Infection of sheep with adult and larval Ostertagia circumcincta: Effects on abomasal pH and serum gastrin and pepsinogen

Abstract

Lawton D. E. B., Reynolds G. W., Hodgkinson S. M., Pomroy W. E. & Simpson H. V. 1996. Infection of sheep with adult and larval Ostertagia circumcincta: effects on abomasal pH and serum gastrin and pepsinogen. International Journal for Parasitology 26: 1063–1074. Infection of sheep with adult or larval O. circumcincta increased serum pepsinogen and gastrin and abomasal pH. The upper limits of the normal range, calculated from over 1000 samples collected from parasite-naive sheep, were set at 2 standard deviations above the mean; these were for serum pepsinogen, 454 mU tyrosine 1 −1; serum gastrin, 64 pM and abomasal pH, 3.26. Five infection regimes were used: sheep previously exposed to field parasitism were infected with 30,000 larvae intraruminally (Group A), while parasite-naive sheep were administered either 50,000 larvae intraruminally (Group B), 150,000 larvae intraruminally followed by a trickle infection of 10,000 larvae thrice weekly from days 21 to 45 (Group C), 150,000 exsheathed larvae via an abomasal cannula (Group D) or 15,000 adult worms via an abomasal cannula (Group E). Whereas the presence of adult worms rapidly increased serum pepsinogen (after 8 h) and abomasal pH and serum gastrin (after about 19 h), the early infective larval stages, regardless of the infection regime, had minimal effects until the abrupt rise in all parameters 5–6 days after infection, Abomasal pH returned to near normal levels when the infections became patent and was not re-elevated by a subsequent trickle infection, whereas serum gastrin and pepsinogen remained high. The initial hypergastrinaemia was coincident with the increased abomasal pH, but was preceded by the increase in serum pepsinogen. In several sheep, serum pepsinogen increased very little during the parasitism, although there were typical effects on abomasal pH and serum gastrin. Serum gastrin was depressed when the abomasal pH exceeded about 5.5. It is suggested that an inhibitor of gastrin release is generated by proliferating abomasal microbes under these conditions and that this is a limitation to the use of elevated serum gastrin in the diagnosis of parasitism in individual sheep.