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| **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 |
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| + | * 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]] |