leshmania

LEISHMANIASIS



BANGAR RAJU DEPT OF MICROBIOLOGY KMC-IC



LEISHMANIA

 Hemoflagellate—Protozoa  Sir William Leishman  Taxonomy - controversial  Vector- Sand fly  Old world( Eurasia, Africa)- genus Phlebotomus  New world (Americas)- Lutzomyia



Primary hosts-Vertebrates Infects hyraxes, canids, rodents, humans Rare in developed countries Common in war torn endemic countries & AIDS patients 12 million people /yr 300 million at risk



Species and clinical groupings

 L.donovani- Visceral Leishmaniasis /kala azar  L.tropica, L. major, L. ethiopicaoriental sore or Old world Cutaneous Leishmaniasis  L. braziliensis , L. mexicanamucocutaeneous Leishmaniasis, New world Leishmaniasis , Espundia



Leishmania

morphology



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Amastigote (leishmania) seen in the mammalian host Promastigote (leptomonad) seen in sand fly



GEOGRAPHICAL DISTRIBUTION

Cutaneous- Afghanistan, Brazil, Iran, Peru, Saudi arabia, Syria Mucocutaneous- Bolivia, Brazil, Peru Visceral /kala azar- Bangla desh , Brazil, India, Nepal, Sudan



Cutaneous: papule at the site of biteraised nodule -ulcerates  Face & extremities, heals in 1-2 yrs  Immune to reinfection Mucocutaneous:  Severe and malignant form of cut lesions  Invasion of oro-nasal mucosa (espundia)  Starts as papulopustular swelling in skin localised around mouth, nostrils or eyes or spread on face, elbows or knees



 Destructive mutilating erosions leading to disfiguration  Complete destruction of nasal septum, perforation of palate, damage to tissues of lips and nasopharynx  Months-20yrs  Death is due to asphyxiation (blockage of trachea), starvation or respiratory infection.



Ecological types of Visceral Leishmaniasis:

Indian kala-azar  L.donovani, young adults, reservoir is man, not zoonotic, vector P. argentipes  Sequelae is PKDL Infantile kala-azar:  Children< 5yrs,  L donovani infantum,  zoonotic Disease  reservoirs –dogs, mongoose,  vector-P orientalis,P martini



South American kala-azar:

 L donovani chagasi, zoonotic, reservoirs foxes, wild canines, vector Lutzomyia longipalpis



KALA-AZAR:

 Black sickness, Dum dum fever, tropical splenomegaly  Spreads from site of inoculation into RE cells (macrophages in liver, spleen lymph nodes, bone marrow)



 Irregular fever, anaemia, enlarged spleen, liver  Multiplication in bone marrow leads to loss of blood forming tissues –  leucopenia, thrombocytopenia ( results in bleeding gums),  untreated die within 2 yrs  PKDL-Cutaneous Leishmaniasis seen in 2-10% Kala-azar patients in India 1-2 yrs later after completion of antimonal treatment



PKDL -3types:

 Hypopigmented patches –earliest lesions on trunk and extremities, face less affected  Erythematous patches -early lesions on nose, cheeks, chin-butterfly erythema photosynthetic-prominent during day  Yellow-pink nodules -on skin (face) rarely on mucous membranes of tongue, eyes. granulomatous, painless, no ulceration



Leishmania

symptoms

type viscera organ Involved liver, spleen, bone marrow, lymph nodes, skin skin symptoms bite reaction; lymphadenopathy, splenomegaly and hapatomegaly; parasitemia, chills and fever; darkening of skin centrifugally growing papular lesion with central crusting; heals spontaneously, permanent scar initially same as cutaneous lesion but it does not heal: necrosis of mucoid tissue; metastasis to distant mucoid tissues; very disfiguring



cutaneous



mucocutaneous



Skin and mucoid tissue



Visceral Leishmania

 1-4 months: fever chills, diarrhea, dysentery  Progressive hepatosplenomegaly  skin hyperpigmentation  Death, if untreated



Prominent feature in visceral Leishmaniasis:



Visceral Leishmaniasis



Cutaneous leishmaniasis



Disseminated cutaneous leishmaniasis



Mucocutaneous leishmaniasis



Mucocutaneous



Cutaneous



Leishmaniasis diagnosis History Lesions or symptoms Organisms in the lesion

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Montenegro test

(type IV hypersensitivity)



Leishmaniasis Pathogenesis and immunology Damage due to CMI Leishmanial proteoglycan Leukopenia with monocytosis and lymphocytosis immunosuppression Interferon and TNF are protective



Lab diagnosis:  Lymph node aspirates, scrapings, biopsies from margin of lesion –Cutaneous forms  Lymph node aspirates, blood, spleen, spleen, liver or bone marrow puncture- kala-azar  ELISA, PCR  Culture on NNN (novy,nick,neal ) mediumbiphasic medium  Aldehyde test of Napier –nonspecific detecting elevated serum globulin in kalaazar  Montenegro skin test: past exposure



Leishmaniasis Preventions and treatment



No vaccine Control of sand fly and infected animals avoidance of sand fly Pentosam (antimony gluconate)



Macrophage engulfing the promastigote form of Leshmania