Secreted effector that hijacks host cell SUMOylation during A.phagocytophilum infection and is important for the pathogen's intracellular survival. Localizes to the A.phagocytophilum-occupied vacuolar membrane (AVM) (PubMed:20212090). Potentially traverses the AVM 3 or fewer times by means of the 3 bilobed hydrophobic alpha-helical domains that are predicted to be in each direct repeat (PubMed:20212090). Colocalizes with SUMO2/3 on the AVM and in the host cytosol throughout the infection cycle (PubMed:25308709). Only late during the infection cycle AmpA colocalizes with SUMO1, which terminally caps poly-SUMO2/3 chains (PubMed:25308709). Is probably not secreted via the type IV secretion system (T4SS) (PubMed:20212090). Is induced within the initial hours of A.phagocytophilum infection and is strongly expressed during the bacterium's intracellular replication phase. Polysumoylated during infection on at least two lysine residues, in the N- and C-terminal section. SUMO2/3 modification of AmpA throughout the infection cycle is likely critical for bacterial intracellular survival, while terminal SUMO1 conjugation of AmpA may promote a late-stage infection cycle event. Only a small portion of the available AmpA pool is actually SUMOylated at any given time. Pharmacologically inhibiting sumoylation in infected cells significantly reduces the bacterial load.