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  • 1. Cutaneous leishmaniasis
  • 2. INTRODUCTION • DEFINITION,CLASSIFICATION • EPIDEMIOLOGY • ETIOLOGY • PATHOPHYSIOLOGY • CLINICAL MANIFESTATIONS • DX &DDX • TREATMENT • PROGNOSIS & PREVENTION
  • 3. • It is a protozoal disease caused by a parasite called leshmania genus. • It is an obligate intracellular parasite. • Which is transmitted to humans by a sand fly bite.
  • 4. EPIDEMIOLOGY • Endemic in 88 countries of the old and new world(Africa,Asia,Europe,N.A& S.A, except Australia. • 1.5-2million new cases seen every year (WHO estimates) • 40,000 – 80,000 deaths every year (esp. MCL,VL). • Race: no racial predilection • Sex: no sex predilection • Age: no specific age susceptibility is known. • The disease is seen in tropics,subtropics & highlands.
  • 5. • Traditionally divided as Old World and New World leishmaniasis. • Old World leishmaniasis: is caused by Leishmania species found in Africa, Asia, the Middle East, the Mediterranean, and India, and • New World leishmaniasis: is caused by Leishmania species found in Central America and South America,
  • 6. THE VECTORS • Leishmania parasites are transmitted by sandflies of • the genus phlebotomus =in the old world and • the genus lutzomyia =in the new world. • Sand flies are small in size mosquito like insects 1.5- 4mm in size can pass through ordinary mesh screen and mosquito netting. Only the females are blood sucking.
  • 7. The parasite has two host life cycles.
  • 8. Leishmania parasites • members of the order kinetoplastida family trypanosomatidae • They are found in two morphologic forms= in mamalian with in macrophages as round to oval non flagellated amastigotes & • in sandfly promastigotes elongated flagellated . • Both forms of parasites have got a nucleus and DNA containing kinetoplast.
  • 9. pathophysiology … • With in the macrophages the promastigotes transform in to amastigotes (leishman-donovan bodies)→multiply by binary fission. • When a macrophage become filled with amastigotes it disrupted →amastigotes reenter the extracellular space and taken up by other macrophages.
  • 10. PATHOPHYSIOLOGY. • Parasites in the form of amastigotes from infected tissue or blood are taken up from the mamalian host during feeding, • Then with in the mid gut of the sandfly the parasites under go change to promastigotes form →multiply • then they migrate to the pharynx and proboscis of the sandfly i.e. with in 8-2o days →they remain until they are injected in to a new host during a subsequent blood meal. • Between 10-200 promastigotes enter the dermis during each feeding but most of them are destroyed by polymorphonuclear leukocytes,eosinophils & serum complement. • Some of the promastigotes become attached to receptors of the dermal macrophages and are phagocytosed = in the macrophages the promastigotes resisting.
  • 11. • Similar to Hansen disease, leishmaniasis is a disease in which the clinical diversity reflects a complex interplay between the virulence of the infecting species and the host's immune response. • At one extreme, localized cutaneous disease demonstrates a strong immune response, with most cases resolving without intervention. • This form of disease exhibits a helper T-cell subtype 1 (TH1) immune response, with cytokines that induce disease resolution.
  • 12. Clinical manifestation • Depending on the degree of the cell mediated host immune response &the type ,virulence of leishmania species the clinical classification are: • Localized cutaneous leishmaniasis • Mucocutaneous leishmaniasis • Diffuse cutaneous lesihmaniasis • Visceral leishmaniasis
  • 13. CUTANEOUS LEISHMANIASIS • OLD WORLD CL -L tropica &L. major ,L.infantum & L.aethiopica. • The disease begin as a small erythematus papule which may appear after the bite of the sand fly→the papules enlarges slowly in size (to 2 cm or more) • Over a period of several weeks a lesion becomes crusted in the center.
  • 14. CL ON THE FACE.
  • 15. CONTD… • L.tropica
  • 16. Moist (ulcerative)cutaneous leishmaniasis • usually caused by L . major • characterized by multiple lesions, • short incubation period (1 to 3 weeks) • rapid and mild course • Spontanosly heals with in 6 months. • good response to therapy.
  • 17. CL WITH S/C NODULES ALONG THE PROXIMAL LYMPHATICS.
  • 18. New world CL • found in Mexico,central America,texas& brazil. • the lesions are similar to L.major • Lesions can develop on any part of the body and • can involve the PINNA of the ears(chiclero ulcer) • L.brazilinesis can some time invade mucous mebrane.
  • 19. Diffuse cutaneous leishmaniasis • DCL in both old and new world caused by L.aethiopica& L.brazilinesis • DCL is found in 20% of leishmania pts in Ethiopia and the Sudan . • Clinically a single nodule spreads locally then by metastasis becomes wide spread with non ulcerating nodules over the face and trunk . • It resembles lepromatous leprosy.
  • 20. • DCL usually runs a protracted course but does not visceralize, • responds to therapy poorly. • Parasites are abundant in skin smear and biopsies.
  • 21. DCL ON FACE.
