leishmania.pptwrdfiydufgukfjgdxffhgjgkckk
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- 2. Blood and Tissue flagellates belonging to the family Trypomastidae six genera but only two of them are responsible to cause disease to man Genus Leishmania Genus Trypanosoma 2
- 3. 3.4.1. General Characteristics blood & tissue flagellates Reproduces by longitudinal binary fission biological insect vectors as intermediate hosts & human as definitive host The species are morphologically indistinguishable, but they can be differentiated on the basis of on their clinical features, geographical distribution, serologic tests 3
- 6. 3.4.2. Leishmania species Causative agent of Leishmaniasis obligate intracellular protozoa of the genus Leishmania Named after Leishman, who first described it in London in May 1903
- 7. Lei… Human infection is caused by about 21 of 30 species that infect mammals. These include: L. donovani complex L. donovani, L. infantum, L. chagasi; L. mexicana complex L. mexicana L. amazonensis L. venezuelensis;
- 8. L. braziliensis complex L braziliensis L. Peruviana L. Guyanensis complex L. Guyanensis L. panamensis L. tropica, L. major & L. aethiopica Lei…
- 9. Leishmaniasis can easily classified clinically as • Visceral leishmaniasis • Cutaneous leishmaniasis • Mucocutaneous leishmaniasis • Diffuse cutaneous leishmaniasis lei…
- 10. Cutaneous leishmaniasis(CL) L. tropica L. major L. aethiopica L. panamensis L. guyanensis L. peruviana Visceral leishmaniasis(VL) Also called Kala azar, Dum- Dum fever, death fever , tropical spleenomegaly L. donovani L. infantum L. Chagasi lei…
- 11. Mucocutaneous leishmaniasis(MCL) L. panamensis L. guyanensis L. bazilliensis L. Aethiopica In immunosuppressed persons, L.donovani, or L. major or L.infantum. Diffuse cutaneous leishmaniasis(DCL) • L. amzonensis • L. aethiopica lei…
- 12. Geographical distribution 350 million people are at risk in 88 countries around the world 72 of which are developing countries an estimated 12 million cases world wide 1.5 to 2 million new cases occur every year CL form representing 50 to 75% of all new cases lei…
- 13. Global Status L. donovani L. donovani L. infantum L. infantum L. tropica L. tropica L. major L. major L. aethiopica L. aethiopica old world: Asia, Africa, Europe new world: outh and central America L L. infantum . infantum ( L. chagasi ) ( L. chagasi ) L.mexicana L.mexicana L.brazilliensis L.brazilliensis L. perurviana L. perurviana L.panamensis L.panamensis L.guyanensis L.guyanensis L.amzonensis L.amzonensis
- 14. lei… In Ethiopia Four species of Leishmania is found, namely, L. aethiopica, L.major L. tropica L. donovani
- 15. Visceral leishmaniasis (VL) L. donovani Occurs mainly in arid and semiarid lowlands below 1,300 m altitude Important endemic foci include Gelana focus at lake abaya, the segen valley (Aba- Roba focus) in Knoso Wereda the Omo river plains and the Metema and Humera plains in north western Ethiopia lei…
- 16. lei… 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
- 17. Transmission and life cycle Common mode of transmission. Bite of infected female sandfly Genera Phlebotomus in Old world Old world Lutzomyia in New world New world Uncommon modes of transmission: Congenital transmission, Blood transfusion, Rarely, inoculation of cultures.
