Leishmaniasis
Leishmania.
1) Cutaneous leishmaniasis.
2) Mucocutaneous leishmaniasis.
3) Visceral leishmaniasis.
1) Cutaneous leishmaniasis
a) Old world cutaneous leishmaniasis (oriental sore, Delhi boil)
b) New world cutaneous leishmaniasis.
sandfly in old world cutaneous
leishmaniasis and lutzomyia for new world cutaneous leishmaniasis.
a) Old world cutaneous leishmaniasis.
1) Leishmania tropica minor (dry or urban cutaneous leishmaniasis, oriental sore,
Aleppo button, Jericho boil, Delhi boil, Baghdad boil).It is anthroponotic disease
transmitted from human to human.
2) Leishmania tropica major (rural or wet cutaneous leishmaniasis).It is zoonotic
disease.
3) Leishmania aethiopica (cutaneous and diffuse or disseminated cutaneous
leishmaniasis of Ethiopia, anergic cutaneous leishmaniasis).
Incubation periods 2 weeks – 3 years
n Leishmania tropica and Leishmania aethiopica as log as 3 years.
Life cycle: As in figure 5.
Clinical features and pathogenesis(Leishmania tropica and Leishmania major):
lesion occur at the dermis at the site of the inoculation of the promastigote.
Mucous membrane are rarely involved.
slightly raised center covered by
a thin blister like layer of epidermis.
lesion then breaks down with discharge of a small amount of clear or purulent
exudate. At the ulcer crater like base in the dermis, a granulation layer is formed and
the margin becomes indurated by infiltration of fibroblast. In the dry type , the disease
is chronic ,occurs in the urban area , single lesion ,face is affected ,the ulceration is slow
and may not occur with little surrounding tissue reaction ,the healing may take > 1 year.
In the wet type, the disease is acute, occurs in the rural area, lower limb is affected,
the ulceration is multiple and prone to early ulceration with high degree of surrounding
tissue reaction and liable for secondary bacterial infection, the healing may take 3-6
months, gerbils and other rodent are the main reservoir.
b) New world cutaneous leishmaniasis (American cutaneous leishmaniasis).
They are caused by Leishmania mexicana complex and Leishmania braziliensis
complex. The American strains of leishmania causing cutaneous leishmaniasis differ in
their tendency to involve the mucous membrane of the mouth and nasopharynx by
extension.
2) Mucocutaneous leishmaniasis
It is caused primarily by Leishmania braziliensis which cause Espundia start as papule
at the site of bite and then metastatic lesion forms, usually at the mucocutaneous
junction of the nose and mouth leading to disfiguring
granulomatous ulcerating lesion destroying the nasal cartilage but not adjacent bone.
Death occurs from secondary bacterial infection.
Immunity to cutaneous leishmaniasis:
Host recovery in cutanous leishmaniasis depends on the development of cell mediated
immunity. The usual cutaneous lesion heals spontaneously.
In certain instances, healing does not occur; these cases may represent the 2 poles of
the spectrum of response. The first spectrum is the anergy as in leishmanial aethiopica.
The second spectrum represent the hypersensitivity reaction in which the patient is
capable for excellent Ab and cellular responses but cannot completely eliminate the
parasites , so as the central lesion heals, active peripheral ones continue to form . This
stage is called leishmaniasis recidiva or lupoid leishmaniasis (in Leishmamnia tropica).
Diagnosis:
1) Specimens: Lymph node aspirate, scrapings and biopsies from the margin of the
lesion. The center of purulent discharge is of no value.
2) Microscopic examination: The specimen smeared onto a clean glass slide, the slide
stained with Giemsa´s stain for demonstration of amastigote within the macrophage or
spread out from ruptured cells.
3) Culture in NNN (Novy-MacNeal-Nicolle) medium or inoculation in hamster.
4) Leishmanin skin test (The test done by i.d injection of a suspension of killed
promastigote) .
3) Visceral leishmaniasis
The three species are (Leishmania donovani, Leishmania infantum, Leishmania
chagasi).
to the mucous membrane
and subcutaneous tissue but throughout the body.
Dermal leishmaniasis:
Post kala-azar dermal leishmaniasis, present first as hypopigmented or erythematous
macules on any part of the body or as nodular eruption especially on the face. The
organism may be present in the lesion. It is a delayed hypersensitivity to parasite antigen
and is interpreted as an indication of inadequate treatment with residuance of parasites
that continue to propagate.
Diagnosis:
1) Specimens. Bone marrow, spleen and lymph node biopsies for detection of
intracellular amasatigote (L-D bodies).Splenic aspirates are the most sensitive method
for the diagnosis.
2) Culture in NNN (Novy-MacNeal-Nicolle) medium.
Note: The diagnosis is established by visualization of amastigotes in smear, biopsies,
or by growth of promastigote in culture.
3) Serological tests: for detection of antigen or antibody.e.g.
I) indirect fluorescent Antibody test (IFAT).
II) Enzyme Linked Immunosorbant Assay (ELISA).
III) Direct agglutination test (DAT).
IV) Immunochromatographic K39 strip test
{Recombinant leishmanial antigens or synthetic
peptides (rK39)} (dipstick test).
The recombinant antigen is a 39 amino acid (rK39) cloned from the C-terminus of the
kinesin protein of Leishmania species that cause visceral infecction. This test is used to
detect antibodies against K39 antigen in patient with visceral leishmaniasis.
The test is simple, rapid (10 minutes), These tests (serological) remain positive for
several months after cure has been achieved, so don’t predictresponse to treatment or
relapse.
4) Leishmanin skin test is negative in the acute disease but positive 2 months after
recovery.
7) Polymerase chain reaction (PCR).
Immunity:
Lifelong immunity.
