ISSN 2398-2977      

Potomac Horse Fever


Synonym(s): Equine monocytic ehrlichiosis, equine ehrlichial colitis, acute equine diarrhea syndrome


  • Formerly known as Equine monocytic ehrlichiosis.
  • CauseNeorickettsia risticii (formerly Ehrlichia risticii) Anaplasmataceae; particularly prevalent in Eastern USA and in summer/autumn; unknown mode of transmission and route of infection but ingestion of aquatic insects infected with metacercariae carrying the organism can result in disease.
  • Signs: sporadic acute enterocolitis: acute onset of fever, depression, anorexia, decreased intestinal sounds, diarrhea, abdominal pain and laminitis.
  • Diagnosis: isolation of organism by culture or polymerase chain reaction (PCR); serologic testing.
  • Treatment: oxytetracycline intravenously for 5-7 days - highly effective; supportive therapy including fluids.
  • Control: vaccination and isolation/hygiene.
  • Prognosis: good with early intervention.



  • Neorickettsia risticii (formerly named Ehrlichia risticii) Anaplasmataceae.
  • N. risticii is an obligate parasite with a predilection for blood monocytes and tissue macrophages.

Predisposing factors


  • Enzootic regions, ie Eastern USA.
  • Individual farms, especially alongside major rivers.


  • Ingestion of trematode stages in intermediate hosts such as aquatic insects infected with E. risticii.


  • Caused by N. risticii Anaplasmataceae.
  • Significant regional and seasonal prevalence.
  • Mode of transmission and route of infection unknown:
    • Although the organism is present in the feces of affected horses, these are not directly infective to other horses.
    • Can be experimentally transmitted by the systemic injection of whole blood from infected horses.
    • Transmission is thought to be related to ingestion of N. risticii-infected cercaria or metacercaria of trematodes (flukes):
      • Adult flukes infected with N. risticii have been found infecting fish.
      • Infected cercaria occur in the freshwater snail (Juga yrekaensis).
      • Infected metacercaria occur in a variety of water associated flies, including caddisflies (Trichoptera), mayflies (Ephemeroptera), damselflies (Odonata, Zygoptera), dragonflies (Odonata, Anisoptera) and stoneflies (Plecoptera).
      • Ingestion of cercaria or metacercaria may protect N. risticii from destruction within the stomach.
      • When the infected fly larvae mature into infected adult flies, they can be ingested by horses inadvertently whilst grazing or on fodder, or they can be infected by drinking infected water. Horses that ingest as few as 5 infected insects, live or dead, can contract PHF.
      • To date, only ingestion of caddisflies containing infected metacercariae has been shown to transmit the organism to horses and result in clinical disease.
    • Penetration through skin wounds may be another possible route of infection.
    • Blackflies do not transmit the disease.
    • N. risticii is closely related to other members of the N. sennetsu genogroup.
  • Target cells are the epithelial cells of the small intestine, colonic, mast and epithelial cells, and macrophages → acute enterocolitis.
  • Target organs are the cecum and large colon, and occasionally the jejunum and small colon.
  • The placenta of pregnant mares is the only other target organ: may → abortion between 190-250 days gestation.
  • Dehydration and shock may develop in severe cases secondary to fluid loss.
  • No long-term carrier state exists but a reservoir in the environment or other species is thought to exist. 
  • There is immediate and persistent infection with the organism within monocytes of the peripheral circulation. 
  • Many animals have low-level seropositive antibody levels but clinical disease is usually sporadic and infections often subclinical. 
  • Management factors seem to have little effect on the incidence. 
  • Although no specific long-term carrier state has been proven, the organism can be isolated from peripheral monocytes after resolution of clinical signs; the organism may persist in the longer term in the intestinal wall or fetus. 
  • Some horses may remain immune following recovery for up to 20 months; early immune response is seen within days of infection.


  • Incubation period: 1-3 weeks.
  • Untreated clinical cases last for 5-10 days.


