium.  J Vet Diag Invest 8: 254-56.