C3 and Rickettsiosis: While complement activation is readily inducible in normal mouse serum (NMS) during Rickettsia infection, C3-deficient mouse serum (C3−/− MS) is incapable of generating complement effector mechanisms, including forming the membrane attack complex, opsonizing bacteria, or, importantly, producing the proinflammatory anaphylatoxin peptides C3a and C5a (24).