Haemophilus parasuis is the aetiological agent of Glässer’s disease in swine, which is characterized by fibrinous polyserositis. In addition, this bacterium can be isolated from the upper respiratory tract of healthy pigs. Several strains can be isolated from a single animal and a high number of strains can be detected in a given farm. Isolates of H. parasuis are very heterogeneous and differ in genotypic and phenotypic features, including pathogenic capacity. Several typing methods have been used to classify H. parasuis strains, but their correlation with virulence has been limited. Prevention and control of Glässer’s disease continues to be challenging.
The pathogenicity and virulence factors of H. parasuis are poorly characterized. Genomic comparisons of strains by microarray detected a group of genes differentially present in strains from different clinical origins; the virulence associated trimeric autotransporters (vtaA). The differential distribution of these genes allowed the development of a diagnostic PCR for the identification of potentially virulent strains. In addition, a combination of VtaAs was shown to be a good vaccine candidate. Comparison of strains from different clinical backgrounds also provided information on mechanisms of virulence. Infection by H. parasuis requires adhesion to and invasion of host cells, resistance to phagocytosis by macrophages, resistance to serum complement and induction of inflammation. The expression of specific genes in the heterologous host, Escherichia coli, allowed the identification of 2 trimeric autotransporters involved in phagocytosis resistance, VtaA8 and VtaA9, which were able to delay the phagocytosis by alveolar macrophages. Early in infection, virulent strains do not induce the activation of alveolar macrophages, increasing the chances of survival and multiplication. Evasion of recognition by the immune system could be related to the capacity of some strains to sialilate their surface. Finally, systemic spread induces strong inflammation, which is reflected in production of the characteristic polyserositis.