Ruminant Pathophysiology of GI Trichostrongyles

1. Ruminant Pathophysiologyof GI Trichostrongyles

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

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

4. 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

5. 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

6. Physiologic changes seen in G.I. Parasitism • anorexia & reduced food intake • anemia • reduced digestion & absorption

7. 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

8. Pathophysiology -Ostertagiasis • Biochemical changes •  in pH of abomasal contents •  in levels of plasma pepsinogen •  in serum proteins, particularly albumin - hypoalbuminemia

9. 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, > 35 days, recovery phase, adult expulsion

10. 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

11. 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

12. 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

13. 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

15. Ostertagia larva 15 DPI

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

17. Abomasum - lining

18. 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

19. 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

20. Larva emerging

21. Phase II • The nodular effect in the abomasal mucosa is now widespread • The Moroccan leather appearance

22. Abomasal lining

23. Phase IIThree changes • An increase in the abomasal pH • directly attributable to the loss of parietal cells • pH goes from ~ 2 to ~ 7

24. OstertagiasisChanges in abomasal pH

26. Phase IISecond change • Reduced pepsinogen output as a result of loss of zymogen cells

27. Phase IIThird 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

28. 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

29. 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

30. Phase II • Clinical Consequences • impaired digestion • loss of appetite • diarrhea • dehydration • weight loss or poor weight gains

31. 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

32. 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

33. 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

34. 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

37. Haemonchosis in SheepMost common observations • Unexpected deaths • Weakness • Anemia • Hypoproteinemia • Subcutaneous edema • Poor weight gains or weight loss