Ruminant Pathophysiology of GI Trichostrongyles

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Ruminant Pathophysiologyof GI Trichostrongyles
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• Pathophysiology describes the morphological and
  physiological changes occurring in disease.
• Disease induced by the presence of worms in the
  gastrointestinal tract

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Parasitic Disease

• the parasitic phase of the life cycle
• the pathophysiological changes caused by the
  parasite
• the clinical syndrome resulting from these changes

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Factors Determining the Degree of
Pathophysiologic Change

• severity of infection
• species of parasite
• age of host
• nutritional status of the host
• immune status of the host

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Physiologic changes seen in G.I. Parasitism

• Loss of blood ? pale mucous membranes
• diarrhea with loss of water and electrolyte
  disturbances
• poor weight gains or even weight loss
• protein loss

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Physiologic changes seen in G.I. Parasitism

• anorexia reduced food intake
• anemia
• reduced digestion absorption

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Pathophysiology -Ostertagiasis

• Life Cycle of Ostertagia
• Adults mature in 17 to 21 days
• Clinical Signs
• diarrhea
• loss of appetite
• loss of weight or reduced weight gains

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Pathophysiology -Ostertagiasis

• Biochemical changes
• ? in pH of abomasal contents
• ? in levels of plasma pepsinogen
• ? in serum proteins, particularly albumin -
  hypoalbuminemia

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Pathophysiology -Ostertagiasis

• Phases of Disease
• Phase I,days 1-17,gastric glands invaded
• Phase II,days 17 -35, adults emerge from the
  gastric glands
• Phase III, gt 35 days, recovery phase, adult
  expulsion

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Pathophysiology -Ostertagiasis

• There are two important types of cells in the
  gastric glands
• Parietal cells - produce HCl
• Chief cells - produce pepsinogen
• The pepsinogen is activated by the HCl to pepsin
  - the functional hydrolytic enzyme of the abomasum

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Pathophysiology -Ostertagiasis

• The integrity of the epithelium is maintained by
  an area of fusion of the lipo-protein layers of
  the plasma membranes of the adjacent cells. This
  area of fusion is called the Zona Occludens

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Phase I

• Development of larvae in the gastric glands
• This is where all the changes occur as the larvae
  develop and moult twice to become immature adults

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Phase I

• The inflammatory response induced by the growing
  larvae produce a constant erosion of the
  epithelial lining of the gastric glands
• These cells are replaced by immature
  non-secretory epithelial cells

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Ostertagia larva 15 DPI
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Phase I

• At post mortem these parasitized glands can be
  seen as white raised nodules on the surface of
  the abomasum

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Abomasum - lining
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Phase I

• Abomasal pH remains at 2.0 to 2.5
• No diarrhea, infected animals eat well and gain
  weight
• Plasma pepsinogen levels rise slightly
• Significant changes are about to occur

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Phase II

• Begins about 17 days after infection
• with the emergence of the young adults from the
  gastric glands
• this further stretches and erodes the glands
• the worms are large enough that they begin to
  destroy the surrounding cells
• net effect is widespread erosion, destroying many
  functional zymogen and parietal cells

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Larva emerging
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Phase II

• The nodular effect in the abomasal mucosa is now
  widespread
• The Moroccan leather appearance

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Abomasal lining
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Phase II Three changes

• An increase in the abomasal pH
• directly attributable to the loss of parietal
  cells
• pH goes from 2 to 7

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Ostertagiasis Changes in abomasal pH
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Phase II Second change

• Reduced pepsinogen output as a result of loss of
  zymogen cells

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Phase II Third change

• Enhanced permeability of abomasal mucosa, caused
  by
• failure to convert pepsinogen to pepsin
• there is little conversion above pH 5
• failure to denature proteins in preparation for
  digestion
• loss of bacteriostatic effect of low pH

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• Enhanced permeability of the mucosa results from
  the normal secretory epithelium being replaced by
  rapidly dividing immature cells whose tight
  junctions (zona occludens) are not fully formed
• Thus the integrity of the stomach lining is lost
  and molecules can cross in both directions

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Phase II

• Pepsinogen will pass into the circulation from
  the lumen
• thus resulting in high plasma pepsinogen levels
• Plasma proteins, primarily albumin, will be lost
  into the gut
• All via these leaky junctions

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Phase II

• Clinical Consequences
• impaired digestion
• loss of appetite
• diarrhea
• dehydration
• weight loss or poor weight gains

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Phase II

• Impaired digestion
• due primarily to the loss of pepsin activity
• Loss of appetite
• related to numbers
• stimulate production of cholecystokinin
• ? CCK depress appetite
• parasites produce a substance that induces
  inappetence

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Phase II

• Diarrhea and Dehydration
• reported for all g.i. Nematodes, except
  Haemonchus
• follows the increased pH and ? in number of
  bacteria
• there are usually high levels of osmotically
  actives substances (bacteria, undigested protein)
  in the gut
• cause water to move into the intestine

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Phase II

• Weight loss
• up to a 20 weight loss is possible
• this may be due to
• loss of protein through leaky mucosa
• anorexia
• impaired digestion
• this means that energy and protein are not coming
  from food intake and digestion, but from
  mobilization of protein reserves in the body,
  i.e. muscle

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Phase III

• Recovery can come about by
• removing the animals from pasture, from the
  source of infection
• removing the worms with an anthelmintic
• Within a relatively short period of time the
  differentiated status of the mucosa has returned
• clinical signs subside and physiology returns to
  normal

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Haemonchosis in Sheep Most common observations

• Unexpected deaths
• Weakness
• Anemia
• Hypoproteinemia
• Subcutaneous edema
• Poor weight gains or weight loss