Potomac horse fever

J E PALMER

GENERAL INTRODUCTION: RICKETTSIAL, CHLAMYDIAL AND HAEMOTROPIC MYCOPLASMAL DISEASES

Introduction

Potomac horse fever is an acute enterocolitis of equids caused by a group of closely related intracellular-occurring ehrlichias collectively known as Ehrlichia risticii, first recognized in 1979 along the Potomac River in Maryland, USA.²⁹ Ehrlichia risticii infection in horses has been referred to as Potomac horse fever, equine monocytic ehrlichiosis, and equine ehrlichial colitis. It has been recognized to occur throughout North America. The original term, ‘Potomac horse fever’, was coined by a television reporter covering the original epidemic along the Potomac River. Although it is the least descriptive term, its wide acceptance and its high level of recognition ensures that it will remain the most common term for the disease. Equine ehrlichial colitis is a more descriptive term for the originally described syndrome of fever, anorexia, depression and diarrhoea. Even mild cases not manifesting diarrhoea have evidence of colitis. Equine ehrlichial abortion is an appropriate term for the abortion syndrome caused by E. risticii.

Aetiology

The causative organism of Potomac horse fever is a member of the tribe Ehrlichieae.²³ Based on nucleotide sequence, the genus Ehrlichia is phylogenetically incoherent. Ehrlichia risticii is most closely related to Ehrlichia sennetsu and Neorickettsia helminthoeca (levels of sequence similarity, > 95 per cent).⁵⁵ Although only definitively proven for N. helminthoeca, it is likely that these three organisms also share the unique property of being the only known obligate intracellular bacteria that are transmitted via a helminth vector.

Although E. risticii grows readily in a number of tissue culture lines as long as antimicrobials are not used in the culture media, the continuous murine macrophage cell line P388D1 is frequently used for isolation and propagation. The original Maryland isolate grows readily in this cell line, initially appearing as a cluster of singly occurring elementary bodies followed by the development of initial bodies and later forming morulae (mature inclusions). Heavily infected cells eventually disintegrate, releasing loosely packed groups of organisms held together by cytoplasmic stroma. ⁶⁹

There is considerable biological diversity of E. risticii isolates from clinical cases of Potomac horse fever. Morphologically, some form large cytoplasmic morulae (inclusions), whereas others form small morulae or are individually dispersed in the cytoplasm in murine P388D1 cells.¹¹ Similarly, patterns of antigenic proteins may differ considerably between isolates.¹¹ The sequences of the 16S rRNA genes of isolates may differ between each other more than from the next most closely related Ehrlichia sp., E. sennetsu. It is evident that Potomac horse fever is not caused by one Ehrlichia sp. but rather by several closely related but distinct Ehrlichia spp.⁸³ This antigenic variation of isolates causing the same clinical disease has resulted in incomplete protection from the first generation of vaccines which all originated from the same type strain of E. risticii.

Epidemiology

Potomac horse fever is confined to North America where it has been reported in a wide variety of geographic regions in most USA states and Canada. Surveys in the USA have shown that 16 to 33 per cent of horses with no history of illness have antibodies to E. risticii^{18, 39, 65} and that these are seasonal fluctuations with the highest number of seropositive horses and highest clinical occurrence in July, August and September.^{18, 39} Over a five-year period 70 per cent of 900 clinical cases recorded in Maryland occurred during the same months.⁵³

Clinical disease shows an unusual sporadic pattern with a low prevalence rate (< 5 per cent) on any one farm despite its frequent occurrence in an endemic area. In fact, when multiple cases occur on a large farm, the pattern is also temporally (within the season of the disease) and geographically (among the pastures and barns on the farm) sporadic. Occasionally an epidemic form occurs which is characterized by a high attack rate (20 to 50 per cent) on an individual farm. The disease may be concentrated on a particular farm or race track, resulting in an outbreak simultaneously involving a large number of horses. The reason for this epidemiological variation is unknown.^{45, 48}

The mode of transmission has been extensively studied but significant questions continue to exist. Direct contact transmission does not occur.⁴⁴ The seasonal occurrence leads to early investigation of a possible arthropod vector. Common vectors of other ehrlichial agents are ticks.⁶⁷ The only adult tick found feeding on horses along the Potomac River during the original epidemic in the early 1980s was Dermacentor variabilis.^{9, 72} The larval and nymphal stages of this tick feed on small ground mammals such as the white-footed mouse (Peromyscus leucopus).⁹ Mice are highly susceptible to experimental E. risticii infection.²⁴ However, attempts to transmit E. risticii to horses using field-captured adult ticks (D. variabilis) from endemic farms failed.⁷² Furthermore, larval and nymphal stages of D. variabilis fed on ehrlichaemic mice did not transmit the organism to other mice or to ponies,^{20, 30} and white-footed mice infested with immature D. variabilis and living in endemic areas of the disease have...