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III- Visceral Leishmaniasis (Kala Azar) Kala AzarDum-dum feverBlack feverDeath fever Tropical Splenomegaly Syndrome Etiology 1- L. donovani 1- L. donovani.

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Presentation on theme: "III- Visceral Leishmaniasis (Kala Azar) Kala AzarDum-dum feverBlack feverDeath fever Tropical Splenomegaly Syndrome Etiology 1- L. donovani 1- L. donovani."— Presentation transcript:

1 III- Visceral Leishmaniasis (Kala Azar) Kala AzarDum-dum feverBlack feverDeath fever Tropical Splenomegaly Syndrome Etiology 1- L. donovani 1- L. donovani common in Adults (over 10 years) India (Man to man) / Africa (Rodents is R.H) / Middle East. 2- L. infantum 2- L. infantum common in children (under 10 years) common Mediterranean / Middle East / Africa. 3- L. chagasi 3- L. chagasi common in children (under 10 years) Central & South America Dr. RAAFAT TAHA MOHAMED

2 III- Visceral Leishmaniasis (Kala Azar) Epidemiology V.L * Cases of V.L. recorded annually are about * Annual death range from * The Disease is endemic in Mediterranean area & became indicator for AIDS patients in Spain. * The Disease is mainly Zoonotic among dogs & Rodents. * In India & Bangladesh it is Anthroponotic. * Endemicity is determined by close contact between Reservoir Host & Vectors. Dr. RAAFAT TAHA MOHAMED

3 Visceral Leishmaniasis Dr. RAAFAT TAHA MOHAMED

4 Pathogenesis of Visceral Leishmaniasis 1-Leishmanioma: Small papule --- Nodule (rarely Ulcerate) Amastigote within skin macrophages. N.B: - Effective cellular immune response controls dissemination of infection. -Malnutrition & Immunosuppression --- contribute in disease development. - V.L. is an immunosuppressive disease. - Children & young Adults are more susceptible to the infection. - Immunocompromized develop highly fatal severely progressive disease. Dr. RAAFAT TAHA MOHAMED

5 Pathogenesis of Visceral Leishmaniasis Incubation period 2- Incubation period: several months to years, now it can be few days Infection skin lesion R.E.S 3- Infection spread from primary skin lesion haematogenously to organs R.E.S. (BONE MARROW – LYMPHOID TISSUE – SPLEEN – LIVER – G.I.T …etc. Amastigotegranulomatous reactionHyperplasia & Hypertrophy 4-Amastigote multiply intracellularly granulomatous reaction Hyperplasia & Hypertrophy of affected organ. Progressive disease may lead to the followings: Bone marrow suppression 1-Bone marrow suppression PANCYTOPENIA ( Anemia – Leucopenia /Neutropenia “tendency to bacterial infection” – Thrombocytopenia “bleeding tendency”). Massive Splemomegaly 2- Massive Splemomegaly early destruction & short life span of R.B.Cs Anemia. Dr. RAAFAT TAHA MOHAMED

6 Pathogenesis of Visceral Leishmaniasis Progressive disease may lead to the followings: Secondary bacterial infection 3- Secondary bacterial infection ( due to Neutropenia / compromised immunity / malnutrition) Otitis media – Pneumonia - Septicemia Liver affection reversed A/G ratio 4- Liver affection reversed A/G ratio Hypoalbuminaemia Oedema. Immune complexes mild glomerulonephritis ( Nephrotic syndrome 5- Immune complexes mild glomerulonephritis (deposition of C.I.C. in glomerular capillaries) Nephrotic syndrome may lead to death. Dr. RAAFAT TAHA MOHAMED

7 Pathogenesis of Visceral Leishmaniasis Leishmanioma is rarely seen at the site of bite Promastigotes Via blood stream to Reticulo-endothelial cells present in human viscera Liver: Spleen: Lymph nodes: Bone marrow: Intestinal mucosa: Taken by hepatomegaly splenomegaly enlarged Amastigotes Reversal of albumin / globulin ratio diarrhoea & dysentery thrombocytopenia marrow RBCs WBCs Platelets Anaemia,leukopenia, Dr. RAAFAT TAHA MOHAMED

