Protection of mice against challenge with homologous and heterologous serovars of Actinobacillus pleuropneumoniae after live vaccination

Protective immune responses and the virulence of Actinobacillus pleuropneumoniae (APP) have been attributed, in part, to toxins (Apx) produced by the bacterium. A mutant of the serovar 7 strain HS93 (HS93Tox(-)), lacking the genes encoding the structural toxin ApxA and the post-translational activating protein ApxC, but retaining the genes required for secretion ApxB and ApxD, was isolated and shown to be attenuated in a mouse model. A plasmid vector system was developed and used to express the ApxA gene from within the HS93Tox(-) strain. The resulting strain, HS93Tox(-)/pIG-T1K, expresses the Apr structural protein in a non-activated form. HS93Tox(-)/pIG-T1K was shown to be attenuated in a mouse model and to be capable of inducing Apr-specific antibodies, which were boosted on reinoculation. Live vaccination of mice with HS93Tox(-)/pIG-T1K offered protection against homologous wild-type serovar 7 challenge, and also heterologous challenge with a serovar 1 strain. This is in contrast to vaccination with the HS93Tox(-) strain, which failed to protect mice against a heterologous challenge.