Includes many different species: Leishmania TrypanosomaGeneral Characters:

1- Present in blood and tissue. 2- Move by Flagellum3- 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.

Haemoflagellatesand

Polymorphic Trypanosomes: Monomorphic Trypanosomes:1 -Trypanosoma gambiense

2 -Trypanosoma rhodesiense Trypanosoma cruzi

Leishmania spp.

Leishmania tropica complex: Leishmania donovani complex:1 -Leishmania tropica

2 -Leishmania major3 -Leishmania aethiopica

1 -Leishmania donovani2 -Leishmania infantum

3 -Leishmania chagasiLeishmania mexicana complex: Leishmania braziliensis complex:Leishmania mexicana Leishmania braziliensis

Blood Flagellates1- Are Protozoa that swim in the blood of patients using

Amastigote

Promastigote Epimastigote

Trypomastigote

Eccentric nucleus

Central nucleus

Free Flagellum

Free Flagellum

Free Flagellum

No free flagellum

Central nucleus

Central nucleus

kinetoplast

kinetoplast

3- Include: Leishmania

Undulating membrane

Undulating membrane

kinetoplast

& Trypanosoma4- Acquire the following shapes:

flagellum (mastigote) then invade their tissues.

oval

elongated

2- Transmitted to man through arthropods bite خيط

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.Cs5- 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.(

DiseaseI- 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:”

III- Visceral Leishmaniasis “Kala-azar:”L. braziliensis

L. donovani - L. infantum - L. chagasi

Disease SPECIES

Cutaneous leishmaniasisLeishmania tropica*Leishmania major*

Leishmania aethiopicaLeishmania mexicana

Mucocutaneous leishmaniasis Leishmania braziliensis

Visceral leishmaniasisLeishmania donovani*Leishmania infantum*

Leishmania chagasi

* Endemic in Saudi Arabia

Leishmania Parasites and Diseases

Leishmania Parasites and Diseases

Leishmania causes leishmaniasis

Liver

Disease is caused by Bite

of ♀ sandfly

Attacks human skinOld world cutaneous leishmaniasis

New world cutaneous leishmaniasisOld world visceral leishmaniasisNew world visceral leishmaniasis Different Leishmania species

Attacks human viscera

Mode of infection of LeishmaniasisThrough the bite of female sand fly (vector)

Infective stage

Promastigotes

Diagnostic stage

Biological transmission

AmastigotePromastigotesblock mouth & pharynx in skin or blood of patientPhlebotomus (OW) Lutzomyia (NW)

Multiply by binary fission

Alimentary canal of sand fly

_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.

Transmission of Leishmaniasis

10

Female sand flies

MaleFemale

Vector

The life cycle of Leishmania

The life cycle of Leishmania

The life cycle of Leishmania

The life cycle of Leishmania

human_life_cycle_leish.swf

The life cycle of Leishmania

life_cycle_sand_fly_leish.swf

Sand fly

Promastigotes of Leishmania Amastigote

Leishmania spp.

Pathogenesis & Clinical Picture of Cutaneous Leishmaniasis

PromastigotesAmastigotes

forms at the site of bite due to multiplication of Leishmania in skin macrophages

forms with sharp-cut edges with raised indurated margin

Healing occurs leaving

The patient develops solid immunity

Nodule

An ulcer

a disfiguring scar

&granulomatous reaction around them.

Skin macrophage

Inflammatory cells

In about 1 year

Leishmania species causing ulcer in the Old World

1- L. tropica

Urban

2- L. major

Rural

In the Middle East

In Ethiopia & Kenya3- L. aethiopica

Affects patients producing diffuse cutaneous lesions resembling lepromatous leprosy.

Oriental sore

المدن الريف

القرحةالشرقية

dry chronic wet acute

In patients with deficient cell-mediated immunityDue to some characteristics of parasite species

I-Cutaneous Leishmaniasis “Oriental Sore”(O.W.C.L)

1 -Single Dry Non-Exudative Lesion Caused by L. tropica URBAN type

2- Long incubation Period (months to years).1 -Present in towns & cities (common in Saudi Arabia).

4- Lesions are slowly progressive.3- Lesions develop in exposed parts such as (face –limbs)

5 -Ulcer heals “self-limiting infection” scar tissue form6 -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

2- Relatively short incubation period (2-6 weeks).1 -Found in villages at edge of deserts(common in KSA).

4- Lesions are rapidly progressive.3- Lesions are more severe than L.tropica – big Ulcers

5- Dense nodules ulcerate & Coalesce big ulcersAppear as follows: Multiple-Big-Wet-painless nodule-Exudative2ry bacterial delay healing –Big disfiguring scar- pruritic.

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 responsePersistent 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

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”.

3 -Appear as Tuberculoid skin lesion “Lupus Vulgaris.”N.B: Montengro’s Test (is strongly +ve), while smear & culture for parasite is –ve????

I-Cutaneous Leishmaniasis “Oriental Sore”(O.W.C.L)

somewhat like a volcano with a raised edge and central crater

Areas where Cutaneous Leishmaniasis exists

L.infantumL.aethiopica

L.tropicaL.major

In the Old World

Leishmania species causing ulcer in the New WorldL.peruviana

Dry ulcer (Uta)

L.braziliensis

spread along lymphatics to mucous membrane producing erosion of

nasal septum, palate & larynx

(Espundia)

Leishmania pifanoi

Diffuse lesion resembles lepromatous

leprosy (does not heal or ulcerate).

Leishmania species causing ulcer in the New World

Leishmania mexicana:

(Chiclero’s ulcer or Bay sore)

single ulcer affects the ear causing destruction of the cartilage.

L.braziliensis

I-Mucocutaneous Leishmaniasis “Espundia”Caused by L. braziliensis present in hot humid forest of central & south America

1- Vector of transmission is Lutzomyia.

3- M.L. may develop 2-10 years following primary C.L..2- majority of cases primarily present with Cutaneous Lesion

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.)