8 Clinical picture of Visceral Leishmaniasis Asymptomatic Asymptomatic “ most common” Symptomatic Symptomatic infections may lead to the following: Leishmanioma 1- Leishmanioma (Primary skin lesion). 2- Fever: irregular – prolonged – intermittent (2-3 peaks daily). dromedary fever Splenomegaly 3- Splenomegaly: progressively enlarged /soft / tender Hepatomegaly 4- Hepatomegaly: progressively enlarged /soft / tender Lymphadenopathy. 5- Lymphadenopathy. Jaundice. 6- Jaundice. Skin 7- Skin is darkly Pigmented at face, hands & feets Diarrhea or Dysentery. 8- Diarrhea or Dysentery. 9- Weight loss. Dr. RAAFAT TAHA MOHAMED

9 OWVL hepatosplenomegaly NWVL hepatosplenomegaly Clinical Picture of Visceral Leishmaniasis 1- Fever: intermittent with double daily rise. Also called Dum-dum fever 2- hepatosplenomegaly (Dum-dum is a town in Calcutta in India) Dr. RAAFAT TAHA MOHAMED

10 Clinical Picture of Visceral Leishmaniasis 3- Skin changes Dark pigmentation or depigmentation (butterfly pigmentation) (also called Kala azar كلمة باللغة الهندية means black fever) 4- Post kala azar dermal leishmanoid (PKDL) Skin nodules. 1- Spontaneous arrest of the disease 2- Incomplete antimony treatment 5- Weight loss, emaciation, death from inter-current infection (cancrum oris, pulmonary, gastrointestinal infections). Persistent allergic reaction to parasite antigens Seen in two conditions Leishmania causes suppression of cell-mediated immunity Disturbance of pigmentation occurs Dr. RAAFAT TAHA MOHAMED

11 Post KALA-AZAR Dermal Leishmaniasis (P.K.D.L) V.LP.K.D.L * About 15-20% of V.L. patients develop P.K.D.L in 1-5 years post infection Skin lesion * Skin lesion develops after apparent cure or shortly after or during treatment Lesions appear as follows: (A)- Multiple depigmented macules /papules/nodules. face (B)- Common in face resemble “Lepromatous leprosy” – Limbs upper trunk Limbs – upper trunk. (C)- Chronic persistent lesion rarely ulcerate. Dr. RAAFAT TAHA MOHAMED

12 Skin changes in visceral leishmaniasis Depigmented areas Post Kala-Azar dermal leishmanoid Usually occur in patients from the old world Butterfly pigmentation Dr. RAAFAT TAHA MOHAMED

13 Areas where Visceral Leishmaniasis exists Old world visceral leishmaniasis New world visceral leishmaniasis L.infantum L.donovani L.chagasi Brazil Dr. RAAFAT TAHA MOHAMED

14 Diagnosis of V. Leishmaniasis Clinically: Ulcer with sharp cut indurated margin Clinically: Fever, hepatosplenomegaly To detect amastigotes at the edge of the ulcer by aspiration or biopsy To detect amastigotes in blood, liver, spleen, lymph node, bone marrow Microscopy: Culture: Animal inoculation Montenegro test Serological tests To detect promastigotes ˃ 95% +ve after successful treatment Necrotic tissue Amastigotes C. Leishmaniasis Dr. RAAFAT TAHA MOHAMED

15 Aspiration and biopsy from the ulcer AspirationScrape or take biopsy Leishmania amastigotes (Giemsa stained) Dr. RAAFAT TAHA MOHAMED

16 Bone marrow Amastigote Aspiration and biopsy from Bone marrow Bone marrow aspiration Supportive Laboratory Findings: 1- Reversal A/G ratio. 2- Hypergammaglobinaemia. 3- Anemia. 4- Neutropenia. 5- Thrombocytopenia. Dr. RAAFAT TAHA MOHAMED

