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Potomac Horse Fever


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Potomac Horse Fever

Potomac Horse Fever (PHF), also known as equine monocytic ehrlichiosis, is a febrile gastrointestinal disease affecting horses of all ages.  PHF was first recognized in 1979 as a distinct clinical entity in Montgomery County, Maryland (the Potomac region).  To date, PHF has appeared as a sporadic disease observed mostly in the summer months throughout many states in the United States and has also been confirmed in Canada and Europe.  Although a clear seasonal pattern exists with cases first reported in late May or June and ending in October or November, the peak prevalence of PHF occurs in July, August, and September.
  PHF is caused by Ehrlichia risticii (now called Neorickettsia risticii), a member of the family Rickettsiaceae.  E. risticii is found in association with trema-todes in freshwater snails.  Although rickettsia are often transmitted by arthropods and the disease is seasonal, an arthropod host has not been identified.  E. risticii is a gram-negative, obligate intracellular bacterium that infects monocytes.  These infected cells have a predilection for the intestine, especially the cecum and colon.  The organism then multiplies in macrophages and mast cells, in the lamina propria and submucosa, and in the cytoplasm of glandular epithelial cells causing cell exfoliation.

Horses affected with PHF usually develop acute depression, fever (102-107ºF) and anorexia.  After 24-48 hours, the horse often develops profuse, watery diarrhea without blood, characteristic odor, or leukocyte excretion.  The diarrhea may be present for up to 10 days but, in most cases, only lasts 1-5 days.  However, not all horses have diarrhea or diarrhea may be transient in nature.  Laminitis, a frequent sequel to PHF, occurs most commonly within three days of the onset of diarrhea.  Other clinical signs include colic and subcutaneous edema of the legs and ventral abdomen.  Borborygmal sounds are typically decreased or absent in the early stages of the disease.  Although horses show different hematologic signs, most horses with PHF have leukopenia characterized by neutropenia, lymphopenia, and eosinopenia.  In addition, some horses may develop thrombocytopenia and, rarely, petechiation.  Acid base and electrolyte

values are typical of most horses with acute diarrhea, namely metabolic acidosis, hyponatremia, hypokalemia, and renal azotemia.

  Since the clinical signs closely resemble those of salmonellosis, multiple samples of fecal matter should be submitted to a laboratory for culture.  In addition, colitis X, antibiotic-associated diarrhea, endotoxic shock, and peritonitis should be ruled out as differential diagnoses for horses with acute diarrhea.  The characteristic epidemiologic features including the seasonal nature, the sporadic occurrence on farms located near rivers, and lack of Salmonella isolation renders PHF a more likely diagnosis.

  Currently, the most convenient way to diagnose PHF is by indirect fluorescent antibody test (IFA).  The IFA detects antibodies in sera to the causative agent E. risticii.  Most horses have detectable antibody titers at the onset of clinical signs although a rapid rise in antibody titer after the first few days of infection with  E. risticii merits paired serum samples.  Though significant changes in titer of affected horses can occur in 2-3 days, paired serum samples should be taken at least two weeks apart.  Nonetheless, the presence of antibodies of the IFA does not indicate that the horse has clinical PHF, only that the horse was exposed to E. risticii sometime in the past.  At least a four-fold increase in antibody titer has been suggested as a criterion for serologic diagnosis.

  A definitive diagnosis of PHF is made by isolation of E. risticii from the peripheral blood of a clinically affected horse.  The organism is best isolated in macrophages in tissue culture media without antibiotics.  In addition, electron microscopic examination of peripheral blood monocytes can be done as a definitive diagnosis by using Giemsa stain to demonstrate the organism in dried blood or buffy coat smears.

  The gross lesions at necropsy may be minimal affecting primarily the cecum and colon and, to a lesser degree, the small intestines.  Affected segments are distended with fluid mixed with ingesta and the fluid is pale brown and fetid.  Very little hemorrhage or damage of the mucosal surface is evident, except for some patchy hyperemia (approximately 4-8 cm of the small intestine affected and approximately 5-20 cm of the cecum or colon.)  In contrast to large areas of necrosis and ulceration with some cases of Salmonellosis, the scattered mucosal erosions and ulcers present in the mucosa

from horses with PHF are less frequent.  In addition, splenomegaly and ventral edema may be present at necropsy.

  Microscopically, the mucosa of the cecum and colon is reduced in thickness due to the loss of surface epithelium, a marked decrease in the number of intestinal crypts, and collapse of the lamina propria.  The denuded surface epithelium may be covered by a pseudomembrane focally, which consists of necrotic cells, fibrin, and bacteria.  Capillaries and veins of the mucosa are engorged with blood.  The remaining intestinal crypt cells have intact epithelium.  The lamina propria is hypercellular, especially at the base of the crypts.  The submucosa is edematous.  Both lamina propria and submucosa contain macrophages with clusters of the infectious agent.  These clusters of E. risticii are demonstrated using a modified Steiner's or Dieterle's silver stain.  The germinal centers of the lymphoid follicles are depleted of lymphocytes and contain karyorrhectic nuclei.

  Treatment of horses with PHF includes antibiotics, fluid and electrolyte replacement therapy for animals exhibiting diarrhea, and nonsteroidal anti-inflammatory drugs for the relief of pain in cases of colic and/or laminitis. 

  Vaccines are available for protection against PHF.  However, protection may be short-lived and incomplete because, in many cases, vaccination has been shown to reduce clinical signs, rather than provide complete protection.  Nonetheless, vaccination may be necessary for horses residing in or traveling to endemic areas.

  The prognosis for survival of PHF has increased to over 85% in recent years with the heightened awareness of the disease among veterinarians and horse owners.  The greatest percentage of mortality is attributed to complications of laminitis.  Outbreaks of PHF will decline in the future with vaccination, increased awareness, and initiating diagnosis and treatment at the early stages of the disease.

-by Ashley Armstrong, Class of 2006
-edited by Dr. Dinesh Singh, ADDL Graduate student


  1. Hillyer M: 2004.  A practical approach to diarrhoea in the adult horse.  In Practice. Pp 2-11.

  2. Madigon JE, Joon-seok C, Pusteria N: 1999.  Potomac Horse Fever: Identification and Transmission of the Causative Agent via Trematodes of Freshwater Snails.  AAEP Proceedings 45:45-47.

  3. McGavin MD et al: 2001.  Thompson's Special Veterinary Pathology, 3rd ed.  Mosby.

  4. Phipps LP: 1994.  Potomac Horse Fever. Equine Vet Edu 6:321-322.

  5. Reed S et al: 1995.  Potomac horse fever.  Equine Practice 17:12-14.

  6. Rikihisa Y et al: 1992.  Loss of absorptive capacity for sodium and chloride in the colon causes diarrhea in Potomac horse fever.  Res in Vet Sci 52: 353-362.

  7. Smith BP: 2002.  Large Animal Internal Medicine, 3rd ed. Elsevier USA.

  8. Whitlock RH: 1986.  Colitis: Differential diagnosis and treatment.  Equine Vet J: 18(4): 278-283.

  9. Whitlock RH, Palmer J: 1986.  Potomac horse fever: Clinical signs, diagnosis and treatment.  AAEP Proceedings 32: 405-413.






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