Pathogenesis of Ostertagiosis

• Presence of Ostertagia ostertagi in the abomasums in sufficient number gives rise to extensive pathological and biochemical changes.

·         The pathological effects are found more when the parasites (immature stage) emerges from the gastric glands (18 days post infection or several months in case of arrested larval development).

Ostertagia

1.      Development of larvae in gastric gland

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Distension of the gland

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Spread to the surrounding cells of gland

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Convert the mucosal gland into rapidly dividing undifferentiated inactive cells

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Decrease production of HCL by parietal cells

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Acidity decreased

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As a result permeability increase

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Plasma protein go to lumen

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Hypo-proteinemia

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Bottle jaw

2.                                       Inactive undifferentiated cells of gastric gland

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New cells try to repair the mucosal layer

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Incompletely line the mucosal layer

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Increase the mucosal permeability to different macromolecule

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Pepsinogen go to blood and plasma protein go to lumen

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Hypo-albuminemia

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3. Decreased acidity cause decreased bacteriostatic capacity.

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Decreased HCL production

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Pepsinogen can not convert into pepsin

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Impairment in protein digestion

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Hypoproteinemia

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Bottle jaw

·         Another more recent theory is that, Zymogen cells secrete increased amount of pepsin directly into        circulation. Clinically, the consequences are reflected as inappetite, weight loss and diarrhea.

·         The precise cause of diarrhea is unknown.

·         In lighter infection, the main effect are sub optimal weight gains.

·         Reduced feed consumption and diarrhea affects the live weight gain.

·         Production loss mainly due to substantial leakage of endogenous protein into GIT        (Hypoprotenemia). It leads to a disturbance in post absorptic nitrogen and energy metabolism due           to increase demands for the synthesis of vital protein (Albumin and immunoglobins) which occur at     the expense of muscle protein and fat deposition.

·         The disturbance are of course influenced by the level of nutrition, exacerated by a low protein       intake and alleviated by a high protein.