17 Promastigotes in rosettes in a culture of an orient sore on N.N.N. medium (Giemsa stain). Diagnosis (cont.) Montenegro “Leishmanin” Test: 1-Detects Delayed type Hypersensitivity. -ve V.L. 2- -ve during acute stage of V.L. 3- +ve after cure. 4- Negative for D.C.L. (suppressed immunity). 5- In Endemic areas, high % of population are positive. Dr. RAAFAT TAHA MOHAMED

18 Immunological Diagnosis: Specific serologic tests: Direct Agglutination Test (DAT), ELISA, IFAT Non specific detection of hypergammaglobulinaemia by formaldehyde (formol-gel) test or by electrophoresis. Diagnosis (cont.) Dr. RAAFAT TAHA MOHAMED

19 Buffy Coat Method RBCs Plasma WBCs, platelets, parasite Patient’s blood Buffy coat Centrifuge A technique used for collection of parasite from blood sample Dr. RAAFAT TAHA MOHAMED

20 Treatment Cutaneous leishmaniasisVisceral leishmaniasis Antimony sodium gluconate (Pentostam) Given intramuscularly Treatment of ulcer Surgical excision Curettage Heat, freezing Physical 2% chlopromazine & clortrimazole Chemical I.D. injection of interferon gamma around the lesion to promote healing of the ulcer Dr. RAAFAT TAHA MOHAMED

21 Control of Leishmaniasis  Treatment of Patients  Protection: by using Wire screens, repellents & mosquito nets  Control of sandfly vector  Vaccination in endemic areas gives long lasting immunity Dr. RAAFAT TAHA MOHAMED

22 Case A female patient went to dermatology clinic suffering from skin lesion. On examination, the doctor noticed a skin ulcer with sharp edge and indurated margin The patient gave a history of an arthropod bite. a- What is your provisional diagnosis? b- How can you confirm your diagnosis? c- How can you manage such condition? A case of Cutaneous leishmaniasis Amastigotes By microscopy, culture, skin test or serological tests. Pentostam I.M., Physical, chemical methods, ID injection of interferon gamma of ulcer Dr. RAAFAT TAHA MOHAMED

23 Case A young Egyptian arriving from Jordan where he was working as a laborer and living in campus. He has a chronic ulcer on his arm with sharp-cut edge that resist treatment by known antibiotics. a- What is your provisional diagnosis? Cutaneous leishmaniasis. c- How can you manage such case? Pentostam I.M. and surgical or chemical treatment for ulcer. c- How can you control such infection? Treat patients, protect the healthy, control of sandfly. b- How can you confirm your diagnosis? By microscopy, culture, skin test or serological tests. Dr. RAAFAT TAHA MOHAMED

24 Compare between Ulcer produced by Detection of amastigotes from edge of the ulcer Detection of amastigotes in blood, liver, spleen, lymph node, bone marrow In urban areas In rural areas Montenegro test positive in 95% of cases Montenegro test positive after successful treatment Diagnosis of Cutaneous and Visceral leishmaniasis. L.tropicaL.major Dry, single chronic Wet, multiple acute Dr. RAAFAT TAHA MOHAMED

25 Stained smears from organs in kala-azar show: b- Promastigote form a- Epimastigote formc- Amastigote form d- Trypomastigote form To diagnose cutaneous leishmaniasis, biopsy is better taken from: a- base of the ulcer b- edge of the ulcerd- skin around the ulcer c- lymph node draining the ulcer The following arthropod transmits visceral leishmaniasis: a- Culicoides b- Chrysops c- Simulium d- Phlebotomus MCQ Dr. RAAFAT TAHA MOHAMED

26  To diagnose cutaneous leishmaniasis a biopsy is better taken from the base of the ulcer. State true or false  Amastigote forms of Leishmania occur in culture. Give reason Leishmania parasites are present in small number in patient's blood. Leishmania parasites are taken by the reticuloendothelial cells of viscera Promastigote forms of Leishmania occur in culture False A biopsy is better taken from the edge of the ulcer where Leishmania amastigotes exist, the base of ulcer contains only necrotic tissue Dr. RAAFAT TAHA MOHAMED


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