Construction and characterization of an Actinobacillus pleuropneumoniae serotype 2 mutant lacking the Apx toxin secretion protein genes apxIIIB and apxIIID.

Apx toxins have been identified as important virulence factors of Actinobacillus pleuropneumoniae, the etiologic agent of porcine pleuropneumonia. In some A. pleuropneumoniae serotypes, Apx toxins are secreted by the cell membrane proteins encoded by apxIIIB and apxIIID genes. In an effort to develop a live vaccine strain against A. pleuropneumoniae, we inactivated the apxIIIB and apxIIID genes in A. pleuropneumoniae 1536, a serotype 2 strain, resulting in the DeltaapxIIIB/DapxIIID mutant strain (1536DeltaBDeltaD). Immunization of pigs with live 1536DeltaBDeltaD A. pleuropneumoniae conferred protection against homologous challenge with wild-type A. pleuropneumoniae 1536. Thus, impaired Apx toxin secretion may decrease the virulence of A. pleuropneumoniae and may be an effective strategy for the development of a live-attenuated A. pleuropneumoniae vaccine.