• It is a protozoal disease caused by a parasite
called leshmania genus.
• It is an obligate intracellular parasite.
• Which is transmitted to humans by a sand fly
• Endemic in 88 countries of the old and new
world(Africa,Asia,Europe,N.A& S.A, except Australia.
• 1.5-2million new cases seen every year (WHO estimates)
• 40,000 – 80,000 deaths every year (esp. MCL,VL).
• Race: no racial predilection
• Sex: no sex predilection
• Age: no specific age susceptibility is known.
• The disease is seen in tropics,subtropics & highlands.
• Traditionally divided as Old World and New World
• Old World leishmaniasis: is caused by Leishmania species
found in Africa, Asia, the Middle East, the Mediterranean,
and India, and
• New World leishmaniasis: is caused by Leishmania species
found in Central America and South America,
• Leishmania parasites are transmitted by sandflies of
• the genus phlebotomus =in the old world and
• the genus lutzomyia =in the new world.
• Sand flies are small in size mosquito like insects 1.5-
4mm in size can pass through ordinary mesh screen
and mosquito netting.
Only the females are blood sucking.
• members of the order kinetoplastida family
• They are found in two morphologic forms= in mamalian with
in macrophages as round to oval non flagellated amastigotes
• in sandfly promastigotes elongated flagellated .
• Both forms of parasites have got a nucleus and DNA
• With in the macrophages the promastigotes
transform in to amastigotes (leishman-donovan
bodies)→multiply by binary fission.
• When a macrophage become filled with
amastigotes it disrupted →amastigotes reenter
the extracellular space and taken up by other
• Parasites in the form of amastigotes from infected tissue or
blood are taken up from the mamalian host during feeding,
• Then with in the mid gut of the sandfly the parasites under
go change to promastigotes form →multiply
• then they migrate to the pharynx and proboscis of the
sandfly i.e. with in 8-2o days →they remain until they
are injected in to a new host during a subsequent blood
• Between 10-200 promastigotes enter the dermis during
each feeding but most of them are destroyed by
polymorphonuclear leukocytes,eosinophils & serum
• Some of the promastigotes become attached to
receptors of the dermal macrophages and are
phagocytosed = in the macrophages the promastigotes
• Similar to Hansen disease, leishmaniasis is a disease in which the
clinical diversity reflects a complex interplay between the virulence
of the infecting species and the host's immune response.
• At one extreme, localized cutaneous disease demonstrates a strong
immune response, with most cases resolving without intervention.
• This form of disease exhibits a helper T-cell subtype 1 (TH1) immune
response, with cytokines that induce disease resolution.
• Depending on the degree of the cell mediated
host immune response &the type ,virulence of
leishmania species the clinical classification
• Localized cutaneous leishmaniasis
• Mucocutaneous leishmaniasis
• Diffuse cutaneous lesihmaniasis
• Visceral leishmaniasis
• OLD WORLD CL -L tropica &L. major ,L.infantum &
• The disease begin as a small erythematus papule
which may appear after the bite of the sand fly→the
papules enlarges slowly in size (to 2 cm or
• Over a period of several weeks a lesion
becomes crusted in the center.
• usually caused by L . major
• characterized by multiple lesions,
• short incubation period (1 to 3 weeks)
• rapid and mild course
• Spontanosly heals with in 6 months.
• good response to therapy.
CL WITH S/C NODULES ALONG THE
New world CL
• found in Mexico,central America,texas&
• the lesions are similar to L.major
• Lesions can develop on any part of the body
• can involve the PINNA of the ears(chiclero
• L.brazilinesis can some time invade mucous
Diffuse cutaneous leishmaniasis
• DCL in both old and new world caused by
• DCL is found in 20% of leishmania pts in Ethiopia and
the Sudan .
• Clinically a single nodule spreads locally then by
metastasis becomes wide spread with non ulcerating
nodules over the face and trunk .
• It resembles lepromatous leprosy.
• DCL usually runs a protracted course but
does not visceralize,
• responds to therapy poorly.
• Parasites are abundant in skin smear and
• MCL = is involvement of both skin & mucus memb of upper
resp tract→ by L.brazelinesis &L.aethiopica.
