Leishmaniasis

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Leishmaniasis

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•	AKA Oriental sore

•	protozoal disease

CL – cutaneous only

ML – mucous membranes only

VL – visceral (spread throughout reticuloendothelial system)

Clinical:

•

localized

•	distribution – unclothed parts of the body (head, neck, arms) easily bitten by the sand fly vector

•	evolution – papule/ ulcer = 1 week to 3 months after bite; spontaneous resolution (with scar) after 6 to 12 months

•	Old World – L. major; multiple primary lesions

•	New World - L. braziliensis and L. mexicana; solitary primary lesion

•	diffuse – anergic variant; lesions are disseminated resembling lepromatous leprosy

•	recidivan = new lesions that develop in the center or periphery of healed leishmania scar

•	post Kala-azar – hypopigmented macules; occurs 1 to 3 years after recovery

•	mostly New World, L. braziliensis

•	involves mucosa, soft tissue, and cartilage of upper respiratory tract (bony structures remain intact in contrast to syphilis and yaws)

•	AKA Kala azar; L. donovani (occurs in both Middle East and South America)

•	primary lesion = small erythematous papule usually on legs, sometimes called “leishmanioma”

•	during active period a patchy blackening of the skin appears (Kala azar = “black fever”)

•	Leishman-Donovan bodies = the amastigotes (can see with H&E but better seen with Giemsa)

•	round with large peripheral nucleus and a smaller rod-shape kinetoplast of mitochondrial DNA

•	part of HIS GIRL P ddx of parasitized histiocytes

•	e.g. vs Histoplasmosis – similar size, but with histoplasmosis a clear space gives the erroneous impression of an unstained capsule, and there is no kinetoplast

•	anergic patients with diffuse CL: heavily parasitized, foamy macrophages throughout dermis

diagnosis:

•	biopsy from active border of lesion (Giemsa stain)

•	obtain media from CDC for culture (to determine species; treatment implications)

•	may be cultured (triple N media)

•	intradermal leishmanin (Montenegro) test – cannot distinguish between active and quiescent disease

•	both the host and the leishmania antigen (i.e. species) are factors in determining the immune response

•	Th1 response dominates à LCL

•	IL2, interferon gamma; augment cell-mediated immune response by activating macrophages;

•	Th2 response dominates à disseminated infection

•	IL4, IL5, IL10; augment humoral response, and inhibit some cell mediated response; (therefore some treat with interferon gamma and antimony)

•	spectrum of clinical disease corresponds to the strength of the host’s cell-mediated response (analogous to leprosy):

•	positive antigen specific T-cell response à spontaneously healing lesions

•	T-cell non-responsiveness à diffuse cutaneous and visceral disease

•	T-cell hyper-responsiveness à mucocutaneous disease

•	arthropod vector for all forms is female sand fly

•	Old World - sand fly = phlebotomus

•	New World - sand fly = lutzomyia

•	during blood feeding, regurgitate saliva injecting promastigotes

•	part of the life cycle is in the gut of the sand fly:

•	promastigote form – extracellular; flagellated (in sand fly gut)

•	amastigote form – nonflagellated obligate intracellular (in humans)

treatment:

•	CL – heal spontaneously in 1 to 3 months; two situations demand specific treatment:

•	to reduce scar size in cosmetically important area (treat to limit scar size)

•	L. braziliensis spp. (treat to decrease risk of mucocutaneous disease developing)

•	pentavalent antimony compounds – Pentostam (sodium stibogluconate)

•	get baseline EKG (most patients in US admitted for cardiac monitoring during treatment)

mnemonic:

in the Middle East major phlebotomus has multiple "legions" of men loyal to him, but Christopher Columbus discovered the New World solo

Organism:	Geography:	Disease:

L. major	Old World	multiple primary lesions in LCL

L. mexicana	New World	solitary primary lesion in LCL

L. braziliensis	New World	solitary primary lesion in LCL and the major cause of ML
L. donovani	Middle East and S. America	VL (AKA Kala azar)