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). This evidence concerns the gene C5AR1 and Rickettsiosis.