McKellar Q A
Department of Veterinary Pharmacology, University of Glasgow Veterinary School, Bearsden, Scotland, U.K.
Int J Parasitol. 1993 Jul;23(4):451-62. doi: 10.1016/0020-7519(93)90033-u.
Ostertagia spp. affect their hosts in several complex interactions involving structural, biochemical, hormonal, nutritional and immunological mechanisms. Following infection with Ostertagia spp. the specialised secretory function and junctional integrity of gastric epithelial cells is lost. The pH of the abomasal contents is elevated and pepsinogen concentration in the plasma increases. There is a concurrent elevation in the concentration of blood gastrin. The effects may be a response to the physical interaction of parasite with epithelial cells, may be mediated through parasite excretory/secretory products, or by neural mechanisms. There may also be interactions between the responses since elevated abomasal pH stimulates secretion of gastrin. Hormonal changes may also have a role in the increased susceptibility of host to parasite during the periparturient period. Prolactin was considered the most likely hormone candidate although there is now a body of evidence to suggest that elevated prolactin concentrations are not solely responsible. Infection with Ostertagia spp. causes a marked inappetance, negative nitrogen balance and reduction in apparent gross energy digestion. The level of nutrition may also affect the response of the host to the parasites and establishment of O. circumcincta is lower in animals on a low plane of nutrition than those on a high plane. Immunity of Ostertagia spp. develops slowly and once established is manifest following challenge by an initial hypersensitivity response, followed by a cell mediated response and then an antibody response. Parasites may fail to establish or may be expelled from immune animals and if they do establish may be stunted with small vulval flaps and lower biotic potential and may become inhibited at the early fourth stage of development.
