1. Giardia duodenalis (G. lamblia; G. intestinalis)
Giardiasis.
Most distinctive of the flagellates.
Has both a trophozoite and cyst stage.

2. Giardia duodenalis Trophozoite
Trophozoites are binucleated (looks like a face) μm.

3. Giardia duodenalis Trophozoite
Trophozoites are binucleated (looks like a face) μm.
Ventral surface bears adhesive disk to adhere to surface of intestinal cell.

4. Giardia duodenalis Trophozoite
Trophozoites are binucleated (looks like a face) μm.
Ventral surface bears adhesive disk to adhere to surface of intestinal cell.
8 flagella (2 anterior, 2 posterior, 2 ventral, and 2 caudal) - all arise from kinetosome.

5. Giardia duodenalis Trophozoite
Trophozoites are binucleated (looks like a face) μm.
Ventral surface bears adhesive disk to adhere to surface of intestinal cell.
8 flagella (2 anterior, 2 posterior, 2 ventral, and 2 caudal) - all arise from kinetosome.
Median bodies occur behind adhesive disk - function is unknown.

6. Giardia duodenalis Trophozoite
Light microscope photos of trophozoites

7. Giardia duodenalis
Lives in the upper part of the small intestine (duodenum, jejunum, and upper ileum).
Here the trophozoites attach to the epithelial cells.

8. Giardia duodenalis Trophozoite
ventral dorsal
Scanning EM view of trophozoite surface showing the adhesive disk.

9. Feeds on mucous that forms in response to irritation.

10. Also absorbs vitamins and amino acids.
Feeds on mucous that forms in response to irritation.
Also absorbs vitamins and amino acids.

11. Interferes with absorption in host especially lipids.
Feeds on mucous that forms in response to irritation.
Also absorbs vitamins and amino acids.
Interferes with absorption in host especially lipids.

12. Giardia can also interfere with vitamin/nutrient absorption.
Feeds on mucous that forms in response to irritation.
Also absorbs vitamins and amino acids.
Interferes with absorption in host especially lipids.
Giardia can also interfere with vitamin/nutrient absorption.
Vitamin A vision
Vitamin D rickets
Both of these are due to long standing infections.

13. Cyst of Giardia duodenalis
The cyst forms as trophozoites become dehydrated when they pass through the large intestine.

14. Cyst of Giardia duodenalis
The cyst forms as trophozoites become dehydrated when they pass through the large intestine.
Morphology:
ovoid in shape; 8-12 µm long x 7-10 µm wide
thin cyst wall.
Four nuclei present, often concentrated at one end.
Flagella shorten and are retracted within cyst.
Axonemes provide internal support.

15. Cyst of Giardia duodenalis
Cyst may remain viable in the external environment (usually water) for many months.

16. Cyst of Giardia duodenalis
Cyst may remain viable in the external environment (usually water) for many months.
-14 billion cysts can be passed in 1 stool sample
-Moderate infections: 300 million cysts.

17. Cyst of Giardia duodenalis

18. Symptoms
Range from none abdominal discomfort causing acute or chronic diarrhea and other GI signs.
Gray, greasy, voluminous malodorous diarrhea!
Flatulence.

19. Giardia duodenalis
Giardia trophs are attracted to bile salts: so sometimes you can get infections in bile ducts and gall bladder, causing jaundice and colic.
This is irritating but not life threatening infection like E. histolytica.

20. Pathogenesis and Pathology
Nutrient malabsorption and physical blockage and damage to microvilli.
Trophs attach to small intestine cause damage (mechanical and toxins).

24. Giardia trophozoite
Trophozoite attaches to surface of epithelial cells with its adhesive disk.

25. Pathogenesis and Pathology
1) Fat/CHO digestion decreases and causes maldigestion.

26. Pathogenesis and Pathology
1) Fat/CHO digestion decreases and causes maldigestion.
2) Absorption decreases due to villus blunting causing malabsorption.

