Author, Donkey, Bureaucrats, Administrators
53,803
edits
Changes
no edit summary
**Unlikely to require treatment at housing
**Unlikely to require treatment at housing
*Cattle exposed to medium/high challenge in late autumn or animals of unknown origin
*Cattle exposed to medium/high challenge in late autumn or animals of unknown origin
**Likely to require treatment at housing using an anthelmintic active against hypobiotic larvae[[Category:Cattle_Nematodes]]
**Likely to require treatment at housing using an anthelmintic active against hypobiotic larvae
* Caused by ''Ostertagia ostertagi''.
** Economically and epidemiologically the most important gastro-intestinal parasite in the bovine in Britain.
===Pathogenesis===
====Type I Ostertagiasis====
* ''Ostertagia ostertagi'' is ingested by calves in their first year at grass.
* The parasites colonise the gastric glands of the fundus and pylorus.
** 17-21 days after ingestion, the parasites reach maturity and emerge from the gastric glands.
* Emergence in sufficient numbers causes extensive pathological changes- [[Gastritis, Chronic|chronic gastritis]]. [[Image:ostertagiasis.jpg|thumb|right|150px|Ostertagiasis (Courtesy of BioMed Image Archive)]]
** The major change is reduction in the functional gastric gland mass
*** Parietal cells and zymogen cells are replaced by rapidly dividing undifferentiated, non-functional cells.
*** A thickened, hyperplastic, non-functional gastric mucosa is formed.
* A non-functional gastric mucosa means that:
*# [[The Abomasum - Anatomy & Physiology|Abomasal]] pH is raised from 2 to 7.
*#* Pepsinogen activation to pesin fails above pH 5.
*#* Proteins are not denatured.
*#* Bacteriostasis fails, increasing the [[The Abomasum - Anatomy & Physiology|abomasal]] bacterial population.
*# Pepsinogen outputis reduced.
*# The bowel wall becomes more permeable to macromolecules.
*#* The junctions between the rapidly dividing undifferentiated cells are not completely formed
*#** Large molecules, particularly proteins, can pass through.
*#** Inactivated pepsinogen passes through the incomplete junctions to the circulation, raising plasma pepsinogen levels
*#** Hypoalbuminaemia occurs, indicating of loss of plasma proteins into the gut lumen.
* Impaired digestion and diarrhoea is the result of these changes, but Ostertagiais does not usually cause an acute problem.
====Type II Ostertagiasis====
* ''Ostertagia ostertagi'' may become hypobiotic in the Autumn.
* In heavy infestations lots of hypobiotic larvae reactivate in the Spring
** Produce severe acute gastritis (fibrinous or haemorrhagic), and even sudden death.
===Pathology===
* Lesions are typical.
** Raised hyperplastic nodules, 2-3mm in diameter with a central orifice (the opening to the parasitized gastric gland).
** In heavy infestations the nodules overlap giving the mucosa a “moroccan leather” or “crazy paving” appearance.
* Following emergence of the parasites, the surface epithelium necrotises and sloughs, and a grey-white diphtheritic membrane of protein, polymorphs and clumps of bacteria forms.
[[Category:Cattle_Nematodes]]
[[Category:Stomach_and_Abomasum_-_Parasitic_Pathology]]