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.