Vaccination of pigs with attenuated Lawsonia intracellularis induced acute phase protein responses and primed cell-mediated immunity without reduction in bacterial shedding after challenge.

Background: Lawsonia intracellularis causes porcine proliferative enteropathy and is one of the most economically important diseases in modern pig production worldwide. The Enterisol Ileitis vaccine have been shown to reduce clinical disease and to increase weight gain, however, while the natural infection with L. intracellularis can provide complete protection against re-infection, this has not been achieved by this vaccine. We therefore undertook a detailed characterization of immune responses to L. intracellularis infection in vaccinated pigs (VAC) compared to previously infected pigs (RE) in order to pinpoint immunological determinants of protection.

Results: The VAC pigs shed L. intracellularis to the same extent as non-vaccinated pigs after challenge, however less L. intracellularis in ileum and lymph nodes was seen post mortem. In the RE group, challenge did not lead to L. intracellularis shedding and no challenge bacteria were found post mortem. In both VAC and RE the acute phase haptoglobin response was diminished and L. intracellularis specific IgG responses were delayed and reduced compared to non-vaccinated pigs. On the other hand L. intracellularis specific IFN-γ responses tended to develop faster in the VAC group compared to controls.

Conclusion: Although vaccinated and non-vaccinated pigs shed L. intracellularis at similar levels after challenge, a lower number of intestinal L. intracellularis was observed in the vaccinated pigs at post mortem inspection. This might be due to the observed faster CMI responses upon challenge in vaccinated pigs. Complete protection against infection without L. intracellularis shedding, however, was only seen after a previous infection resulting in IFN-γ production predominantly by CD8(+) and CD4(+) CD8(+) cells. Improved protective vaccines against L. intracellularis should therefore target stimulation of these T cell subsets.