  • The organism has a complex aquatic epizootiology.
  • N. risticii DNA is found in virgulate cercariae released from freshwater operculate snails. The cercariae are associated with trematodes of the family Lecitheodendriidae - common parasites of bats, birds and amphibians in North America.
  • There is a regional (Eastern USA) and seasonal (summer and autumn) prevalence of seropositivity and clinical disease.
  • Most cases occur in July-September in the northern hemisphere (summer months).
  • The disease is, in general, sporadic in enzootic areas both temporally and geographically (usually 1-2 cases per farm) but in some areas farms may have a high prevalence with up to 80% clinical cases and 100% serologically positive.
  • Experimental transmission of the disease via an aquatic insect (caddisfly, Dicosmoecus gulvipes) suggests a probable vector. The caddisfly is most numerous from July to November and would be consumed in high numbers on pasture, drunk from still water, or ingested in stable feed and water after being attracted by stable lights.
  • Other hypothesized modes of transmission:
    • Vectors such as blood-sucking arthropods, but many species of flies, gnats, midges and mosquitoes have been found to be negative.
    • Transmission via liver fluke has been proposed.
    • Direct contact with recovered or ill animals is usually not associated with disease development.
  • The reservoir for the agent is not known:
    • The disease commonly occurs in successive years in the same area suggesting some overwintering mechanism.
    • There may be other sources than horses.
    • Serologic studies have detected antibodies in other species including dogs, pigs, goats, rabbits and non-human primates.
    • Mild clinical signs can occur in primates indicating a zoonotic possibility.


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Further Reading


Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Dutra F, Schuch L F et al (2001) Equine monocytic Ehrlichiosis (Potomac horse fever) in horses in Uruguay and southern Brazil. J Vet Diagn Invest 13 (5), 433-437 PubMed.
  • Chae JoonSeok et al (2000) Infection of aquatic insects with trematode metacercariae carrying Ehrlichia risticii, the cause of Potomac horse fever. J Medical Entomology 37, 619-625 PubMed.
  • Madigan J Eet al (2000) Transmission of Ehrlichia risticii, the agent of Potomac horse fever, using naturally infected aquatic insects and helminth vectors - preliminary report. Equine Vet J 32, 275-279 PubMed.
  • Pusterla N et al (2000) Molecular detection of an Ehrlichia-like agent in rainbow trout (Oncorhynchus mykiss) from northern California. Vet Parasitol 92, 199-207 PubMed.
  • Pusterla N et al (2000) Infection rate of Ehrlichia risticii, the agent of Potomac horse fever, in freshwater stream snails (Juga yrekaensis) from northern California. Vet Parasitol 92, 151-156 PubMed.
  • Mott J et al (1997) Comparison of PCR and culture to the indirect fluorescent-antibody test for diagnosis of Potomac horse fever. J Clin Microbiol 35 (9), 2215-2219 PubMed.
  • McLaughlin B et al (1996) Potomac horse fever in southwestern Ontario. Can Vet J 37 (6), 367-368 PubMed.
  • Shapiro J et al (1995) Potomac horse fever in eastern Ontario. Can Vet J 36 (7), 448 PubMed.
  • Palmer J E et al (1994) Studies on oral transmission of Potomac horse fever. J Vet Intern Med (2), 87-92 PubMed.
  • Palmer J E (1993) Potomac horse fever. Vet Clin North Am Equine Pract (2), 399-410 PubMed.
  • Rikihisa Y et al (1992) Loss of absorptive capacity for sodium and chloride in the colon causes diarrhea in Potomac horse fever. Res Vet Sci 52 (3), 353-362 PubMed.
  • Mulville P (1991) Equine monocytic ehrlichiosis (Potomac horse fever) - a review. Equine Vet J 23 (6), 400-404 PubMed.
  • Friedhoff K T et al (1990) Haemoparasites of equines - impact on international trade of horses. Rev Sci Tech (4), 1187-1194 PubMed.
  • Dutta S K et al (1988) Disease features in horses with induced equine monocytic ehrlichiosis (Potomac horse fever). Am J Vet Res 49 (10), 1747-1751 PubMed.
  • Gordon J C et al (1988) An epidemiological investigation of farms with Potomac horse fever (equine monocytic ehrlichiosis). Acta Vet Scand Suppl 84, 319-322 PubMed.
  • Palmer J E et al (1988) Oral transmission of Ehrlichia risticii resulting in Potomac horse fever. Vet Rec 122 (26), 635 PubMed.
  • Ziemer E L et al (1987) Clinical and haematological variables in ponies with experimentally induced equine ehrlichial colitis (Potomac horse fever). Am J Vet Res 48 (1), 63-67 Europe PMC.
  • Cordes D O et al (1986) Enterocolitis caused by Ehrlichia sp. in the horse (Potomac horse fever). Vet Pathol 23 (4), 471-177 PubMed.
  • Palmer J E et al (1986) Equine ehrlichial colitis (Potomac horse fever) - recognition of the disease in Pennsylvania, New Jersey, New York, Ohio, Idaho, and Connecticut. JAVMA 189 (2), 197-199 PubMed.
  • Whitlock R H (1986) Colitis - differential diagnosis and treatment. Equine Vet J 18 (4), 278-283 PubMed.

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