Human granulocytic anaplasmosis and Anaplasma phagocytophilum

• Published in: Emerging infectious diseases Vol. 11; no. 12; pp. 1828 - 1834
• Main Authors: Dumler, J Stephen, Choi, Kyoung-Seong, Garcia-Garcia, Jose Carlos, Barat, Nicole S, Scorpio, Diana G, Garyu, Justin W, Grab, Dennis J, Bakken, Johan S
• Format: Journal Article
• Language: English
• Published: United States U.S. National Center for Infectious Diseases 01-12-2005; Centers for Disease Control and Prevention
• Subjects: Anaplasma phagocytophilum; Anaplasma phagocytophilum - classification; Anaplasma phagocytophilum - genetics; Anaplasma phagocytophilum - pathogenicity; Anaplasmataceae; Animals; Care and treatment; Communicable Diseases; Diagnosis; Ehrlichiosis - epidemiology; Ehrlichiosis - immunology; Ehrlichiosis - microbiology; Emerging; Humans; Neutrophils - immunology; Neutrophils - microbiology; Phylogeny; Rickettsial diseases; Rickettsiales; Risk factors; Tickborne Diseases; United States
• ISSN: 1080-6040; 1080-6059
• DOI: 10.3201/eid1112.050898

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.