Wolbachia pipientis is a bacterium that induces cytoplasmic incompatibility (CI), the phenomenon in which infected males are reproductively incompatible with uninfected females. CI spreads in a population of hosts because it reduces the fitness of uninfected females relative to infected females. CI encompasses two steps: modification (mod) of sperm of infected males and rescuing (resc) of these chromosomes by Wolbachia in the egg. Infections associated with CI have mod resc phenotypes. However, mod⁻resc phenotypes also exist; these do not result in CI. Assuming mod/resc phenotypes are properties of the symbiont, theory predicts that mod⁻resc infections can only spread in a host population where a mod resc infection already occurs. A mod⁻resc infection spreads if the cost it imposes on the infected females is lower than the cost inflicted by the resident (mod resc ) infection. Furthermore, introduction of a mod⁻ Wolbachia eventually drives infection to extinction. The uninfected population that results can be recolonized by a CI-causing Wolbachia. Here, we investigated whether variability for induction of CI was present in two Tetranychus urticae populations. In one population all isofemale lines tested were mod⁻. In the other, mod resc and mod⁻resc isofemale lines coexisted. We found no evidence for a cost difference to females expressing either type (mod /⁻). Infections in the two populations could not be distinguished based on sequences of two Wolbachia genes. We consider the possibility that mod⁻ is a host effect through a population dynamics model. A mod⁻ host allele leads to infection extinction in the absence of fecundity differences. Furthermore, the uninfected population that results is immune to reestablishment of the (same) CI-causing Wolbachia.