The virulence factors of Actinobacillus pleuropneumoniae (App) have been described. The most important among them are: Apx toxins, proteases, lipopolysaccharides (LPS), capsule polysaccharides (CPS), outer membrane proteins and adhesins. All App strains possess CPS, which facilitates their invasion by protecting bacteria from the defense of the host immune system (phagocytosis and lysis). It also prevents the opsonization and removing of bacteria from the respiratory tract. Being a component of the external membrane, LPS induces production of the tumor necrosis factor, interleukins, interferons, activated oxygen compounds, prostaglandins, platelet activating factor and leukotrienes. Proteases released by App have the capacity of IgA cleavage and degradation of hemoglobin. These facilitate mucosal colonization and acquisition of iron ions necessary for the survival of bacteria. Actinobacillus pleuropneumoniae synthesizes four toxins: ApxI, ApxII, ApxIII and ApxIV. They have the ability to form pores in biological membranes and stimulate secretion of proinflammatory mediators. They possess hemolytic and cytotoxic capacities. Apx toxins damage endothelial cells and activate the thrombocytes which result in microclot formation leading to necrosis. Apx toxins are also highly immunogenic. They play a dominant role in the pathogenesis of swine pleuropneumonia. The lack of Apx genes definitely causes a loss of bacterial virulence. Nevertheless, other App structures may also significantly affect the course of App infection.
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