1. Parasitic Protozoans
Lecture 4

2. 2- Flagellates 1- Trypanosoma spp. 2- Leishmania spp. 3- Giardia spp.
4- Trichomonas spp.

3. 1- Hemoflagellates 1- Trypanosoma spp. 2- Leishmania spp.
Called Hemoflagellates because they have a flagellum and require blood medium to culture them.
A.K.A. Kinetoplasta
Flagellum is attached to an undulating membrane attached to a kinetoplast.
There is evidence for sexual reproduction but when it occurs is not known.
They can also absorb and use foreign DNA.

4. 1- Hemoflagellates Two host life cycle
Humans and their domestics are Definitive Host
Insect vectors are the Intermediate Host
Four life stages
Not all stages occur in all species
Certain stages are found in specific hosts
Epimastigotes and promastigotes in insect IH
Amastigoes and trypomastigotes in DH

5. 1- Trypanosoma spp. 1- Trypanosoma gambiensi 2- T. rhodesiensi
3- T. curzi
4- T. lewisi

6. 1- Trypanosoma gambiensi
2- T. rhodesiensi
Definitive Host: Humans. Not pathenogenic to any other species. Native ruminates serve as reservoirs for T.b. rhodesiense, but not T.b. gambiense.
Intermediate Host: Tsetse fly (Glossina)
Mode of transmission: Bite of infected tsetse fly
Tsetse fly (Glossina)

7. Geographic Distribution
T. b. gambiense is found in west central and central Africa.
T. b. rhodesiense found in central and east central Africa
T. b. gambiense
T. b. rhodesiense

8. Life cycle

9. 1- Trypanosoma gambiensi
2- T. rhodesiensi
Location: Throughout the body in the blood and tissues
Pathology: Both subspecies cause African Sleeping Sickness.
T.b. gambiense causes chronic, long-term form.
T.b. rhodesiense causes an acute form.
Starts with a small sore at bite.
Trypimastigotes divide rapidly and spread throughout body

10. Pathology Pathology (con’t): Lymph nodes become swollen and congested
Particularly the nodes in neck
Called Winterbottom’s sign

11. Pathology T.b. gambiense frequently goes to CNS
Causes the chronic, sleepiness associated with African Sleeping Sickness
Apathy, mental dullness, disturbance of coordination
Increase in sleepiness, finally to coma, and death.
Death may also occur from malnutrition, falling, or other infections

12. Pathology
T.b. rhodiensiense rarely invade the CNS but causes death much faster.
Usually due to invasion of heart tissue
Both subspecies produce intermittent periods of fever, particularly in early stages.
Due to antigen shifts of the parasite.
They can also take antigens from host body and put them on their body
Much pathology may be due to heightened immune response killing uninfected body cells.

13. Diagnosis Trypomastigotes in the blood smear.
Can also be in cerebrospinal fluid
Serological test available

14. 3- Trypanosoma curzi
Definitive Host: Humans, dogs, cats, opossums, armadillos, and wood rats.
Intermediate Host: Reduviid bugs (Kissing bug or assassin bugs).
Location in the Definitive Host: Throughout the body.
Trypomastigotes in blood
Amastigotes most common in spleen, liver, and muscles, including heart
Mode of Transmission: Host rubs tryps into bite wound.

15. Geographic Distribution
Throughout much of central and South America.
12-19 million infected
Annual incidence 561,000
2-3 million with chronic symptoms
45,000 die from disease every year.
A few cases in U.S. in Maryland, Georgia, Florida, Texas, Arizona, New Mexico, California, Alabama, and Louisiana.

16. Life cycle

17. 2- Leishmania spp.
Leishmania donovani
L. tropica.

18. Leishmania donovani
Definitive Hosts: Humans. Reservoir includes most mammals
Intermediate Hosts: Phlebotomus sand fly.
Mode of Transmission: Bite of infected Sand Fly
Location in D.H.: Immune system, including spleen, liver, lymph nodes and bone marrow

19. Geographic Distribution
Probably originated in Old World
Moved to New World with slave trade

20. Pathology Causes Visceral Leishmaniasis
A.K.A. Kala-azar, Dum-Dum Fever
Amastigote is engulfed by macrophage.
Macrophage doesn’t kill amastigote.
Neutrophils and eosinophils will kill amastigotes.
Multiplies, breaks out, and each invades another macrophage.
Also destroys macrophages in the spleen, liver, and lymph nodes
Body starts manufacturing macrophages to replace them.
Results in severe wasting and anemia

21. Pathology
Macrophage Infected with amastigotes
of Leishmania

22. Pathology Early symptoms include malaise, vomiting, low-grade fevers.
Followed with chronic wasting, anemia, enlargement of abdomen due to greatly enlarged spleen and liver.
Death usually follows in 1-2 years if untreated.
Some people recover spontaneously
Related to age and nutrition
Some people who were treated later develop Post-Kala-azar dermal leishmanoid
“Face bumps”
Repeat of treatment usually clears up the bumps.

23. Life Cycle

24. Diagnosis
Amastigotes in liver tissue, macrophages, spleen, other organs.
IFA, ELISA tests have been developed but can’t tell between L. donovani and L. tropica.
Need to eliminate possibility of typhoid, paratyphoid, malaria, syphilis, tuberculosis, dyssentery, and relapsing fever which cause similar symptoms.

25. 2- Somato-flagellates 1- Genital flagellates 2- Intestinal flagellates
Trichomonas spp.
2- Intestinal flagellates
Giardia spp.

26. Trichomonas vaginalis
Genital flagellates
Trichomonas spp.
Trichomonas vaginalis
Definitive Hosts: Humans. Reservoir includes most mammals and birds
Intermediate Hosts: Nothing
Mode of Transmission: during sexual inter course by trophozoite

27. Geographic Distribution
Trichomonas are found in man, monkeys, rodents, fowls, pigeons, doves, termites and slugs.
Distributed in all countries

28. Pathology Causes milky yellowish irritant vaginal discharge in female
Ulceral discharge may occur in male

29. Life Cycle

30. Diagnosis
In female: Examination of vaqginal discharge for trophozoites and urine sample
In male: Examination of prostatic fluid and urine sample

31. Intestinal flagellates
Giardia spp.
Definitive Hosts: Humans.
Intermediate Hosts: Nothing
Mode of Transmission: quadri-nucleated cyst in contaminated food and drink
Flies and cockroaches play an important role in transmission

32. Geographic Distribution
Worldwide, more prevalent in warm climates

33. Pathology Children are affected
Mucus production, diarrha, dehydration, intestinal pain, weight loss.

34. Life Cycle

35. Diagnosis
Microscopic examination of fecal material for identification of trophozoite.
PCR analysis for detection of giardia DNA from both trophozoites and cysts