- 18. General life cycle of Leishmania species female sandflies inject promastigotes stage during blood meals about 30 species of sand flies acts a vector lei…
- 19. lei… Promastigotes are phagocytized by macrophages & transform into intracellular amastigotes 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)
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- 21. lei… Sandflies become infected during blood meals when they ingest macrophages infected with amastigotes the host cell break down and releasing the amasigotes which is then transform to promastigotes multiply , fill the lumen of the gut and migrate to the proboscis
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- 24. Pathogenesis Entrance into the host and establishment of infection by leishmanias is enhanced by saliva from the vector Two substances were 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 lei…
- 25. lei… 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
- 26. lei… 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 lysosmes by regulating their internal PH
- 27. Clinical features and pathology Cutaneous Leishmaniasis Cutaneous Leishmaniasis The clinical forms of CL vary according to The species of parasite Region and Response of patient lei…
- 28. Old World CL L. Tropica SW Asia, N.Africa • Anthroponotic or dog reservoir • dry ,urban ,chronic, old world oriental sore • 'dry painless lesion’ • 25-70mm diameter lei…
- 29. lei… Officer holding Iraqi child with Leishmania tropica on face Soldier in Afghanistan with Leishmania tropica on hand
- 31. hyper-pigmentation of scar • Are self-healing,1-2yrs • Often leave disfiguring scars • Immune to re-infection • Rarely develop: leishmaniasis recidivans (LR) lei…
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- 34. L. major • central Asia, middle East, Africa • rural (rodent reservoir) • wet oreintal sore • Early papules is inflamed (5- 10mm) • Develop to large uneven ulcer • Self-healing (3-6mths) • Protect against reinfection & also with L.tropica ulcers are moist or open with seropurulent exudate lei…
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- 36. L. infantum • Mediterranea, Europe • dermotrophic strains recently recognized • L. aethiopica • highlands of Kenya and Ethiopia • Similar to oreintal sore • Self-heal 1-3 yrs • Can cause DCL in patients • also cause MCL lei…
- 37. New World CL • Initially, the lesion is a small, red papule up to 2 cm in diameter • change in size and appearance over time Chiclero Ulcer (L. mexicana) L. mexicana) lei…
- 38. • chronic ulcerated, papular, or nodular lesion • lesion is painless, non- tender, non-pruritic Chiclero Ulcer (L. mexicana) lei…
- 39. • Lesions of the body tend to self-healing • but those on the ear may last up to 30 years and entirely destroy the pina of the ear lei…
- 40. Diffuse Cutaneous Leishmaniasis • caused by L. aethiopica and L. amazonensis • Skin lesion develop over large areas of the body • Scaly, not ulcerated, nodules • Chronic and painless • Numerous parasites in lesions • Seldom heal despite treatment lei…
- 42. Mucocutaneous Leishmaniasis • Known as espudia • two stages • simple skin lesion • 2o mucosal involvement • metastasis via blood or lymphatic systems • can occur after primary lesion (up to 16 years) • frequently in naso-pharyngeal mucosae • junction of skin and mucosa lei…
- 43. • variable types and sizes of lesions • chronic and painless • non-ulcerative type • local edema (upper lip) • ulcerative type • rapid and extensive mutilation lei…
- 44. Disfiguration is often extreme with complete destruction of the nasal septum, perforation of the palate and damage of the tissues of the lips and larynx lei…
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- 46. Visceral Leishmaniasis (VL) • reticuloendothelial system affected • spleen, liver, bone marrow, lymph nodes • The disease may be asymptomatic and self-resolving but usually runs a chronic course and may be fatal without treatment • . Untreated VL carries have progressive disease • 75-95% mortality • death generally within 2 years • Death usually occurs because of severe secondary bacterial infections in advanced disease lei…
- 47. lei… Pneumonia is the common complication incubation period • generally 2-6 months ( range 10 days to years)
- 48. • fever, malaise, weakness • wasting despite good appetite • spleno- and hepatomegaly, enlarged lymph nodes • epistaxis (nose bleeding) and bleeding of gums • depressed hematopoiesis • severe anemia • leucopenia • thrombopenia lei…
- 49. A 12-year-old boy suffering from visceral leishmaniasis. The boy exhibits splenomegaly and severe muscle wasting 49 lei…
- 50. Post Kala Azar Dermal leishmaniasis (PKDL) Cutaneouse form of leishmaniasis, which can occur after resolution (after treatment and recovery) of VL It require expensive and prolonged treatment characterized by hypo pigmented and raised erythematous patches on the face, trunk of the body and limbs may develop in to nodules and resembles those of lepromatous leprosy, fungi infections or other skin disorders 50 lei…
- 51. lei… Occasionally there is ulceration of lips and tongue occurs in 1-3% of Indian and 50% of Sudanese VL patients
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- 53. Leishmaniasis and HIV Infection Coexistence of leishmaniasis with HIV infection is a serious concern Leishmaniasis is spreading in several areas of the world because of the rapidly spreading epidemic AIDS The immune deficiency has lead to increased susceptibility to infections, including leishmaniasis Co-infection with HIV has lead to the spread of leishmaniasis, typically a rural disease, into urban areas lei…
- 54. In patients infected with HIV, leishmaniasis accelerates the onset of AIDS by cumulative immunosuppression and by stimulating the replication of the virus It may also change asymptomatic Leishmania infections into symptomatic infections lei…
- 55. Laboratory Diagnosis of CL, MCL, DCL • suspected because of: • geographical presence of parasite • history of sandfly bite • + skin lesion: • chronic, painless, ‘clean’ ulcer • nasopharyngeal lesions • nodular lesions lei…
- 56. lei… The laboratory diagnosis of CL, MCL & DCL is by 1. Detecting amastigotes from scrapings, biopsy, aspirates 2. Culture from ulcer material 3. Leishmainin test 4. serology
- 57. Treatment Treatment • Sodium stibogluconate (Pentostam) • Pentamidine isethionate • amphotericin B • cryotherapy and thermotherapy lei…
- 58. Prevention and control 1. Early detection by serological diagnosis (VL) and treatment of infected persons 2. Health information dissemination 3. Personal protection from sand fly bites by: Using insect replants Avoiding endemic areas especially at times when sand flies are most active Use of pyrethroid impregnated bed nets and curtains lei…
- 59. lei… 4. Vector control by the use of light traps or residual insecticide spraying of houses 5. Destruction of stray dogs and infected domestic dogs 6. Elimination and control of rodents 7. sitting human dwellings away from the habitats of animal reservoir hosts where sand flies are known to breed
Editor's Notes
- #4: kinetoplast : contain DNA of single mitochondrion . Most enzymes are produced by the direction of DNA.
