A staphylococcal complement inhibitor that specifically blocks human C4b2a and C3bBb, interfering with additional C3b deposition through classical, lectin or alternative pathways (Rooijakkers et al., 2005) . Sung et al. (2008) found several genes conserved in all Staphylococcus aureus isolates from humans were variable or missing in one or more animal isolates, including fnbA, fnbB, and coa. Human and murine chlamydial infections depend on different virulence factor genes that coevolved to counter host species specific IFN-γ-mediated effector responses mounted by the particular host species (Nelson et al., 2005) .