Equine granulocytic ehrlichiosis is an infectious, noncontagious, seasonal disease, seen chiefly in the USA in northern California but also recognized in several other states; it also occurs in Europe and South America. (Also see Potomac Horse Fever.)
Etiology, Epidemiology, and Transmission
The causal riskettsial agent was initially termed Ehrlichia equi, but based on DNA sequence relationships, the organism is now referred to as Anaplasma phagocytophilum. The organism has a wide host range; naturally occurring infections have been seen in horses, burros, dogs, llamas, and rodents. A rickettsia closely resembling A phagocytophilum, the human granulocytic ehrlichiosis (HGE) agent, has been identified in cases of human illness in the upper midwestern and northeastern states in the USA.
A phagocytophilum frequently infects horses in the foothills of northern California. Other states in which clinical infection has been confirmed include Connecticut, Illinois, Arkansas, Washington, Pennsylvania, Colorado, Minnesota, and Florida. It has also been confirmed in British Columbia, Sweden, Great Britain, and South America.
A phagocytophilum resembles the etiologic agents of tickborne fever, bovine petechial fever, and the HGE agent based on morphology, cell tropism, and 16S rRNA gene sequence data. It is present in cytoplasmic vacuoles of neutrophils and occasionally eosinophils during the acute phase. Blood smears stained with Giemsa or Wright-Leishman stains reveal one or more loose aggregates (morulae or inclusion bodies, 1.5–5 μm in diameter) of blue-gray to dark blue coccoid, coccobacillary, or pleomorphic organisms within the cytoplasm of neutrophils.
The infection can be transmitted experimentally to susceptible horses by whole blood from infected horses or from people with HGE. The incubation period is 1–3 wk. Ixodes pacificus (the western black-legged tick) can transmit A phagocytophilum to horses.
The zoonotic risk is unknown at this time. Although horses and people appear to be infected with strains of the same agent, it is believed that human exposure occurs through tick bites, and not by direct transmission from horses to people.
Severity of signs varies with age of the animal and duration of the illness. Signs may be mild. Horses <1 yr old may have a fever only; horses 1–3 yr old develop fever, depression, mild limb edema, and ataxia. Adults exhibit the characteristic signs of fever, partial anorexia, depression, reluctance to move, limb edema, petechiation, and icterus. The fever, which is highest during the first 1–3 days of infection at 103–104°F (39.5–40°C), persists at 102–104°F (39–40°C) for 6–12 days. Signs become more severe over several days. Rarely, myocardial vasculitis may cause transient ventricular arrhythmias. Other clinical presentations for acute infection have included recumbency and severe myopathy. Any concurrent infection (eg, a leg wound or respiratory infection) can be exacerbated. Cytoplasmic inclusion bodies are few during the first 48 hr and increase to 30–40% of circulating neutrophils at days 3–5 of infection. The disease is seasonal in California, occurring in the late fall, winter, and spring.
Gross petechiation, ecchymoses, and edema develop in the subcutis and fascia. Vasculitis is regional, with the subcutis and fascia of the legs predominantly affected.
Demonstration of the characteristic cytoplasmic inclusion bodies in a standard blood smear is diagnostic. However, inclusion bodies are difficult to see in the first day or two of fever. PCR can detect A phagocytophilum DNA in unclotted blood or buffy coat smears. An indirect fluorescent antibody test can detect rising antibody titers to A phagocytophilum. Differential diagnoses include viral encephalitis, primary liver disease, equine infectious anemia, purpura hemorrhagica, and viral arteritis.
Treatment and Control
Oxytetracycline is extremely effective against A phagocytophilum, and tetracycline, 7 mg/kg, IV, sid for 8 days, has eliminated the infection. Penicillin, chloramphenicol, and streptomycin have no inhibitory effect. Horses with severe ataxia and edema may benefit from short-term corticosteroid treatment (dexamethasone, 20 mg, sid for 2–3 days). Recovered horses are solidly immune for ≥2 yr and are not believed to be carriers. A recent finding suggests persistence of infection with some European strains, but further verification is required. Tick control measures are mandatory for control of disease. There is no vaccine.
Last full review/revision March 2012 by John E. Madigan, DVM, MS