4 Visceral, Mucocutaneous and Cutaneous Leishmaniasis Leishmaniasis is a diseases of different clinical manifestations .Leishmania donovanihome the liver and spleen causing (usually fatal) visceral leishmaniasis;2. Leishmania brasiliensishomes the lining of the nose and throat causing the mucocutaneous disease,3.Leishmania tropicahomes the skin causing the self limiting skin ulcers, called cutaneous leishmaniasis
5 L. tropica L. braziliensis LEISHMANIASIS species of Leishmania : L. donovanicauses visceral leishmaniasis(Kala-azar, black disease, dumdum fever);L. tropica(L.t.major, L.t. minor and L.ethiopica) causecutaneous leishmaniasis(oriental sore, Delhi ulcer, Aleppo,or Baghdadboil).L. braziliensis( L. mexicana is a etiologic agents of mucocutaneous leishmaniasis (espundia, Uta, chiclero ulcer).
6 -Amastigote (leishmanial form) is oval and measures 2-5 microns Morphology-Amastigote (leishmanial form)is oval and measures 2-5 microns-Leptomonad (promastigote form)measures micronsa similar size to trypanosomes
7 South east Asia, Indonesia, Pakistan, Mediterranean, Epidemiology Leishmaniasis is prevalent world wide:South east Asia, Indonesia,Pakistan,Mediterranean,North and central Africa,South and central America.
20 Life cycleThe 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 transform into flagellate promastigotes and multiply in the gut.Dogs and rodents are common reservoirs.
22 Cutaneous leishmaniasis PathologyCutaneous 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, even if 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.
26 Cutaneous and mucocutaneous Diagnosis:Cutaneous and mucocutaneous1. aspirate material from edge of ulcer andstain (Giemsa). 2. biopsy - pathology sections.(amastigotes = Leishmania donovanibodies =LD bodies) are seen inmacrophages of aspirate and biopsy. 3. culture aspirate or biopsy material inspecial media (NNN) producingpromastigotes.
27 Treatment Medical pentavalent antimony Surgical No treatment- It self healing lesions.Medical pentavalent antimony(Pentostam), Amphotericin B.+/- Antibiotics for secondary bacterialinfection.Surgical- Cryosurgery- Excision- Curettage
29 L. tropica L. braziliensis LEISHMANIASIS species of Leishmania : L. donovanicauses visceral leishmaniasis(Kala-azar, black disease, dumdum fever);L. tropica(L.t.major, L.t. minor and L.ethiopica) causecutaneous leishmaniasis(oriental sore, Delhi ulcer, Aleppo,or Baghdadboil).L. braziliensis( L. mexicana is a etiologic agents of mucocutaneous leishmaniasis (espundia, Uta, chiclero ulcer).
30 Leishmania donovani visceral leishmaniasis L Leishmania donovani visceral leishmaniasis L.infantum :mainly in infant L.donovani :mainly in adult
37 (kala-azar, dumdum fever) pathologyVisceral 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 (relative monocytosis and lymphocytosis) -anemia and thrombocytopenia Bone marrow:-leukopenia(relative monocytosis and lymphocytosis)-anemia and thrombocytopeniahyperpigmented granulomatous skin(kala-azar means black disease).Chronic disease renders patients susceptible to other infections.Untreated disease results in death.
40 Presentation Fever . splenomegaly, hepatomegaly, hepatosplenomegaly Weight loss.Anemia, Epistaxis.Cough, Diarrhea.Untreated case can be fetal.After recovery may be postkala –azar dermal leishmaniasis.
41 Parasitological diagnosis *. bone marrow aspirate or spleenpuncture and stain (Giemsa) .*.culture material aspirated on(NNN)..Lymph node least sensitive..tissue biopsy
43 Serological diagnosis: - direct agglutination test, ELISA,IFAT.- Skin test leishmanin test for surveyand follow up after treatment.- non spesfic detection ofhyper-gammaglobulinemia byformaldehyde (formol gel test ) orby electrophoresis.- PCR
44 Treatment - Pentavalent antimony (Pentostam) is the drug of choice.- Amphotericin B.- Treatment of anemia, bleeding, andinfection.
51 African Trypanosomiasis (African Sleeping Sickness) A hemo-flagylate found only in Africa.In East Africa disease, transmitted from resevoir animal to man by the vector tsetse fly (Glossina) zoonosis.In west Africa it is transmitted by tsetse human to human..
53 Life cycleThe infective metacyclic trypanosome is injected into host during a bite by tsetse fly .it enters the draining lymphatic and blood stream.The trypanosomal form enters the vector during the blood meal and travels through the alimentary canal to the salivary gland where it proliferates as epimastigotes form and matures to infectious metacyclic forms.
55 PathogenesisTsetse bites man and injects saliva containing trypanosomes into the wound.These multiply locally producing a local lesion.trypanosome multiplies by binary fission extracellularly producing fever and lymphadenopathy .then reaches the central nervous system producing a meningoencephalitis.
57 Trypomastigotes can traverse the walls of blood and lymph capillaries into the connective tissues at a later stage, cross the choroid plexus into the brain and cerebrospinal fluid.The organism can be transmitted through blood transfusion.
58 Clinical picture - trypanosomal chancre - parasitemia with fever - lymphadenopathygeneralized organ involvement. - central nervous system meningoencephalitis, coma and death
59 Bite reaction:T.chancreA non-pustular, painful, itchy chancre appears 1-3 weeks after the bite and lasts 1-2 weeks. It leaves no scar
75 1-The primary lesion, chagoma, appearing at the site of bite Symptoms Chagas' disease can be divided into three stages:1-The primary lesion, chagoma, appearing at the site of bite. Infection in the eyelid, resulting in a unilateral conjunctivitis and orbital edema (Ramana's sign)
78 2-Acute Stage: Fever, bone and muscle pains. hepatomegaly, and rash. lymphadenopathy.Diffuse myocarditis, sometimes pericarditis and endocarditis.In children, Chagas' disease may cause meningo-encephalitis and coma.Death occurs in 5-10 percent.
79 3-The chronic: stage results in an abnormal function of the hollow organs, particularly the heart, esophagus and colon.The cardiac changes include myocardial insufficiency, cardiomegaly.Disturbances of peristalsis lead to megaesophagus and megacolon .