27. Pathogenesis and Pathology
1) Fat/CHO digestion decreases and causes maldigestion.
2) Absorption decreases due to villus blunting causing malabsorption.
3) Malabsorption and maldigestion causes diarrhea.

28. Pathogenesis and Pathology
4) Physical damage: clubbing of villi; decreases villus-to-crypt ratio; brush borders of cells are irregular.

29. Epidemiology
Get infected by ingesting cysts through contaminated water.

30. Epidemiology Most common intestinal flagellate of people.
Get infected by ingesting cysts through contaminated water.
Most common intestinal flagellate of people.

31. Epidemiology
Get infected by ingesting cysts through contaminated water.
Most common intestinal flagellate of people.
World wide distribution; prevalence ranges from %.

32. Epidemiology Reservoir hosts can play a significant role.
Get infected by ingesting cysts through contaminated water.
Most common intestinal flagellate of people.
World wide distribution; prevalence ranges from %.
Reservoir hosts can play a significant role.

33. Reservoir Hosts
Transmission from animals to humans is controversial; dependent on strain or type involved.

34. Human Infections
There are hot spots: Vacations and Travels Camping.

35. Human Infections
There are hot spots: Vacations and Travels Camping.
Colorado ski resorts are notorious for outbreaks drinking from Mountain springs, washing utensils/drinking water that is not treated.

36. Human Infections Day care centers.
There are hot spots: Vacations and Travels Camping.
Colorado ski resorts are notorious for outbreaks drinking from Mountain springs, washing utensils/drinking water that is not treated.
Day care centers.

37. Diagnosis Trophs in diarrheic feces; cysts in formed feces.
At least 3 exams (one every other day) before judge negative.
ELISA tests: detect soluble antigen.
PCR

38. Enzyme-linked immunosorbent assay

39. Enzyme-linked immunosorbent assay

40. Treatment and Prognosis
Drug of choice is Flagyl.
Giardia thrives in people not necessarily hard to treat, but keeping those who were infected from becoming reinfected.

41. Blood and Tissue Flagellates Phylum Euglenoidea
Known as Hemoflagellates or Kinetoplastids.
Some have forms that live in the alimentary canal of insects such as flies, bugs, etc.

42. Adaptation to Parasitism
Most parasites evolved from free-living forms.

43. Adaptation to Parasitism
Most parasites evolved from free-living forms.
They became parasites when hosts ingested them and they survived the process.

44. Adaptation to Parasitism
Most parasites evolved from free-living forms.
They became parasites when hosts ingested them and they survived the process.
They were then selected for and adapted to colonize hosts.

45. Adaptation to Parasitism
This is not the case for blood and tissue flagellates.

46. Adaptation to Parasitism
This is not the case for blood and tissue flagellates.
Because most insect species have flagellates that live within them and these share characters with human blood and tissue flagellates.

47. Adaptation to Parasitism
This is not the case for blood and tissue flagellates.
Because most insect species have flagellates that live within them and these share characters with human blood and tissue flagellates.
Therefore, biting insects probably gave these parasites to us!

48. Blood and Tissue Flagellate Anatomy and Life Stages
There are seven ontogenetic stages, but not all species have all seven.
These stages are continuous.

49. Life-cycle stages of trypanosomatidae. A. promastigote; b
Life-cycle stages of trypanosomatidae. A. promastigote; b. ophistomastigote; c. epimastigote; d. trypomastigote; e. choanomastigote; f. amastigote; g. paramastigote; K. kinetoplast; N. nucleus; F. flagellum.

50. You will be responsible for 4 of them.
Remember not all 4 stages will be found in each species life cycle.

51. Promastigote anterior Flagellum Kinetosome Kinetoplast Nucleus
posterior

52. Epimastigote
anterior
Undulating membrane
posterior

53. Trypomastigote
Undulating membrane
anterior
posterior

54. These are intracellular, stages that occur within cells.
Amastigote
anterior
Flagellum
Kinetosome
Kinetoplast
Nucleus
posterior
These are intracellular, stages that occur within cells.