Dogs were found to be susceptible to human granulocytotropic Ehrlichia spp. Infection was produced through the bite of Ixodes scapularis Say (= dammini Spielman, Clifford, Piesman & Corwin) nymphs and adults that acquired infection while feeding as larvae on experimentally infected mice. Dogs were also infected by intravenous injection of mouse blood or dog blood from parasitemic donors. Parasites were demonstrable in neutrophils within 8 or 9 d after nymphs began feeding; prepatent periods were longer when infection was induced by adult tick feeding (18 d) or by transfusion of mouse blood (12 d). The shortest prepatent period observed was 5 d in a dog infected by transfusion of blood from a parasitemic dog. Infections in dogs were mild and apparently transient. Mild thrombocytopenia was the most commonly observed abnormality. Parasites could be detected by light microscopy during the acute phase of infection (4 or 5 d) and parasite DNA by polymerase chain reaction as early as 5 d after exposure but not at 6-9 d after morulae were first observed in neutrophils. Likewise, dog blood was infectious for mice at 2 d but not at 25 d, and for dogs at 3 d but not at 13 d after morulae were first observed in neutrophils. Seroconversion occurred as early as 11 d after onset of tick feeding and persisted until dogs were euthanatized. Gross and histopathologic lesions were similar to those observed in dogs with E. canis (Donatien & Lestoquard), E. chaffeensis Anderson, Dawson & Wilson, and E. ewingii Anderson, Greene, Jones & Dawson infections but were generally milder than any of these. The moderate enlargement of lymphoid organs observed grossly was reflected histologically as mild to moderate reactive hyperplasia, which was largely follicular (B cell).