By inactivating fXII, CpaA may attenuate important antimicrobial defense mechanisms such as intravascular thrombus formation, thus allowing <i>A. baumannii</i> to disseminate.<b>IMPORTANCE</b> Ventilator-associated pneumonia and catheter-related bacteremia are the most common and severe infections caused by <i>Acinetobacter baumannii</i> Besides the capsule, lipopolysaccharides, and the outer membrane porin OmpA, little is known about the contribution of secreted proteins to <i>A. baumannii</i> survival <i>in vivo</i> Here we focus on CpaA, a potentially recently acquired virulence factor that inhibits blood coagulation <i>in vitro</i> We identify coagulation factor XII as a target of CpaA, map the cleavage sites, and show that glycosylation is a prerequisite for CpaA-mediated inactivation of factor XII.