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
Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Emerg Infect Dis. 2005 Dec;11(12):1828-34. 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.
人粒细胞无形体病是由嗜吞噬细胞无形体引起的一种通过蜱传播的嗜中性粒细胞立克次体感染。尽管该病原体在1932年被定义为一种兽医病原体,但人类疾病直到1990年才首次被确认。自1990年以来,美国的病例显著增加,目前在欧洲也发现了感染病例。较高的国际血清阳性率表明感染广泛存在但未被认识到。嗜吞噬细胞无形体的生态位是嗜中性粒细胞,这表明该病原体具有独特的适应性和致病机制。深入研究已证明其与宿主细胞信号转导以及可能与真核转录存在相互作用。这种相互作用导致嗜中性粒细胞功能的改变,并可能引发免疫病理变化、严重疾病和机会性感染。需要更多的研究来确定免疫学和致病机制,并了解为何某些人会发展为严重疾病,以及为何某些动物会成为长期的许可储存宿主。