Since cydA::Tn mutants did not phenocopy ΔmenD mutants for intracellular survival, we hypothesized that disruption of both cytochrome oxidases might be necessary to completely abolish membrane potential; hence, we generated a double cytochrome oxidase mutant, the ΔcydAB/ΔqoxA strain. This mutant was more attenuated for virulence than either single cytochrome oxidase mutant (Fig. 5E), suggesting at least partial redundancy of the two cytochrome oxidases in L. monocytogenes. Unexpectedly, the double ΔcydAB/ΔqoxA mutants lysed at the same level as single ΔcydAB mutants (Fig. 5F). Although the cytochrome oxidase mutants exhibited moderate intracellular survival defects, our data suggest that noncanonical functions of MK, independently of MK-dependent functions in the ETC, protect L. monocytogenes from cytosolic bacteriolysis.