Anaplasma Phagocytophilum

Maiara S Severo; Kimberly D Stephens; Michail Kotsyfakis; Joao HF Pedra


Future Microbiol. 2012;7(6):719-731. 

In This Article


A. phagocytophilum has emerged as an important public health tick-borne pathogen in the USA, Europe and Asia. A. phagocytophilum is a rickettsial pathogen that has evolved a remarkable ability to colonize and replicate inside tick and mammalian cells. A. phagocytophilum survival has been facilitated by the deletion of LPS and peptidoglycan genes, acquisition of a cholesterol uptake pathway to support membrane integrity, expansion of outer-membrane proteins and the presence of a T4SS. When transmitted to humans by a tick bite, this bacterium may cause HGA. While adaptive immune responses direct pathogen clearance, innate immunity contributes to HGA pathology. The underlying mechanisms that control this dichotomy are still elusive and controversies among different groups call for further experimentation. In the mammalian host, A. phagocytophilum subverts neutrophil apoptosis and autophagy, and it also inhibits oxidative and inflammatory responses to promote its persistence. With the same intent, A. phagocytophilum modulates gene expression in the ixodid tick vector, thus increasing tick survival in cold temperatures. This leads to the principle that complex and distinct mechanisms are used by this pathogen to perpetuate its cycle despite having a small genome size and an obligate intracellular life.


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