• Mucosal lesions develop from CL in more than 75% of those
• A small red papule develops at the site of a sandfly bite
gradually enlarges,ulcerates and the infections extends to
the mucus of the mouth,nose,pharynx,to carrtillages of the
upper resp tract(nose&the larynx)
• Oedema &inflam.changes occur →destruction of the
cartilagenous structures(nasal septum,floor of the mouth
→to marked disfigurement.
• BUT bony stuctures are spared.
MCL WITH NASAL SEPTUM CARTILLAGE
• VL(KALAZAR)=Mainly affects the reticulo-endothelial systems
(spleen , BM,liver,lymphnodes)
• L.DONOVANI,L.CHAGASI &L.INFANTUM
• The disease present in china,india mid.east,east ,Africa
• It is one of the Common opprtunistic infection in HIV.
• Patients will have splenomegally,pancytopenia,anaemia
fever,wasting& imbalance of serum protiens.
• Diagnosis =smears,cultures from BM
biopsies,or spleen aspirates,serology tests are
POST KALAZAR DERMAL
• lesions usually appear with in a year after a
course of therapy.
• Consists of macular,papular & nodular lesions
on the face,trunk & extremities.
• PKDL has been reported to develop in 20% of
Indian & in more than 50% of pts in the Sudan
treated for VL.
• Lab Studies:
• Cutaneous lesions
– Skin scrapings are obtained from the base of an active ulcer or
biopsy of the edge of a suspicious lesion or ulcer.
– Visualization of all 3 features (nucleus, cell membrane, and
kinetoplast) is required to make the Dx. microscopically.
• Cultures of tissue are regularly obtained to identify Leishmania
• PCR is now routinely used in experienced laboratories as a rapid
a direct agglutination test (DAT), and even a nitrocellulose dipstick
to date is an L chagasi recombinant amastigotes K39 (rK39)–based
antigen test system that has been used with enzyme-linked
immunosorbent assay (ELISA),
– The degree of conservation of the K39 gene is high among isolates
of the L donovani family, including L chagasi and L infantum.
– Therefore, this test is useful for most recognized cases of visceral
– Assays based on rK39 antigen are highly sensitive and specific and
validated in several large studies worldwide.
Local heat therapy(electrocautery)
• The mainstay of antileishmanial therapy has been
pentavalent antimony (sodium stibogluconate or
• Cutaneous disease: 20 mg/kg/d IV/IM for 20 D
• Lesion borders: 1 mg/kg intralesional qwk.
• Cure rates are 90-97%.
These drugs are expensive and difficult to obtain.
• Cure rates near 100%, except possibly in HIV infection.
• Dose Amphotericin B (with deoxycholate): 1 mg/kg IV for 20 d
• Azole antifungals have antileishmanial properties.
• Not effective in visceral disease and should be used only as
second-line therapy in limited forms of cutaneous disease
with known species sensitivity (eg, rapidly self-curing
disease due to L mexicana but not L tropica).
• Gastric acid required for absorption.
• Adult Dose 600 mg PO qd for 4 wk.
Pentamidine (Pentam-300, Pentacarinat, NebuPent)
• - Inhibits growth of protozoa by blocking oxidative phosphorylation
and incorporation of nucleic acids into RNA and DNA, inhibiting
protein and phospholipid synthesis.
• Cutaneous disease: 2 mg/kg IV (4 doses)
• Resistance common in India; high relapse rates reported.
• Paromomycin (Aminosidine) -- Amebicidal and antibacterial
aminoglycoside obtained from Streptomyces rimosus grain.
• Dose15 mg/kg/d IV for 20 d
• Cytokines -- Interferon-gamma a TH1 cytokine, is used to enhance
host immunity to Leishmania parasites.
• Interferon-gamma-1b (Actimmune) -- Recombinant DNA product.
Administered with sodium antimony gluconate (probably ineffective
• Adult Dose 100 mg/m2/d IV for 28 d (with 20 mg/kg/d sodium
In addition to parenteral and oral medications , local therapies for some
forms of cutaneous leishmaniasis:
• Intralesional heat therapy with 40-42°C for 12 hours (One novel FDA-
approved device is called the Thermo Med device.); and
• Topical paromomycin preparations, typically 15% with 10% urea.
• As many as 90% of localized cutaneous forms of leishmaniasis heal
spontaneously with scarring.