Presentation on theme: "Includes many different species: LeishmaniaTrypanosoma General Characters: 1- Present in blood and tissue.2- Move by Flagellum 3- Require vector (blood."— Presentation transcript:
Includes many different species: LeishmaniaTrypanosoma 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. Haemoflagellates and 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 major 3- Leishmania aethiopica 1- Leishmania donovani 2- Leishmania infantum 3- Leishmania chagasi Leishmania mexicana complex: Leishmania braziliensis complex: Leishmania mexicanaLeishmania braziliensis
Blood Flagellates 1- Are Protozoa that swim in the blood of patients using Amastigote PromastigoteEpimastigote Trypomastigote Eccentric nucleus Central nucleus Free Flagellum No free flagellum Central nucleus kinetoplast 3- Include: Leishmania Undulating membrane kinetoplast & Trypanosoma 4- Acquire the following shapes: flagellum (mastigote) then invade their tissues. oval elongated 2- Transmitted to man through arthropods bite خيط
Leishmania spp Leishmania spp. Introduction 1- Leishmania established everywhere in Forest, desert, mountains, towns, countries Leishmaniasis 2- Leishmaniasis is a variety of syndromes that are wide-spread giving rise to: Cutaneous – Mucocutaneous – Visceral Leisons 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) Sandfly 8- Vector of transmission is Sandfly “Phlebotomus” (old world) and “Lutzomyia” (new world).
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”: III- Visceral Leishmaniasis “Kala-azar”: L. braziliensis L. donovani - L. infantum - L. chagasi
Leishmania causes leishmaniasis Liver Disease is caused by Bite of ♀ sandfly Attacks human skin Old world cutaneous leishmaniasis New world cutaneous leishmaniasis Old world visceral leishmaniasis New world visceral leishmaniasis Different Leishmania species Attacks human viscera
Mode of infection of Leishmaniasis Through the bite of female sand fly (vector) Infective stage Promastigotes Diagnostic stage Biological transmission Amastigote Promastigotes block mouth & pharynx in skin or blood of patient Phlebotomus (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 Male Female Vector
The life cycle of Leishmania
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 & Kenya 3- L. aethiopica Affects patients producing diffuse cutaneous lesions resembling lepromatous leprosy. Oriental sore المدنالريف القرحة الشرقية dry chronicwet acute In patients with deficient cell-mediated immunity Due 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 form 6- C.M.I. curtails the infection leading to resistance to reinfection Appear as follows: 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 ulcers Appear as follows: Appear as follows: Multiple-Big-Wet-painless nodule-Exudative 2ry 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 response Persistent chronic infection (over years) The Lesions appear as follows: 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: 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.infantum L.aethiopica L.tropica L.major In the Old World
Leishmania species causing ulcer in the New World L.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. M.LC.L. 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: N.B: only non-visceral Leishmaniasis lesion that may cause death from (Pneumonia- Septicemia as superimposed 2ry bacterial infection – malnutrition – Deficient C.M.I.)