Objectives At the end of this sub-unit, students will be able to: Explain the classification and characteristics of blood and tissue flagellates Discuss the epidemiology, life cycle, and clinical aspects of Leishmania parasites Discuss the epidemiology, life cycle, and clinical aspects of Trypanosoma species

1. Blood and Tissue flagellates
Objectives
At the end of this sub-unit, students will be able to:
1. Explain the classification and characteristics of blood and tissue
flagellates
2. Discuss the epidemiology, life cycle and clinical aspects of
Leishmania parasites
3. Discuss the epidemiology, life cycle and clinical aspects of
trypanosoma species
By: Asmamaw Tesfaye

2. Outline
 Classification of blood and tissue flagellates
 Characteristics of blood & tissue flagellates
 Leishmania (different forms)
 Trypanosoma brucie complex
 Trypanosoma cruzi
By: Asmamaw Tesfaye

3. Classification
kingdom -------- protista
subkingdom -----protozoa
phylum -----------sarcomastigophora
subphylum -------mastigophora
class ---------------zoomastigophora
order --------------kinetoplastida
family -------------trypanosomatidae
genus --------------Leishmania, trypanosoma
By: Asmamaw Tesfaye

4. General Characteristics
 Reproduce by longitudinal binary fission.
 Use biological insect vectors as intermediate hosts & human
as definitive host.
 The species are morphologically indistinguishable, but they
can be differentiated on the basis of their:
Clinical features
Geographical distribution
Vector species
Reservoir hosts
Immunological and molecular tests
By: Asmamaw Tesfaye

5. Developmental forms
The different developmental forms are differentiated on the basis of
 Presence or absence of free flagellum
 Presence or absence of undulating membrane
 Position of the kinetoplast relative to the nucleus
1. Amastigote(Leishmanial form)
 Rounded body, large nucleus and
eccentric kinetoplast visible
 No free flagellum
 No undulating membrane
 The only intracellular forms of all
leishmania species and Trypanosoma
cruzi
By: Asmamaw Tesfaye

6. Developmental forms…
• Elongated body, central nucleus, anterior kinetoplast
• Single anterior flagellum arises from kinetoplast
• Found in the invertebrate host, and in culture media
of all Leishmania species
By: Asmamaw Tesfaye

7. Developmental forms…
3. Epimastigote (crithidial forms)
• Elongated body, single free flagellum, single nucleus
• Has undulating membrane
• Kinetoplast is just anterior to the nucleus
• Found in the invertebrate host and in culture media of
Trypanosome species
By: G. A.

8. Developmental forms…
4. Trypomastigote (Trypanosomal forms)
• Pleomorphic, it can be seen as “U” or “C” shaped
• Central nucleus, posterior kinetoplast
• Single Flagellum arises posteriorly
• Has undulating membrane
• Found in the peripheral blood of vertebrates and
• is the diagnostic stage of Trypanosome species
By: G. A.

9. Developmental forms…
5. Metacyclic Trypomastigote
• Morphologically similar to trypomastigote stage but it is short
and stumpy
• Final developmental stage in the gut of the insect vectors
• Infective stage of Trypanosome species
By: Asmamaw Tesfaye

10. Leishmania species
 Causative agent of leishmaniasis
 Obligate intracellular to mononuclear phagocytes
 Human infection is caused by > 20 of 30 species that infect
mammals.
 L. donovani complex
 L. donovani
 L. infantum
 L. chagasi
 L. chinensis
 L. archibaldi
By: Asmamaw Tesfaye

11. …
Cutaneous leishmaniasis(CL)
Visceral leishmaniasis(VL)
L. donovani
L. infantum
 L. Chagasi
 L. tropica
 L. major
 L. aethiopica
 L. panamensis
 L. guyanensis
 L. peruviana
 L. mexicana
Mucocutaneous leishmaniasis(MCL)
 L. panamensis
 L. guyanensis
 L. Brazilliensis
 L. aethiopica
Diffuse cutaneous leishmaniasis (DCL)
• L. amazonensis
• L. aethiopica
Clinical classification
By: Asmamaw Tesfaye

12. Epidemiology
 350 million people are at risk in 98 countries around the world
 Annual incidence estimated to be 0.9 – 1.6 million (all forms)
 Incidence of VL: 200,000-400,000 cases /year
 Mortality due to VL: 20,000 - 40,000 /year
 An estimated 12 million cases world wide
 CL form representing 50 to 75% of all new cases
 Most of the affected countries are in tropics and sub tropics
 90% of all VL cases occur in Bangladesh, Brazil, India, Ethiopia, Sudan
and south Sudan.
 90% of all MCL cases occurs in Bolivia, Brazil and Peru
 90% of all CL cases occur in Afghanistan, Brazil, Iran, Peru, Saudi Arabia
Algeria, pakistan and Syria
By: Asmamaw Tesfaye

