E. platys is the causative agent of CCT. Tick transmission is presumed, but an actual vector has not been identified. E. platys organisms enter platelets and reproduce by binary fission, forming morulae within parasitized platelets. Platelets counts decline precipitously to about 20,000-50,000/µl over a 3-4 day period, parasitemia diminishes, and platelet counts return to normal within another 3-4 days. Subsequent parasitemic and thrombocytopenic episodes occur at 10-14 day intervals. The degree of parasitemia and thrombocytopenia diminishes with time, and eventually hematologic changes resolve. Naturally occurring and experimental infections result in few clinical signs, unless hemostasis is compromised by some other problem. Mild nonregenerative anemia, leukopenia, hypoalbuminemia, and hyperglobulinemia have been reported with experimental E. platys infections. Coinfections with E. canis and Babesia canis are common, which may aggravate clinical signs.

Feline ehrlichiosis is an emerging infectious disease recognized in Europe, Africa and North America. It has been documented with E. risticii, the etiologic agent of Potomac Horse Fever, and E. equi. Clinical signs of disease include anorexia, depression, fever, weight loss, lymphadenopathy, and diarrhea. Laboratory abnormalities include anemia, neutropenia, thrombocytopenia, and hyperglobulinemia. Serologic testing of cats with clinical signs of ehrlichiosis over a 7 year period at Colorado State University revealed antibodies to E. canis and E. risticii in 69 of 340 (20%). Of 12 cats given a presumptive diagnosis of ehrlichiosis, E. canis titers were consistently higher than E. risticii titers, leading to speculation that the organism involved was closely related to E. canis.

The historical, clinical and clinical pathologic findings of canine ehrlichiosis must be differentiated from other infectious diseases (eg., RMSF, gram negative sepsis), immune-mediated diseases (eg., ITP, IMHA, immune-mediated polyarthritis, aplastic anemia), and neoplastic diseases (eg., myeloma, chronic lymphocytic leukemia, myelophthisis). Serologic testing using the indirect immunofluorescent assay (IFA), is an important adjunct to the diagnosis of ehrlichiosis. The IFA test for E. canis is very sensitive and specific, though cross reactivity has been reported between E. canis and E. ewingii, and between E. canis and Neorickettsia helminthoeca, the etiologic agent of salmon poisoning disease. Serologic cross-reaction has not been reported with Rickettsia rickettsii or Babesia canis. In acute ehrlichiosis, dogs will be seronegative during the initial 3 weeks of disease. Documentation of seroconversion is necessary to confirm a diagnosis. Serum samples from initial presentation, and from about 3 weeks later, should demonstrate a 4-fold increase in titer. Positive titers indicate infection, since these persist until treatment is given. Infection with E. canis does not confer protective immunity.

Antirickettsial agents recommended for the treatment of ehrlichiosis include tetracycline (22 mg/kg tid for 14-21 days), doxycycline (10 mg/kd sid or divided bid for 10-14 days), chloramphenicol (20 mg/kg tid for 14 days) and imidocarb diproprionate (5 mg/kg IM, 2 injections at 14 day intervals). In CME, there is controversy regarding length of therapy, with some authors advising 6-12 weeks of antibiotic therapy. Additional supportive therapy, including fluids, blood transfusions, and short-term immunosuppressive glucocorticoids, may be required. In dogs with severe chronic CME, response to treatment may be minimal, and establishing success can be challenging. Rapid clinical improvement is frequently noted, but antibody titers may persist for months to years. Complete hematologic recovery may take up to 1 year. Progressive decrease in gamma globulin level coincides with elimination of infection. Detection of E. canis DNA in peripheral blood samples using PCR has also been used to evaluate treatment success.

References: Lappin, Proc 11th ACVIM Forum, Washington, DC, 1993, p 447; Kordick et al, In Current Vet Therapy XII (Kirk and Bonagura, eds.), WB Saunders, Philadelphia, 1995, p 287; Stubbs et al, Proc 16th ACVIM Forum, San Diego, CA 1998, p 720.