Med Helmenths Kalazar
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  • 1. LEISHMANIASIS : Dr.Mohamad Shaikhani.
  • 2. LEISHMANIASIS :
    • Caused by unicellular flagellate intracellular protozoa with 3 clinical syndromes:
    • Visceral leishmaniasis (VL, kala-azar)
    • Cutaneous leishmaniasis (CL)
    • Mucosal leishmaniasis (ML).
    • Most caused by zoonotic transmission from animals (chiefly canine /rodent reservoirs) to humans through phlebotomine sandfly.
    • Humans are the only known reservoir (anthroponotic) in major VL foci in India /Sudan.
    • The disease occurs in 88 countries, with annual incidence of 2 million new cases (500 000 for VL,1.5 million for CL).
  • 3. 3- Another sandfly bites human and ingests blood infected with Leishmania 2- Sandfly bites human and injects Leishmania into skin 1- Sandfly bites animal and ingests blood infected with Leishmania 4- Cycle continues when sandfly bites another human or animal reservoir
  • 4. LEISHMANIASIS :
  • 5. VISCERAL LEISHMANIASIS (KALA-AZAR):
    • Caused by protozoon Leishmania donovani complex, transmitted by the phlebotomine sandfly.
    • Rarely, a dermatotropic species (e.g. Leishmania tropica ) may cause visceral disease.
    • India, Sudan, Bangladesh,Brazil account for 90% of cases of VL, ,others include the Mediterranean, East Africa, China, Arabia, Israel & other South American countries.
    • Transmission reported to follow blood transfusion in N Europe.
    • Can present unexpectedly in immunosuppressed as renal transplantation & AIDS
  • 6. VISCERAL LEISHMANIASIS (KALA-AZAR):
  • 7. VISCERAL LEISHMANIASIS (KALA-AZAR):
  • 8. Pathogenesis:
    • The great majority remain asymptomatic&control the infection.
    • Those unable to do so develop clinical disease.
    • In visceral diseases the spleen, liver, bone marrow & lymph nodes are primarily involved.
  • 9. Clinical features:
    • In India both adults/ children equally affected; in others predominantly children / infants, except if HIV co-infection.
    • Malnutrition increases susceptibility to the visceral disease.
    • The IP: weeks-months (occasionally several years).
    • The first sign is high fever, usually accompanied by rigor /chills.
    • Fever intensity decreases over time & patients may become afebrile for intervening periods ranging from weeks to months, followed by a relapse of fever, often of lesser intensity.
    • Splenomegaly develops quickly in the first few weeks & becomes massive as the disease progresses, hepatomegaly occurs later, to a lesser degree than splenomegaly.
    • Lymphadenopathy is seen in the majority in Africa,Mediterranean &South America but is rare in India.
  • 10. Clinical features:
    • Black skin or kala-azar (Hindi word), is a feature of advanced illness, now rarely seen.
    • Pancytopenia with its clinical manifestations is a common feature.
    • Moderate to severe anemia develops rapidly& result in CHF &associated clinical features.
    • Thrombocytopenia, often with hepatic dysfunction, may result in bleeding from retina, GIT& nose.
    • In progressive disease, hypoalbuminaemia causes leg oedema , ascites & anasarca & if advanced, profound immunosuppression &secondary infections are very common,as TB, pneumonia, amoebic or bacillary dysentery, gastroenteritis, herpes zoster& chickenpox.
    • Skin infections, boils, cellulitis & scabies are common occurrences.
    • Without adequate treatment most die.
  • 11. Investigations:
    • Pancytopenia is the most dominant feature, with granulocytopenia &monocytosis.
    • Polyclonal hypergammaglobulinaemia, chiefly IgG followed by IgM& hypoalbuminaemia are seen later.
    • Patients are anergic to the leishmanin antigen skin test (LST)& there is antigen-specific immunosuppression when peripheral blood mononuclear cells are challenged with Leishmania antigen ex vivo.
    • After successful chemotherapy there is recovery of immunity & the LST becomes positive.
  • 12. Diagnosis:
    • Demonstration of amastigotes (Leishman-Donovan bodies) in splenic smears is the most efficient means of diagnosis, with 98% sensitivity; but carries a risk of serious haemorrhage.
    • Safer methods like BM or LN smears are not as sensitive.
    • Parasites may be demonstrated in buffy coat smears, especially in immunosuppressed patients.
    • Sensitivity can be improved by culturing the aspirate material,but expensive only available in well-equipped labs.
    • PCR for DNA detection from the peripheral blood is an efficient non-invasive method for diagnosis, but is only in specialised labs& also used for species identification.
  • 13. Diagnosis:
    • Serodiagnosis, by ELISA or immunofluorescence antibody test, is employed in developed countries.
    • In endemic regions, a highly sensitive/specific direct agglutination test of stained promastigotes & an equally efficient rapid immunochromatographic k39 strip test have become popular.
    • These tests remain positive for several months after cure, so do not predict response to treatment or relapse.
