• Tick-borne diseases of dogs and cats causing vasculitis leading to multisystemic dysfunction often characterized by thrombocytopenia and hyperglobulinemia.
     • Recently reclassified – moved from the family Rickettsiaceae to the Anaplasmataceae.

Overview of etiologic agents
     • 3 pathogenic genera: Ehrlichia, Anaplasma, and Neorickettsia; we are concerned here with the first 2.
     • Ehrlichia spp. – divided into 3 groups:-
     • E. canis – intracyctoplasmic morulae found in circulating leukocytes.
     • E. chaffeensis – like E. canis, found in mononuclear cells; mainly a human pathogen but can causes disease in dog.
     • E. ewingii – canine granulocytic ehrlichiosis; like A. phagocytophila, infects granulocytic cells in dogs, but differs in geographic distribution (mainly found in southeastern and south-central USA).
     • Anaplasma spp. – 2 organisms of importance:-
           o phagocytophila – previously E. equi, E. phagocytophila, and HGE; infects mainly horses; infects granulocytic cells of dogs; serologic cross reactivity occurs with other Anaplasma spp. but uncommon with Ehrlichia spp.; same distribution as Lyme dz (same tick vector) - northeastern and upper Midwestern states, and California. No serologic cross reactivity with Borrelia, Bartonella or Rickettsia rickettsii.
           o platys – previously E. platys; tropism for platelets; does not share serologic cross reactivity with E. canis.
In this presentation, we will focus on E. canis and A. phagocytophilum.

Pathogenesis
Ehrlichia canis – Canine monocytotrophic ehrlichiosis.
     • Rhipicephalus sanguineus (brown dog tick) and occasionally Dermacentor variabilis transmits disease to dogs in saliva.
     • Incubation period – 1 to 3 weeks.
     • Severity and outcome of disease depends on infecting strain and dose of inoculum; German shepherd dogs seem more clinically affected
     • After infection – organisms multiply in macrophages then spread throughout hose:-
     • 3 stages of disease:-
           o Acute – spreads from bite site to the spleen, liver, and lymph nodes (causes organomegaly); then subclinical with mild thrombocytopenia; mainly endothelial cells affected; vasculitis; anti-platelet antibodies exacerbates thrombocytopenia; variable leukopenia; mild anemia; severity depends on organism.
           o Subclinical – organism persists; antibody response increases (hyperglobulinemia); thrombocytopenia persists.
           o Chronic – impaired bone marrow production (platelets, erythroid suppression); marrow hypercellular with plasma cells.
           o Multisystemic disease – including bleeding tendencies (thrombocytopenia and vasculitis), lymphadenopathy, splenomegaly, CNS, ocular (anterior uveitis), and lung.
Anaplasma phagocytophilum – Canine granulocytic anaplasmosis.
     • Ixodes spp (I. scapularis in northeast, I. pacificus in California). transmit Dz in saliva
     • Incubation period – 1to 2 weeks (much shorter than for Lyme disease).
     • Reservoir hosts - white-footed mouse, chipmunks, wood rats, voles, and white-tailed deer; various bird species are also implicated in spread of disease.
     • After infection, organism binds and enters mainly neutrophils – multiply (morula) – rupture cell to release more organisms which infect more cells.
     • How organisms cause disease is not known; after ~ 10 days of infection, cellular and humoral immune mechanisms control infection.
     • Clinical findings are virtually always associated with acute disease period during the bacteremic phase – chronic disease has not been reported.
     • Mild illness typified by fever, lethargy and thrombocytopenia; polyarthritis occurs but rare in comparison to infection with E. ewingii; most dogs present in the spring, early summer and again in the fall.