1. Haemoflagellates General Characters: Includes many different species:
Leishmania
and
Trypanosoma
General Characters:
1- Present in blood and tissue. 2- Move by Flagellum
3- Require vector (blood sucking insect) for transmission.
4- Alternate cycles & acquire 2 interchangeable stages in host & vector.
5- Multiply by simple binary fission.
Trypanosoma spp.
Polymorphic Trypanosomes: Monomorphic Trypanosomes:
1- Trypanosoma gambiense
Trypanosoma cruzi
2- Trypanosoma rhodesiense
Leishmania spp.
Leishmania tropica complex: Leishmania donovani complex:
1- Leishmania tropica
1- Leishmania donovani
2- Leishmania major
2- Leishmania infantum
3- Leishmania aethiopica
3- Leishmania chagasi
Leishmania mexicana complex:
Leishmania braziliensis complex:
Leishmania mexicana
Leishmania braziliensis

2. flagellum (mastigote) then invade their tissues.
Blood Flagellates
1- Are Protozoa that swim in the blood of patients using
خيط
flagellum (mastigote) then invade their tissues.
2- Transmitted to man through arthropods bite
Leishmania
& Trypanosoma
3- Include:
4- Acquire the following shapes:
Trypomastigote
Amastigote
Undulating membrane
kinetoplast
oval
No free flagellum
Free Flagellum
Eccentric nucleus
Central nucleus
Promastigote
Epimastigote
kinetoplast
elongated
kinetoplast
Free Flagellum
Free Flagellum
Central nucleus
Undulating membrane
Central nucleus

3. Leishmania spp. Introduction
1- Leishmania established everywhere in Forest, desert, mountains, towns, countries
2- Leishmaniasis is a variety of syndromes that are wide-spread giving rise to:
Cutaneous – Mucocutaneous – Visceral Leisons.
3- Species variation & the cellular immune response determine the type of lesion
4- Leishmania spp. are strictly obligatory intracellular parasite of macrophages/ monocyte series (Histiocytes – Epitheloid cells – Kupfer cells – R.E.Cs
5- Multiply by binary fission within macrophages of : SKIN – RETICULO- ENDOTHELIAL SYSTEM & other VISCERA
6- Acquire interchangeable stages:
Amastigotes: in Man- Dogs –Rodents Promastigotes: in vector & culture
7- Transmission of the disease is seasonal – mainly zoonotic.
Exceptions are L. donovani in india & L. tropica ….. Whereas man is the only
source of maintaining infection (Anthroponotic)
8- Vector of transmission is Sandfly “Phlebotomus” (old world) and “Lutzomyia”
(new world).

4. Disease I- Cutaneous Leishmaniasis “Oriental Sore”:
A- Old World Cutaneous Leishmaniasis (O.W.C.L.):
1- Single Dry Non-Exudative Lesion L.tropica
2- Multiple Wet Exudative Lesion L.major
3- Disseminated Cut. Leishmaniasis L.aethiopica
4- Chronic (Recidivan) Relapsing Cut. Leishmaniasis L.tropica
B- New World Cutaneous Leishmaniasis (N.W.C.L.):
1- Relapsing skin Lesion (Chiclero’s Ulcer) L.mexicana
2- Mucocutaneous Leishmaniasis (Espundia) L.braziliensis
II- Mucocutaneous Leishmaniasis “ESPUNDIA”:
L. braziliensis
III- Visceral Leishmaniasis “Kala-azar”:
L. donovani - L. infantum - L. chagasi

5. Leishmania Parasites and Diseases
SPECIES
Cutaneous leishmaniasis
Leishmania tropica*
Leishmania major*
Leishmania aethiopica
Leishmania mexicana
Mucocutaneous leishmaniasis
Leishmania braziliensis
Visceral leishmaniasis
Leishmania donovani*
Leishmania infantum*
Leishmania chagasi
* Endemic in Saudi Arabia

6. Leishmania Parasites and Diseases

7. Leishmania causes leishmaniasis
Disease is caused by Bite of ♀ sandfly
Liver
Attacks human skin
Old world cutaneous leishmaniasis
Attacks human viscera
New world cutaneous leishmaniasis
Old world visceral leishmaniasis
Different Leishmania species
New world visceral leishmaniasis

8. Mode of infection of Leishmaniasis
Through the bite of female sand fly (vector)
Phlebotomus (OW)
Lutzomyia (NW)
in skin or blood of patient
block mouth & pharynx
Amastigote
Promastigotes
Diagnostic stage
Infective stage
Alimentary canal of sand fly
Promastigotes
Multiply by binary fission
Biological transmission

9. Transmission of Leishmaniasis
_ by sand flies.
_ artificial transmission of leishmania via the sharing of contaminated syringes and needles, from one intravenous drug user to another.
Rarely, Leishmaniasis is spread from a pregnant woman to her baby (Materno-fetal transplacental transmission).
Blood transfusion or contaminated needles also can spread Leishmaniasis.