  • 22. Mucocutaneous lesihmaniasis • MCL = is involvement of both skin & mucus memb of upper resp tract→ by L.brazelinesis &L.aethiopica. • Mucosal lesions develop from CL in more than 75% of those infected. • A small red papule develops at the site of a sandfly bite gradually enlarges,ulcerates and the infections extends to the mucus of the mouth,nose,pharynx,to carrtillages of the upper resp tract(nose&the larynx) • Oedema &inflam.changes occur →destruction of the cartilagenous structures(nasal septum,floor of the mouth →to marked disfigurement. • BUT bony stuctures are spared.
  • 23. MCL WITH NASAL SEPTUM CARTILLAGE DESTRUCTION &DISFIGURMENT
  • 24. MCL
  • 25. MCL.
  • 26. Visceral leishmaniasis • VL(KALAZAR)=Mainly affects the reticulo-endothelial systems (spleen , BM,liver,lymphnodes) • L.DONOVANI,L.CHAGASI &L.INFANTUM • The disease present in china,india mid.east,east ,Africa &S.America. • It is one of the Common opprtunistic infection in HIV. • Patients will have splenomegally,pancytopenia,anaemia fever,wasting& imbalance of serum protiens.
  • 27. Visceral leishmniasis…. • Diagnosis =smears,cultures from BM biopsies,or spleen aspirates,serology tests are important.
  • 28. POST KALAZAR DERMAL LEISHMANIASIS • lesions usually appear with in a year after a course of therapy. • Consists of macular,papular & nodular lesions on the face,trunk & extremities. • PKDL has been reported to develop in 20% of Indian & in more than 50% of pts in the Sudan treated for VL.
  • 29. PKDL
  • 30. PKDL
  • 31. WORKUP • Lab Studies: • Cutaneous lesions – Skin scrapings are obtained from the base of an active ulcer or biopsy of the edge of a suspicious lesion or ulcer. – Visualization of all 3 features (nucleus, cell membrane, and kinetoplast) is required to make the Dx. microscopically.
  • 32. • Cultures of tissue are regularly obtained to identify Leishmania species. • PCR is now routinely used in experienced laboratories as a rapid diagnostic technique.
  • 33. Serologic test a direct agglutination test (DAT), and even a nitrocellulose dipstick test. to date is an L chagasi recombinant amastigotes K39 (rK39)–based antigen test system that has been used with enzyme-linked immunosorbent assay (ELISA), – The degree of conservation of the K39 gene is high among isolates of the L donovani family, including L chagasi and L infantum. – Therefore, this test is useful for most recognized cases of visceral leishmania. – Assays based on rK39 antigen are highly sensitive and specific and validated in several large studies worldwide.
  • 34. Management Topical therapy Topical azole Cryotherapy Local heat therapy(electrocautery) Topical parmomycine • The mainstay of antileishmanial therapy has been pentavalent antimony (sodium stibogluconate or meglumine antimonate). • Cutaneous disease: 20 mg/kg/d IV/IM for 20 D • Lesion borders: 1 mg/kg intralesional qwk. • Cure rates are 90-97%. These drugs are expensive and difficult to obtain.
  • 35. Amphotericin B • Cure rates near 100%, except possibly in HIV infection. • Dose Amphotericin B (with deoxycholate): 1 mg/kg IV for 20 d
  • 36. Ketoconazole • Azole antifungals have antileishmanial properties. • Not effective in visceral disease and should be used only as second-line therapy in limited forms of cutaneous disease with known species sensitivity (eg, rapidly self-curing disease due to L mexicana but not L tropica). • Gastric acid required for absorption. • Adult Dose 600 mg PO qd for 4 wk.
  • 37. Pentamidine (Pentam-300, Pentacarinat, NebuPent) • - Inhibits growth of protozoa by blocking oxidative phosphorylation and incorporation of nucleic acids into RNA and DNA, inhibiting protein and phospholipid synthesis. • Cutaneous disease: 2 mg/kg IV (4 doses) • Resistance common in India; high relapse rates reported.
  • 38. • Paromomycin (Aminosidine) -- Amebicidal and antibacterial aminoglycoside obtained from Streptomyces rimosus grain. • Dose15 mg/kg/d IV for 20 d • Cytokines -- Interferon-gamma a TH1 cytokine, is used to enhance host immunity to Leishmania parasites. • Interferon-gamma-1b (Actimmune) -- Recombinant DNA product. Administered with sodium antimony gluconate (probably ineffective alone). • Adult Dose 100 mg/m2/d IV for 28 d (with 20 mg/kg/d sodium antimony gluconate)
  • 39. In addition to parenteral and oral medications , local therapies for some forms of cutaneous leishmaniasis: • Cryotherapy; • Intralesional heat therapy with 40-42°C for 12 hours (One novel FDA- approved device is called the Thermo Med device.); and • Topical paromomycin preparations, typically 15% with 10% urea.
  • 40. Mortality/Morbidity: • As many as 90% of localized cutaneous forms of leishmaniasis heal spontaneously with scarring.