11:02:00 PM
- 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
¯
Distension of the gland
¯
Spread to the surrounding cells of
gland
¯
Convert the mucosal gland into
rapidly dividing undifferentiated inactive cells
¯
Decrease production of HCL by
parietal cells
¯
Acidity decreased
¯
As a result permeability increase
¯
Plasma protein go to lumen
¯
Hypo-proteinemia
¯
Bottle jaw
2. Inactive
undifferentiated cells of gastric gland
¯
New cells try to repair the mucosal
layer
¯
Incompletely line the mucosal layer
¯
Increase the mucosal permeability
to different macromolecule
¯
Pepsinogen go to blood and plasma
protein go to lumen
¯
Hypo-albuminemia
¯
Bottle jaw
3.
Decreased acidity cause decreased bacteriostatic capacity.
4.
Decreased HCL production
¯
Pepsinogen can not convert into
pepsin
¯
Impairment in protein digestion
¯
Hypoproteinemia
¯
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.
·
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.
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