13. By: Asmamaw Tesfaye

14. Global Status
L. donovani
L. infantum
L. tropica
L. major
L. aethiopica
old world:
Asia, Africa, Europe
new world:
south and central America
L. infantum
( L. chagasi )
L.mexicana
L.brazilliensis
L. peruriana
L.panamensis
L.guyanensis
L.amzonensis
By: Asmamaw Tesfaye

15.  The incidence of leishmaniasis is increasing, mainly because of:
 Man-made environmental changes
 Poverty and malnutrition
 Climate change
 Movement of susceptible populations into endemic areas
By: Asmamaw Tesfaye

16. Distribution in Ethiopia
Visceral leishmaniasis (VL): L. donovani
Occurs mainly in arid and semiarid lowlands below 1500 m
altitude. Important endemic foci are:
Northwest Ethiopia (2/3 of national burden)
 Metema, Armacho, Quara, Humera and T/Adiabo -low lands
 Libokemkem/ Fogera districts of Amhara Regional state -high
lands( new foci 2005)
South and southwest Ethiopia
 Dawa, Genale, Konso/Segen, Woito, and Omo River Valleys
 Ethio–Kenyan Boarder, Guji and Borena zones
 Ethio - Sudanese Boarder
Northeastern Ethiopia
 Awash Valley areas
 Ethio-Djibout Boarder–cases reported
Eastern Ethiopia – Somali region
By: Asmamaw Tesfaye

17. Distribution in Ethiopia….
Cutaneous leishmaniasis: L. aethiopica, L.major, L. tropica
 Endemic at altitudes 1400 - 2700 m in most administrative regions
 Prevalence rates of 5.5 – 40% were reported from villages in
Shewa , Wello and G.Gofa with the highest rate in Ocholo village
in G. Gofa
 Rock (Procavia habessinica) & tree (Heterhyrax brucei ) hyraxes
serving as reservoir host for L. aethiopica
By: Asmamaw Tesfaye

18. Transmission and life cycle
 Common mode of transmission: Bite of sand fly
Genera Phlebotomus vs Lutzomyia
 Uncommon modes of transmission:
Congenital transmission
Blood transfusion
Sharp materials
Breeding sites for the sand flies
Balanite Trees
Acacia Forests
Black cotton soil
Termite Hills
 Favorable Environmental conditions
 Altitude below 1500 meters (low land)
 High level humidity (70-80% Relative
Humidity)
High T: 25-32o C
For VL transmitting vectors
By: Asmamaw Tesfaye

19. 19
BALANITE TREE
ACACIA TREE
 P.orientalis in the North
is associated with black
cotton soil, red Accacia
and Balanite trees
By: Asmamaw Tesfaye

20.  P.orientalis in the North
is associated with black
cotton soil, red Accacia
and Balanite trees
 Phlebotomus martini/ celiae
in the South are usually
associated with termite hills.
By: Asmamaw Tesfaye

21. By: Asmamaw Tesfaye

22. Sloth
Gebril Hyrax
Bat
Porcupine
opossum
dog
fox
Primates
anteater
Mammalian Reservoir Hosts

23. Maxadilin, SIP
Life cycle
6-10 days
By: Asmamaw Tesfaye

24. Life cycle….
 Female sandflies inject promastigote stage during blood meals
 Promastigotes are phagocytized by macrophages & transform into
intracellular amastigote form
 Amastigotes multiply by binary fission, rapture from macrophages ,
and infect new cells
• In VL the amastigotes are carried through blood circulation , then invade
and multiply in the macrophages of spleen, liver, bone marrow, lymph glands
• In CL , MCL – the amasigote multiply in skin macrophages (histocytes)
 Sand flies become infected during blood meals when they ingest
macrophages infected with amastigotes
 The host cell break down and release amasigotes which are then
transformed to promastigotes
 Multiply, fill the lumen of the gut and migrate to the proboscis
By: Asmamaw Tesfaye

25. Pathogenesis
 Entrance into the host and establishment of infection by leishmanias
is enhanced by saliva from the vector
 Two substances are involved
 maxadilin, or maximum dilation molecule: keeps the capillary
bed open at the site of feeding for about 48 hours
 SIP or salivary immunosuppressive protein : restrains the
immune system’s early efforts to eliminate the parasites
 Infective promastigotes entering the blood of the vertebrate are
covered by two key molecules: the protein gp 63 and
lipophosphoglycan (LPG). Both mediate the uptake of
promastigotes by macrophages
 The promastigotes are engulfed & form phagosome
By: Asmamaw Tesfaye

26. Pathogenesis…
 Phagosome fuse with the lysosome to form a phagolysosome
 As the promastigotes transform into amastigotes, which
produce compounds that counter lysosomal enzymes
 The gp 63 molecule inactivates proteolytic enzymes
 LPG protects against other enzymes
 Leishmanial organisms are able to survive the highly acidic
environment of lysosomes by regulating their internal PH.
By: Asmamaw Tesfaye