Seropositive, clinically healthy dogs
Animals from endemic areas are often exposed to A. phagocytophilum, and 40% or more of dogs in these areas may be seropositive.9 However, since the morbidity is low, it appears that many animals may have antibodies to A. phagocytophilum without having any concurrent evidence of clinical disease. Since persistent infection in clinically healthy dogs has been
demonstrated,6,7,15 it is likely that a portion of the seropositive animals are chronically infected carriers of the organism. Experimentally,
chronically infected carriers did not have any hematologic abnormalities,7 and, thus far, it appears that seropositive animals with no clinical evidence of disease are hematologically normal. Incidents
of chronically infected carriers later developing clinical disease have not been clearly documented.
The cyclic appearance of clinical cases that coincide with tick season indicates that canine anaplasmosis is an acute disease
that occurs in dogs a week or two after organism inoculation by ticks.5,12 Because chronic infection has not been directly related to clinical disease and because a therapeutic regimen effective
in clearing the organism from an infected animal has not been established, treating clinically healthy, seropositive animals
is of questionable benefit. However, a seropositive reaction to A. phagocytophilum in a clinically healthy dog should not be disregarded. At a minimum, implement an aggressive tick-control program designed
to minimize exposure to ticks, and, hence, to other tick-borne diseases. It is clear that coinfection with two or more tick-borne
agents is common and that dogs coinfected with B. burgdorferi and A. phagocytophilum are nearly two times more likely to develop clinical disease than are dogs infected with either agent alone.9 There is also some concern that chronically infected carriers could be adversely affected by therapeutic agents that compromise
the immune system or by a concurrent illness that might alter an animal's immune status. The administration of immunosuppressive
doses of corticosteroids to infected, asymptomatic dogs resulted in the reappearance of bacteremia, although the animals remained
ANAPLASMA PLATYS INFECTION
Anaplasma platys (formerly Ehrlichia platys) is the causative agent of infectious cyclic thrombocytopenia in dogs.
Anaplasma platys was first reported in the United States in 1978 and has since been recognized to have a worldwide distribution, being reported
in many European, Asian, and South American countries.18 This agent is unique—it is the only intracellular infectious agent described in people or animals to specifically infect
platelets (Figure 4).
4. Two large, dark-blue-staining Anaplasma platys morulae in a circulating platelet from an infected dog. The normal, smaller, pink-staining platelet granules are also observed
in the cytoplasm of the infected platelet (Wright's-Giemsa; 100X).
Tick vector and mammalian hosts
The natural mode of disease transmission has not been conclusively determined, but A. platys DNA has been amplified from Rhipicephalus and Dermacentor species ticks.19,20 Therefore, tick transmission is highly suspected. Dogs are by far the most common mammalian host, although rare reports
of infections in cats, impalas, and sheep have been documented outside the United States.21,22