Secreted effector that irreversibly inactivates host MAP kinases by catalyzing the dephosphorylation of the phosphothreonine residue in the pT-X-pY motif in MAPK2/ERK2, MAPK3/ERK1, and p38, via a beta-elimination reaction leading to a dehydrobutyrine residue. Is also able to remove the phosphate group from phospho-JNK in vitro, but JNK may not be a substrate in vivo. Could help suppress localized pro-inflammatory responses at infection foci in the spleen and liver, and thereby facilitate bacterial growth. kcat is 10.60 sec(-1) with the Erk2 phosphopeptide DHTGFL-pT-E-pY-VATR as substrate. Optimum pH is 8.5. Can be secreted in vitro by either the SPI-1 or SPI-2 type III secretion systems (T3SS). Translocation of the protein into the cytosol of infected macrophages by intracellular bacteria is dependent on the SPI-2 T3SS. Translocated SpvC proteins appear to be distributed evenly in the cytoplasm of infected cells, and neither colocalize with the SCV membrane nor accumulate in the nucleus of infected cells. Strains lacking this gene are attenuated for systemic virulence in mice. Belongs to the phosphothreonine lyase family.