Studies of representative members, primarily Anaplasma phagocytophilum and Ehrlichia chaffeensis, have shed much light on the exquisite mechanisms by which Anaplasmataceae pathogens manipulate their host cells, and are discussed following overviews of the diseases that they cause, their notable genomic features, and their infection and developmental cycles. The secretion of type IV secretion system (T4SS) effectors into host cells is critical for survival of facultative and obligate intracellular bacterial pathogens. Apoptosis is initiated by enzymatic caspases, which are inactive until they are activated by apoptotic signaling pathways. The A. phagocytophilum-occupied vacuole (ApV) excludes fusion with secretory vesicles and specific granules harboring NADPH oxidase and proteolytic enzymes. Preferentially recruiting Rab GTPases that are predominantly found on slow recycling endosomes potentially provides A. phagocytophilum with four intracellular survival advantages. First, A. phagocytophilum is auxotrophic for 16 amino acids. Second, the mechanism by which A. phagocytophilum obtains LDL endocytic pathway-derived cholesterol for incorporation into its cell wall is unknown. Third, continual delivery of recycling endosomes to the ApV would conceivably provide an unlimited supply of host membrane material to allow for expansion of the AVM, which would be necessary to accommodate growing intravacuolar bacterial populations. Fourth, by coating the AVM with recycling endosome- associated Rab GTPases, the ApV camouflages itself as a recycling endosome, which is likely a means by which it protects itself from fusing with lysosomes. Finally, much of what authors know regarding Anaplasmataceae pathogen manipulation of host cell functions is derived from studies of A. phagocytophilum and E. chaffeensis.