- #12: Most of the affected countries are in tropics and sub tropics 90% of all visceral leishmaniasis (VL) cases occur in Bangladesh, Brazil, India, Nepal and Sudan; 90% of mucocutaneous leishmaniasis (MCL) occurs in Bolivia, Brazil and Peru 90% of cutaneous leishmaniasis (CL) cases occur in Afghanistan, Brazil, Iran, Peru, Saudi Arabia and Syria. leishmaniasis are related to environmental changes such as deforestation, building of dams, new irrigation schemes, urbanization and migration of non-immune people to endemic areas. They seriously hamper socioeconomic progress. Epidemics have significantly delayed the implementation of numerous development programmes.
- #15: visceral leishmaniasis (VL) and is widely distributed throughout the lowlands of north-western Ethiopia.
- #24: Entrance into the host and establishment of infection by leishmanias is enhanced by saliva from the vector. Early experiments showed that the probability of infection as well as the increases in the numbers of amastigotes was many times greater when sand fly saliva was administered with the promastigotes
- #25: Leishmania Spp. live in a most unlikely place in the vertebrate host-macrophages. Macrophages are a key element of the immune system. They engulf and destroy small invading organisms. They also present antigens from these destroyed organisms to other members of the immune system. protein gp 63 and a lipophosphoglycan (LPG) mediate the uptake of promastigotes by interacting with components of the complement system and with surface molecules on the macrophages.
- #26: The promastigotes are engulfed by macrophages and contained in a so-called phagosome. The phagosome, in turn, fuses with a lysosome to form a phagolysosome. These organelles contain numerous enzymes, which normally break down organic compounds. As the promastigotes transform into amastigotes, they produce an arsenal of compounds to counter lysosomal enzymes such as catalase, superoxide dismutase, and glutathione peroxidase. The gp 63 molecule inactivates proteolytic enzymes and LPG protects against other enzymes.
- #30: Upper Eyelid. Note the dry, crusted/scabbed appearance which is different than previous sores shown. Photograph provided by COL Naomi Aronson
- #36: L. aethiopica however, can cause diffuse cutaneous leishmaniasis (DCL) in patients with little or no cell-mediated immunity against the parasite. This is an incurable condition characterized by the formation of disfiguring nodule over the surface of body. The nodule contains large number of amastigote. L. aethiopica can also cause mucocutaneous leishmaniasis.
- #39: NEW WORLD CL L. peruviana: mainly infects children. The single or few lesions are painless and usually heal spontaneously after about 4 months. The infection is known locally as ‘uta’. It occurs at high altitude in dry valleys. L. guyanensis: may give rise to painless dry single ulcers or multiple lesions scattered all over the body. There is lymph node involvement in 10% of patients .The disease often referred to as ‘forest yaws’ (‘pain bois’). Spontaneous healing is rare and relapses are frequent.
- #40: DCL caused by L. amazonensis is resistant to treatment. With L. aethiopica relapses tend to occur after treatment.
- #42: MCL is caused by new world leishmania species, L. braziliensis, L. panamensis and occasionally by L.guyanensis. In immunosuppressed persons, mucosal lesion can be caused by L.donovani, or L. major or L.infantum.
- #46: VL caused by the Leishmania donovani complex, Leishmania donovani L. infantum L. chagasi The clinical features of VL caused by different species are different, and each parasite has a unique epidemiological pattern. On the Indian subcontinent, the disease is almost exclusively caused by L.donovani. L. infantum is responsible for VL in children in the Mediterranean basin. L.chagasi causes VL in children in Latin America, where lymphadenopathy is a dominant clinical feature. Some VL cases affected their lungs, pleura, oral mucosa, larynx, oesophagus, stomach, small intestine