OBJECTIVE: To characterize antibody response in horses with clinical signs of Ehrlichia equi infection. DESIGN: Prospective study. ANIMALS: 13 horses with confirmed acute E equi infection. PROCEDURE: Sequential serum sampling was performed in Connecticut and New York during 1995 and 1996 to identify horses with naturally acquired equine granulocytic ehrlichiosis (EGE). Horses with clinical signs of EGE (i.e., fever without respiratory involvement) were confirmed as having E equi infection by polymerase chain reaction detection of ehrlichial DNA and by a minimum fourfold increase in total antibody titer by indirect fluorescent antibody staining methods. Infection was corroborated by use of DNA sequencing. RESULTS: 11 of 13 horses did not have detectable antibody in serum samples obtained at onset of disease. Seroconversion was evident in samples obtained 19 to 81 days thereafter. Median time to peak antibody response was 46 days after onset and median titer was 1:320. For 11 of 13 horses, antibody titers were < or = 1:40 by 215 days after onset. CLINICAL IMPLICATIONS: E equi was found in horses in the northeastern United States and caused EGE. Concentration of antibodies to E equi increased within 19 to 81 days of disease onset and were low during early weeks of infection. Therefore, antibody detection may be of limited value for early serologic diagnosis. We suggest that disease may develop from a reinfection, and retrospective serologic studies to determine exposure to E equi may reflect a disproportionate number of negative reactions.
OBJECTIVE: To characterize antibody response in horses with clinical signs of Ehrlichia equi infection. DESIGN: Prospective study. ANIMALS: 13 horses with confirmed acute E equi infection. PROCEDURE: Sequential serum sampling was performed in Connecticut and New York during 1995 and 1996 to identify horses with naturally acquired equinegranulocytic ehrlichiosis (EGE). Horses with clinical signs of EGE (i.e., fever without respiratory involvement) were confirmed as having E equi infection by polymerase chain reaction detection of ehrlichial DNA and by a minimum fourfold increase in total antibody titer by indirect fluorescent antibody staining methods. Infection was corroborated by use of DNA sequencing. RESULTS: 11 of 13 horses did not have detectable antibody in serum samples obtained at onset of disease. Seroconversion was evident in samples obtained 19 to 81 days thereafter. Median time to peak antibody response was 46 days after onset and median titer was 1:320. For 11 of 13 horses, antibody titers were < or = 1:40 by 215 days after onset. CLINICAL IMPLICATIONS: E equi was found in horses in the northeastern United States and caused EGE. Concentration of antibodies to E equi increased within 19 to 81 days of disease onset and were low during early weeks of infection. Therefore, antibody detection may be of limited value for early serologic diagnosis. We suggest that disease may develop from a reinfection, and retrospective serologic studies to determine exposure to E equi may reflect a disproportionate number of negative reactions.