leishmaniasis (leishmania)

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Leishmaniasis (Leishmania)

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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: - PowerPoint PPT Presentation

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Page 1: Leishmaniasis  (Leishmania)

Leishmaniasis (Leishmania)

Page 2: Leishmaniasis  (Leishmania)

caused by intracellular protozoan parasites of the genus Leishmania

transmitted by phlebotomine sandfliesdisease involving the skin and mucosal

surfaces and the visceral reticuloendothelial organs.

Page 3: Leishmaniasis  (Leishmania)

ETIOLOGYparasite is dimorphic:1. flagellate promastigote in the insect vector2. aflagellate amastigote that resides and

replicates only within mononuclear phagocytes

Page 4: Leishmaniasis  (Leishmania)

kala-azarinoculation of the organism :1. asymptomatic infection 2. 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.

Page 5: Leishmaniasis  (Leishmania)

kala-azarDuring the 1st few weeks to months of

disease evolution the fever is intermittentthere is weakness and loss of energyspleen begins to enlargeThe 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

Page 6: Leishmaniasis  (Leishmania)
Page 7: Leishmaniasis  (Leishmania)

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.

Page 8: Leishmaniasis  (Leishmania)

LABORATORY FINDINGSanemia (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).

Page 9: Leishmaniasis  (Leishmania)

DIFFERENTIAL DIAGNOSISmalaria, typhoid fever, miliary tuberculosis schistosomiasis brucellosis amebic liver abscess infectious mononucleosis lymphoma and leukemia

Page 10: Leishmaniasis  (Leishmania)

DIAGNOSISSerologic 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

Page 11: Leishmaniasis  (Leishmania)

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.

Page 12: Leishmaniasis  (Leishmania)

TREATMENTpentavalent antimony compounds and

meglumine antimoniate (20 mg/kg/day intravenously or intramuscularly for 28 days )

Amphotericin B desoxycholate amphotericin lipid formulationsParomomycininterferon-γMiltefosine

Page 13: Leishmaniasis  (Leishmania)

PREVENTIONavoidance of exposure to the

nocturnal sandfliesinsect repellent and permethrin-

impregnated mosquito nettingvaccine