There has been increasing awareness of disease states caused by Ehrlichia species, both in veterinary and human medicine. This newsletter reviews canine and feline ehrlichiosis.

Ehrlichia species are gram negative pleomorphic bacteria of the family Rickettseaceae. Many genera of ticks are vectors for Ehrlichia species, which are transmitted within salivary secretions of infected ticks. Organisms are phagocytized by circulating leukocytes, or enter platelets by endocytosis. In the acute stages of disease, organisms may be visualized within membrane-lined intracytoplasmic vacuoles, called morulae.

Canine ehrlichiosis is classified by the cellular trophism of the infecting organisms. Monocytic morulae represent infection with E. canis, and produce the disease called canine monocytic ehrlichiosis. Neutrophilic morulae are seen with E. equi and E. ewingii infections, and the resulting disease is called canine granulocytic ehrlichiosis. Morulae found within platelets represent infection with E. platys, which causes canine cyclic thrombocytopenia.

Feline ehrlichiosis can occur naturally or be induced experimentally with E. risticii and E. equi., but not E. canis.

CME, caused by infection with E. canis, is transmitted by the brown dog tick Ripicephalus sanguineus. Although this vector is found primarily in the southern United States, CME can be found in all states due to the chronic nature of the disease, and transportation of dogs from endemic to nonendemic areas. Concurrent infection with Babesia canis, Hepatozoon canis, and other Ehrlichia species is possible.

CME is divided into 3 phases of infection: acute, subclinical, and chronic. The acute phase occurs 1-3 weeks after infection, and clinical signs last for 2-4 weeks. During this phase, organisms multiply in circulating lymphocytes and monocytes, and in fixed tissue macrophases within lymph nodes, liver, and spleen. Infected monocytes adhere to the vascular endothelium in multiple organs, inducing a vasculitis. Clinical signs during the acute phase include anorexia, fever, weight loss, dyspnea, lymphadenopathy, splenomegaly, and occasional central nervous system ( CNS) signs. Clinical signs here can mimic Rocky Mountain Spotted Fever (RMSF). Dogs typically recover from the acute phase and become subclinical for months to years. Immunocompetent dogs eliminate the parasite during this phase, and so do not develop the chronic phase. Dogs with ineffective immune responses become chronically infected. Clinical signs during the chronic stage can be mild to severe, and include depression, weight loss, abdominal pain; bleeding episodes such as epistaxis, petechiation and ecchymoses, melena, and hematemesis; ocular lesions of anterior uveitis, chorioretinitis, and retinal hemorrhages; and CNS signs compatible with meningitis. Polyarthritis can also occur in dogs with chronic CME. Death of these dogs is often due to secondary infections from severe leukopenia.

Cytopenias and hyperglobulinemia are the major laboratory abnormalities seen in CME. Thrombocytopenia is the most consistent abnormality, and is present in most dogs through all phases of the disease. Transient mild leukopenia is present during the acute phase, but will often normalize during the subclinical phase. Nonregenerative anemia is encountered in all phases, and Coomb's positive hemolytic anemia can be found.

Hyperglobulinemia and hypoalbuminemia may be evident during the subclinical and chronic phases. Polyclonal gammopathies are most common, but monoclonal gammopathies have also been reported. Lymphocytosis (up to 20,000/µl) has been reported in subclinical and chronic CME.

Bone marrow plasmacytosis is commonly present in all phases of disease. The bone marrow is hypercellular during the acute and subclinical phases of disease, but becomes hypocellular during the chronic stage. Severe pancytopenia or aplastic anemia may be seen in advanced chronic disease, and may not reverse with therapy. Less frequently reported laboratory findings include protein-losing nephropathy, azotemia, and elevated liver enzyme activities. Dogs with the CNS form may have mononuclear pleocytosis and increased protein in CSF. Synovial fluid in dogs with polyarthritis contains high numbers of neutrophils and elevated protein content, consistent with immune-mediated polyarthritis.

E. ewingii and E. equi are the etiologic agents of CGE. Tick transmission is suspected, but a definite vector has not been confirmed. Nonerosive polyarthritis and fever are the most common clinical signs. Laboratory abnormalities associated with CGE include mild anemia, neutropenia, thrombocytopenia, lymphocytosis, monocytosis, and eosinophilia. Synovial fluid analysis reveals nonseptic, suppurative inflammation.