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

Nematode larvae developing within the glands cause local loss of parietal c ells and mucous cell hyperplasia whereas reduced acid secretion, increased serum gastrin and pepsinogen concentrations and generalized histological ch anges are associated with parasites in the abomasal lumen. Parietal cells w ith dilated canaliculi and/or degenerative changes typical of necrosis are present soon after the transplantation of adult worms, and abomasal secreti on is also affected. Anaerobic bacteria survive in greater numbers as the p H rises, with bacterial densities becoming similar to ruminal populations a t an abomasal pH of 4 and above. Failure to lyse bacteria may affect advers ely the nutrition of the host. The parasites may initiate the pathophysiolo gy through the release of excretory/secretory (ES) products which either ac t directly on parietal cells or indirectly through enterochromaffin-like (E CL) 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 hypergastrinaem ia. Inflammation increases circulating pepsinogen concentrations and may al so contribute to increased gastrin secretion. Stimulation of mucosal prolif eration and differentiation of parietal cells in the isthmus by the raised serum gastrin levels will be beneficial by generating a new population of a ctive parietal cells and adequate acid secretion. (C) 2000 Harcourt Publish ers Ltd.