    • A significant proportion of the healthy population in an endemic region will be positive for these tests due to past exposure.
  • 14. Diagnosis:
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  • 17. Differential diagnosis:
    • Malaria
    • Typhoid
    • Tuberculosis
    • Schistosomiasis
    • Many other infectious &neoplastic conditions, some of which may coexist with VL.
    • Fever, splenomegaly, pancytopenia & non-response to antimalarial therapy may provide the clue before specific lab diagnosis is made.
  • 18. Treatment: Pentavalent antimonials
    • Antimony (Sb) compounds were the first drugs used & remain the mainstay.
    • The exception is the India, where almost two-thirds of cases are refractory.
    • Traditionally, pentavalent antimony is available as sodium stibogluconate (100 mg/ml) & meglumine antimoniate (85 mg/ml).
    • The daily dose is 20 mg/kg body weight, given either intravenously or intramuscularly for 28-30 days.
    • Side-effects are common and include arthralgias, myalgias, raised hepatic transaminases, pancreatitis, especially in patients co-infected with HIV&ECG changes (T wave inversion and reduced amplitude).
    • Severe cardiotoxicity, manifested by concave ST segment elevation, prolongation of QTc > 0.5 msec, ventricular ectopics, runs of ventricular tachycardia, torsades de pointes, ventricular fibrillation & sudden death, is not uncommon.
    • The incidence of cardiotoxicity & death can be very high with improperly manufactured Sb
  • 19. Amphotericin B
    • Given once daily or on alternate days for 15-20 doses, is used in patients with Sb failure or unresponsiveness.
    • It has a cure rate of nearly 100%.
    • Infusion-related side-effects, e.g. high fever with rigor, thrombophlebitis, diarrhoea & vomiting, are extremely common.
    • Serious adverse events, as renal or hepatic toxicity, hypokalaemia, thrombocytopenia, myocarditis& occasional death, are not uncommon.
    • Lipid formulations & liposomal amphotericin B are less toxic.
  • 20. Miltefosine
    • An alkyl phospholipid, approved for the treatment of VL.
    • A daily dose of 50 mg (patient's body weight < 25 kg) to 100 mg (≥ 25 kg), or 2.5 mg/kg body weight for children, for 28 days cures over 90%.
    • Side-effects include mild to moderate vomiting /diarrhoea/ rarely skin allergy or nephrotoxicity.
    • Since it is a teratogenic drug, it cannot be used in pregnancy; female patients are advised not to become pregnant for the duration of treatment &another 2 months, because of its half-life of nearly 1 week.
  • 21. Paromomycin
    • An aminoglycoside, highly effective if given intramuscularly at 15 mg/kg body weight daily for 3 weeks.
    • No significant auditory or renal toxicity is seen.
  • 22. Post-kala-azar dermal leishmaniasis
    • (PKDL) After treatment &recovery from the visceral disease in India & Sudan some patients develop dermatological manifestations.
    • In India dermatological changes occur in a small minority of patients 6 months to ≥ 3 years after the initial infection seen as macules, papules, nodules (most frequently) & plaques which have a predilection for the face, especially the area around the chin.
    • The face often appears erythematous.
    • Hypopigmented macules can occur over all parts of the body &are highly variable in extent and location.
    • There are no systemic symptoms & no spontaneous healing.
  • 23. Post-kala-azar dermal leishmaniasis
    • The diagnosis is clinical, supported by demonstration of scanty parasites in lesions by slit skin smear&culture.
    • Immunofluorescence & immunohistochemistry are other methods for demonstration of the parasite in skin tissues.
    • In the majority of patients serological tests (direct agglutination test or k39 strip tests) are positive.
    • Treatment of PKDL is difficult. Sb for 120 days or several courses of amphotericin B infusions are required.
    • In the absence of a physical handicap, most patients are reluctant to complete the treatment.
    • PKDL patients are a human reservoir& focal outbreaks have been linked to patients with PKDL in areas previously free of VL.
  • 24. kala-azar prevention:
    • Multipronged approach is needed.
    • Sandflies are extremely sensitive to insecticides & vector control through insecticide spray is very important.
    • Mosquito nets or curtains treated with insecticides will keep out the tiny sandflies.
    • In endemic areas with zoonotic transmission, infected or stray dogs should be destroyed.
    • In areas with anthroponotic transmission, early diagnosis & treatment of human infections, to reduce the reservoir & control epidemics of VL, is extremely important.
    • Serology is useful for screening of suspected cases in the field.
    • No vaccine is currently available .
  • 25. Cutaneous & mucous leishmaniasis: Solitary facial lesions with satellites Hyraxes L. aethiopica Rapid necrosis, wet sores Gerbils, desert rodents L. major Oriental sore(Baghdad boil) Dogs L. tropica Clinical features Host Leishmania species
  • 26. Post-kala-azar dermal leishmaniasis
  • 27. Cutaneous leishmaniasis.
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