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Leishmaniasis (Leishmania)

Leishmaniasis (Leishmania). caused by intracellular protozoan parasites of the genus Leishmania transmitted by phlebotomine sandflies disease involving the skin and mucosal surfaces and the visceral reticuloendothelial organs. ETIOLOGY. parasite is dimorphic:

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Leishmaniasis (Leishmania)

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  1. Leishmaniasis (Leishmania)

  2. caused by intracellular protozoan parasites of the genus Leishmania • transmitted by phlebotomine sandflies • disease involving the skin and mucosal surfaces and the visceral reticuloendothelial organs.

  3. ETIOLOGY • parasite is dimorphic: • flagellate promastigote in the insect vector • aflagellate amastigote that resides and replicates only within mononuclear phagocytes

  4. kala-azar • inoculation of the organism : • asymptomatic infection • Oligosymptomatic (malaise, intermittent diarrhea, poor activity tolerance) and intermittent fever,mildly enlarged liver In most of these children the illness will resolve without therapy 3 approximately ¼ it will evolve to active kala-azar within 2–8 mo.

  5. kala-azar • During the 1st few weeks to months of disease evolution the fever is intermittent • there is weakness and loss of energy • spleen begins to enlarge • The classic clinical features of • 1- high fever, 2-marked splenomegaly, 3-hepatomegaly, and4- severe cachexia typically develop approximately 6 mo after the onset of the illness

  6. At the terminal stages of kala-azar hepatosplenomegaly is massive, gross wasting, pancytopenia is profound, and jaundice, edema, and ascites may be present. • Anemia may be severe enough to precipitate heart failure. Bleeding episodes, especially epistaxis, are frequent. • The late stage of the illness is often complicated by secondary bacterial infections, which frequently are a cause of death. • Death occurs in >90% of patients without specific antileishmanial treatment.

  7. LABORATORY FINDINGS • anemia (hemoglobin 5–8 mg/dL), • thrombocytopenia, • leukopenia (2,000–3,000 cells/μL), • elevated hepatic transaminase levels, • hyperglobulinemia (>5 g/dL) that is mostly immunoglobulin G (IgG).

  8. DIFFERENTIAL DIAGNOSIS • malaria, • typhoid fever, • miliary tuberculosis • schistosomiasis • brucellosis • amebic liver abscess • infectious mononucleosis • lymphoma • and leukemia

  9. DIAGNOSIS • Serologic testing : enzyme immunoassay, indirect fluorescence assay, or direct agglutination is very useful in VL because of the very high level of antileishmanial antibodies • enzyme-linked immunosorbent assay using a recombinant antigen (K39) has a sensitivity and specificity for VL that is close to 100% • A negative serologic test result in an immunocompetent individual is strong evidence against a diagnosis of VL

  10. Definitive diagnosis is established by the demonstration of amastigotes in tissue specimens or isolation of the organism by culture. • In patients with VL, smears or cultures of material from splenic, bone marrow, or lymph node aspirations are usually diagnostic.

  11. TREATMENT • pentavalent antimony compounds and meglumine antimoniate (20 mg/kg/day intravenously or intramuscularly for 28 days ) • Amphotericin B desoxycholate • amphotericin lipid formulations • Paromomycin • interferon-γ • Miltefosine

  12. PREVENTION • avoidance of exposure to the nocturnal sandflies • insect repellent and permethrin-impregnated mosquito netting • vaccine

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