[9] The major mammalian reservoir for A. phagocytophilum in the eastern United States is the white-footed mouse, Peromyscus leucopus.

Although white-tailed deer and other small mammals harbor A. phagocytophilum, evidence suggests that they are not a reservoir for the strains that cause HGA.

[12] Anaplasma phagocytophilum shares its tick vector with other human pathogens, and about 10% of patients with HGA show serologic evidence of coinfection with Lyme disease, babesiosis, or tick-borne meningoencephalitis.

[12] While it is rare, it is possible for HGA to be transmitted human-to-human via a blood transfusion, in which case it is called Transfusion-Transmitted Anaplasmosis (TTA).

[14] A. phagocytophilum infects the most vast array of living things, including humans, and all around the world.

[14] Anaplasma MSPs can not only cooperate with vertebrates, but also invertebrates, which make these phenotypes evolve faster than others, because they have a lot of selective forces acting on them.

[14] Clinically, HGA is essentially indistinguishable from human monocytic ehrlichiosis, the infection caused by Ehrlichia chaffeensis, and other tick-borne illnesses such as Lyme disease may be suspected.

If anaplasmosis is suspected, treatment should not be delayed while waiting for a definitive laboratory confirmation, as prompt doxycycline therapy has been shown to improve outcomes.

[20] The first outbreak of Human Granulocytic Anaplasmosis (HGA) in the United States began with a patient in early 1990 in Wisconsin.

[12] Although the infectious agent is known to be from the Anaplasma genus, the term "human granulocytic ehrlichiosis" (HGE) has been previously used, reflecting the prior classification of the organism.