Overview of Equine Granulocytic Ehrlichiosis
Equine granulocytic ehrlichiosis is an infectious, noncontagious, seasonal disease, originally seen in the USA in northern California but now recognized in many states where the tick vector occurs; it is also seen in Europe, Africa, and South America. (Also see Potomac Horse Fever.)
The causal rickettsial agent was initially termed Ehrlichia equi, but based on DNA sequence relationships, the organism is now referred to as Anaplasma phagocytophilum. It is not similar or clinically related to anaplasmosis in cattle. The organism has a wide host range; naturally occurring infections have been seen in horses, burros, dogs, llamas, and rodents. A rickettsia infection in people, the human granulocytic anaplasmosis (HGA) agent, caused by a similar strain as the equine infection, has been identified in cases of human illness in the upper midwestern and northeastern states in the USA and many other countries worldwide.
A phagocytophilum frequently infects horses wherever the tick vector (Ixodes sp) is present. States in which clinical infection has been confirmed include Connecticut, Illinois, Arkansas, Washington, Pennsylvania, Colorado, Minnesota, New York, Massachusetts, 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 (see Tickborne Fever), bovine petechial fever (see Bovine Petechial Fever), and the HGA 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 HGA. The incubation period is 1–3 wk. I pacificus (the western black-legged tick) and I scapularis can transmit A phagocytophilum to horses.
The zoonotic risk of infection to people via horses has not been observed to occur. 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 horse 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.
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.
Oxytetracycline is extremely effective against A phagocytophilum, and systemic treatment with tetracycline, 7 mg/kg/day, IV, for 8 days, has eliminated the infection. Penicillin, chloramphenicol, and streptomycin have no inhibitory effect. Horses treated early in infection for shorter durations may relapse within the following few weeks. Horses with severe ataxia and edema may benefit from short-term corticosteroid treatment (dexamethasone, 20 mg/day, for 2–3 days). The risk of laminitis appears to be very low; no laminitis has occurred in clinical cases or experimental infections. Recovered horses are solidly immune for ≥2 yr and are not believed to be carriers. Persistence of infection has been suggested with some European strains, but further verification is required. Tick control measures are mandatory for control of disease. There is no vaccine.