Human granulocytic anaplasmosis and Anaplasma phagocytophilum

Abstract

Human granulocytic anaplasmosis is a tickborne rickettsial infection of neutrophils caused by Anaplasma phagocytophilum. The human disease was first identified in 1990, although the pathogen was defined as a veterinary agent in 1932. Since 1990, US cases have markedly increased, and infections are now recognized in Europe. A high international seroprevalence suggests infection is widespread but unrecognized. The niche for A. phagocytophilum, the neutrophil, indicates that the pathogen has unique adaptations and pathogenetic mechanisms. Intensive study has demonstrated interactions with host-cell signal transduction and possibly eukaryotic transcription. This interaction leads to permutations of neutrophil function and could permit immunopathologic changes, severe disease, and opportunistic infections. More study is needed to define the immunology and pathogenetic mechanisms and to understand why severe disease develops in some persons and why some animals become long-term permissive reservoir hosts.

Figure 1

Anaplasma phagocytophilum in human peripheral blood band neutrophil (A. Wright stain, original magnification ×1,000), in THP-1 myelomonocytic cell culture (B, LeukoStat stain, original magnification, ×400), in neutrophils infiltrating human spleen (C, immunohistochemistry with hematoxylin counterstain; original magnification ×100), and ultrastructure by transmission electron microscopy in HL-60 cell culture (D; courtesy of V. Popov; original magnification ×21,960).

Figure 2

Current phylogeny and taxonomic classification of genera in the family Anaplasmataceae. The distance bar represents substitutions per 1,000 basepairs. E. coli, Escerichia coli.