10. Vector
Female sand flies
Male
Female

11. The life cycle of Leishmania

12. The life cycle of Leishmania

13. The life cycle of Leishmania

14. The life cycle of Leishmania

15. The life cycle of Leishmania

16. Leishmania spp.
Sand fly
Amastigote
Promastigotes of Leishmania

17. Pathogenesis & Clinical Picture of Cutaneous Leishmaniasis
Nodule
forms at the site of bite due to multiplication of Leishmania in skin macrophages
& granulomatous reaction around them.
Inflammatory cells
Promastigotes
Amastigotes
Skin macrophage
forms with sharp-cut edges with raised indurated margin
An ulcer
In about 1 year
Healing occurs leaving
a disfiguring scar
The patient develops solid immunity

18. Leishmania species causing ulcer in the Old World
In the Middle East
1- L. tropica
القرحة الشرقية
2- L. major
Oriental sore
المدن
الريف
Urban
Rural
dry chronic
wet acute
In Ethiopia & Kenya
3- L. aethiopica
Affects patients producing diffuse cutaneous lesions resembling lepromatous leprosy.
In patients with deficient cell-mediated immunity
Due to some characteristics of parasite species

19. I-Cutaneous Leishmaniasis “Oriental Sore”(O.W.C.L)
1- Single Dry Non-Exudative Lesion
Caused by L. tropica URBAN type
1- Present in towns & cities (common in Saudi Arabia).
2- Long incubation Period (months to years).
3- Lesions develop in exposed parts such as (face –limbs)
4- Lesions are slowly progressive.
5- Ulcer heals “self-limiting infection” scar tissue form
6- C.M.I. curtails the infection leading to resistance to reinfection
Appear as follows: single-small-Dry-painless nodule-nonexudative-delayed ulceration-small scar- non pruritic- uncommon 2ry bacterial infection.
2- Multiple Wet Exudative Lesion
Caused by L. major RURAL type
1- Found in villages at edge of deserts(common in KSA).
2- Relatively short incubation period (2-6 weeks).
3- Lesions are more severe than L.tropica – big Ulcers
4- Lesions are rapidly progressive.
5- Dense nodules ulcerate & Coalesce big ulcers
Appear as follows: Multiple-Big-Wet-painless nodule-Exudative
2ry bacterial delay healing –Big disfiguring scar- pruritic.

20. I-Cutaneous Leishmaniasis “Oriental Sore”(O.W.C.L)
3- Chronic (Recidivan) Relapsing Cut. Leishmaniasis
Caused by L. tropica
Few cases following primary skin lesion become hyper-
Sensitive to parasite antigen --- vigorous immune response
Persistent chronic infection (over years)
The Lesions appear as follows:.
1- Papules develop around the healed skin & scar tissue
2- Ulcerate & heal by SCAR tissue formation
3- Appear as Tuberculoid skin lesion “Lupus Vulgaris”.
N.B: Montengro’s Test (is strongly +ve), while smear & culture for parasite is –ve ????
4- Diffuse Cut. Leishmaniasis (D.C.L.)
L. aethiopica (also L. amazonensis)
Inefficient cellular immune response limited cellular infiltration around infected macrophages failure of immune response to abort infection spread of amastigote
The Lesions appear as follows:.
1- Multiple nodules with abundant parasite – Rarely ulcerate.
2- Skin becomes thick due to hyperplasia & hypertrophy.
3- The lesion appear as “Lepromatous Leprosy”.

21. I-Cutaneous Leishmaniasis “Oriental Sore”(O.W.C.L)
somewhat like a volcano with a raised edge and central crater

22. Areas where Cutaneous Leishmaniasis exists
L.tropica
L.major
In the Old World
L.aethiopica
L.infantum

23. Leishmania species causing ulcer in the New World
L.peruviana
L.braziliensis
(Espundia)
Dry ulcer
(Uta)
spread along lymphatics to mucous membrane producing erosion of nasal septum, palate & larynx
Leishmania pifanoi
Diffuse lesion resembles lepromatous leprosy (does not heal or ulcerate).

24. Leishmania species causing ulcer in the New World
Leishmania mexicana:
single ulcer affects the ear causing destruction of the cartilage.
(Chiclero’s ulcer or Bay sore)
L.braziliensis

25. I-Mucocutaneous Leishmaniasis “Espundia”
Caused by L. braziliensis present in hot humid forest of central & south America
1- Vector of transmission is Lutzomyia.
2- majority of cases primarily present with Cutaneous Lesion
3- M.L. may develop 2-10 years following primary C.L..
4- Deficient C.M.I Spread of infection either directly or haematogenously to involve soft tissues of the Oronasal & Pharyngeal mucosa (NOSE-PHARYNX-LARYNX –UPPER LIP)
5-Lesion may be hypertrophy or severely destructive:
Hypertrophy mainly NOSE & MOUTH.
Destructive Mouth –Pharynx- Nasal (mucosa/cartilage
Septum) nasal obstruction – bleeding – erosion
massive destruction, severe pain & great deformity.
N.B: only non-visceral Leishmaniasis lesion that may cause death from (Pneumonia- Septicemia as superimposed 2ry bacterial infection – malnutrition – Deficient C.M.I.)