بسم الله الرحمن الرحيم

1. بسم الله الرحمن الرحيم

4. Visceral, Mucocutaneous and Cutaneous Leishmaniasis Leishmaniasis is a diseases of different clinical manifestations . Leishmania donovani home the liver and spleen causing (usually fatal) visceral leishmaniasis; 2. Leishmania brasiliensis homes the lining of the nose and throat causing the mucocutaneous disease, 3.Leishmania tropica homes the skin causing the self limiting skin ulcers, called cutaneous leishmaniasis

5. LEISHMANIASIS species of Leishmania : L. donovani causes visceral leishmaniasis (Kala-azar, black disease, dumdum fever); L. tropica (L.t.major, L.t. minor and L.ethiopica) cause cutaneous leishmaniasis (oriental sore, Delhi ulcer, Aleppo,or Baghdad boil). L. braziliensis ( L. mexicana is a etiologic agents of mucocutaneous leishmaniasis (espundia, Uta, chiclero ulcer).

6. Morphology -Amastigote (leishmanial form) is oval and measures 2-5 microns -Leptomonad (promastigote form) measures 14 - 20 microns a similar size to trypanosomes

7. EpidemiologyLeishmaniasis is prevalent world wide: South east Asia, Indonesia, Pakistan, Mediterranean, North and central Africa, South and central America.

9. * Endemic in Saudi Arabia

10. Types of cutaneous leishmaniasis * L.major: zoonotic cutaneous leishmaniasis: wet lesion with sever reaction. . *L.tropica: Anthroponotic cutaneous leishminiasis: dry lesions with minimal ulceration. Oriental sore (most common) classical self-limited ulcer.

11. Leishmania major –wet lesion

12. Leishmania tropica: dry type

16. Uncommon types * Diffuse cutaneous leishmaniasis (DCL): caused by L. aethiopica, diffuse nodular non-ulcerating lesion. low immunity to leishmania antigens, numerous parasites. * Leishmaniasis recidiva (lupoid leishmaniasis): sever immunological reaction to leishmania antigen leading to persistent dry skin lesions, few parasites.

17. 2 1 1-Diffuse cutaneous leishmaniasis 2-leishmaniasis recidiva (lupoid)

20. Life cycle The organism is transmitted by blood-feeding sand flies (Phlebotomus) which carry the promastigote . The parasites gain to mononuclear phagocytes where they transform into amastigotes and divide, infected cell ruptures. The released organisms infect other cells. The sand fly take the organisms during the blood meal; the amastigotes transformintoflagellate promastigotes and multiply in the gut. Dogs and rodents are common reservoirs.

22. Pathology Cutaneous leishmaniasis (Oriental sore, Delhi ulcer, Baghdad boil): the organism (L.tropica) multiplies locally, producing a papule . The papule gradually grows to form a relatively painless ulcer. The ulcer heals in 2-10 months, evenif untreated but leaves a disfiguring scar . The disease may disseminate in the case of depressed immune function.

24. Mucocutaneous leishmaniasis (espundia, Uta, chiclero) It is the same as those of cutaneous leishmaniasis, but the lesions spread to near mucous membrane (oral, pharyngeal and nasal) lead to their destruction and hence sever deformity . The organisms responsible are L. braziliensis, L. mexicana.

25. mucocutaneous leishmaniasis

26. Diagnosis: Cutaneous and mucocutaneous 1.aspirate material from edge of ulcer and stain (Giemsa).2.biopsy - pathology sections. (amastigotes = Leishmania donovani bodies =LD bodies) are seen in macrophages of aspirate and biopsy.3. culture aspirate or biopsy material in special media (NNN) producing promastigotes.

27. Treatment No treatment- It self healing lesions. Medicalpentavalent antimony (Pentostam), Amphotericin B. +/- Antibiotics for secondary bacterial infection. Surgical - Cryosurgery - Excision - Curettage

29. LEISHMANIASIS species of Leishmania : L. donovani causes visceral leishmaniasis (Kala-azar, black disease, dumdum fever); L. tropica (L.t.major, L.t. minor and L.ethiopica) cause cutaneous leishmaniasis (oriental sore, Delhi ulcer, Aleppo,or Baghdad boil). L. braziliensis ( L. mexicana is a etiologic agents of mucocutaneous leishmaniasis (espundia, Uta, chiclero ulcer).

30. Leishmania donovanivisceral leishmaniasisL.infantum :mainly in infantL.donovani :mainly in adult

33. * Endemic in Saudi Arabia

36. L.Donovani -visceral leishmaniasis

37. pathology Visceral leishmaniasis (kala-azar, dumdum fever) Organismes are localized and multiply in the mononuclear phagocytic cells of spleen, liver, lymph nodes, bone marrow, intestinal mucosa and other organs. fever. Hepatosplenomegaly.

38. Bone marrow: -leukopenia (relative monocytosis and lymphocytosis) -anemia and thrombocytopenia • hyperpigmented granulomatous skin (kala-azar means black disease). • Chronic disease renders patients susceptible to other infections. • Untreated disease results in death.

39. Post kala- azar dermal leishmaniasis

40. Presentation Fever . splenomegaly, hepatomegaly, hepatosplenomegaly Weight loss. Anemia, Epistaxis. Cough, Diarrhea. Untreated case can be fetal. After recovery may be post kala –azar dermal leishmaniasis.

41. Parasitological diagnosis *. bone marrow aspirate or spleen puncture and stain (Giemsa) . *.culture material aspirated on (NNN). .Lymph node least sensitive. .tissue biopsy

42. 1-Bone marrow biopsy 1 2 3-promastigotes 2- rosette shape promastigotes

43. Serological diagnosis: - direct agglutination test, ELISA, IFAT. - Skin test leishmanin test for survey and follow up after treatment. - non spesfic detection of hyper-gammaglobulinemia by formaldehyde (formol gel test ) or by electrophoresis. - PCR

44. Treatment - Pentavalent antimony (Pentostam) is the drug of choice. - Amphotericin B. -Treatment of anemia, bleeding, and infection.

46. African trypanosomiasis

47. African trypanosomiasis 2 species:   -Trypanosoma brucei gambiense (Africa :west of Rift valley)-Trypanosoma brucei rhodesiense (Africa :east of Rift valley)

49. The reservoir Humans and wild animals (zoonosis) The vector Glossina (Tsetse) flies

50. Glossina