While the ∆tolC mutants are competent for phagosomal escape, intracellular replication, and dissemination to distal organs during in vivo infection, compared to the wild-type (WT) bacteria, the mutants activate increased caspase-3 cleavage, replicate to lower numbers, and are eventually cleared by the host (21, 23, 41, 43). This evidence concerns the gene CASP3 and infection.