Pathogenesis of proliferative enteropathy caused by Lawsonia intracellularis

Abstract

Proliferative enteropathy is a common infectious disease affecting pigs, horses and other animals; it is caused by Lawsonia intracellularis, an obligately intracellular bacterium. Lawsonia infection causes a distinctive pathological change, characterized by a rugose thickening of the intestinal mucosa, due to the adenomatous proliferation of immature intestinal crypt epithelial cells, with local depletion of goblet and enteroendocrine cells.

The disease has a low infectious dose; transmission occurs readily between young animals via oral contact with infected faecal material derived from other infected animals and the environment.

Intracellular L. intracellularis infection causes the transient amplifying epithelial cells in the crypts of the aboral intestine to fail to differentiate, leading to the distinctive adenomatous proliferation. This differentiation failure reflects Lawsonia's ability to disrupt paracrine crosstalk signalling between epithelial cells and the layers of supporting cells surrounding each crypt. A working hypothesis is that the intracellular infection of transient amplifying cells in the crypt by Lawsonia disrupts the quiescence activity of bone morphogenetic protein at the crypt–villus junction zone.

Lawsonia infection is a rare example of host tissue hyperplasia due to a reaction induced by a bacterium.