Pathophysiology of abomasal parasitism: is the host or parasite responsible?

Nematode larvae developing within the glands cause local loss of parietal cells and mucous cell hyperplasia whereas reduced acid secretion, increased serum gastrin and pepsinogen concentrations and generalized histological changes are associated with parasites in the abomasal lumen. Parietal cells with dilated canaliculi and/or degenerative changes typical of necrosis are present soon after the transplantation of adult worms, and abomasal secretion is also affected. Anaerobic bacteria survive in greater numbers as the pH rises, with bacterial densities becoming similar to ruminal populations at an abomasal pH of 4 and above. Failure to lyse bacteria may affect adversely the nutrition of the host. The parasites may initiate the pathophysiology through the release of excretory/secretory (ES) products which either act directly on parietal cells or indirectly through enterochromaffin-like (ECL) cells by provoking inflammation or by disrupting the protective mucosal defence system. Parietal cell dysfunction is proposed as a key event which leads to loss of mature chief cells and mucous cell hyperplasia, as well as hypergastrinaemia. Inflammation increases circulating pepsinogen concentrations and may also contribute to increased gastrin secretion. Stimulation of mucosal proliferation and differentiation of parietal cells in the isthmus by the raised serum gastrin levels will be beneficial by generating a new population of active parietal cells and adequate acid secretion.