Contagious porcine pleuropneumoniae is caused by Actinobacillus pleuropneumoniae. The agent isable to adhere to the epithelium of the lower respiratory tract and lung alveoli. Type IV fimbriae play,amongst other virulence factors, an important role in the adhesion phase. Transferrin binding proteinsmediate the uptake of iron by this bacterium, which is necessary for its multiplication. The typicalhemorrhagic to necrotizing lesions in the lungs are primarily caused by the production of Apx toxins.By forming biofilms and producing proteases, Apx toxins and ammonia, A. pleuropneumoniae is ableto circumvent the immune system of the host. Antibodies directed against the lipoprotein PalA mayaggravate the course of infection, and counteract the protective effect of antibodies targeting the Apxtoxins. In-depth knowledge on host-pathogen interactions may lead to the development of efficientvaccines. The protection observed after vaccination with bacterins, such as autologous vaccines, isserotype-specific and variable. This may be attributed to variable levels of PalA in these vaccines. Untilnow, the best results have been obtained using an experimental vaccine containing type IV fimbriae,transferrin binding proteins and Apx toxins.