UNIVERSITY OF BAHRI

COLLEGE OF MEDICINE
DEPARTMENT OF COMMUNITY MEDICINE
COMMUNICABLE AND NONCOMMUNICABLE DISEASES

CUTANEOUS LEISHMANIASIS

Prepared by: Kenyi Alex Daniel Kenyi

Supervised by Prof. Mohammed Ali Mustafa
Date: 28/02/2016
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CUTANEOUS LEISHMANIASIS
Introduction:
Cutaneous leishmaniasis as the name implies, it is due to infection of
reticuloendothelial cells of the skin caused by the genus leishmania
Cutaneous leishmaniasis is the most common form of leishmaniasis and
causes skin lesions, mainly ulcers, on exposed parts of the body, leaving
lifelong ulcers and serious disability
Epidemiology
Around 350 million people in the world are estimated to be residing in
endemic areas of leishmaniasis and are at higher risk for acquiring the
infection
About 95% of CL occur in America, the Mediterranean basin, the Middle
East and central Asia
Over 2/3 of the new CL occur in 6 countries; Afghanistan, Algeria, Brazil,
Columbia, Iran and the Syrian Arab Republic
Cutaneous leishmaniasis flares up from time to time among the indigenous
population of endemic areas who were not infected before e.g. military
campers and expatriates working or visiting endemic areas
LIFE CYCLE:
Involves a vertebrate host and Phlebotomus fly as a vector.
In the mammalian host, Leishmania is an obligate intracellular parasite and
exists in the amastigote form inside cells of the mononuclear phagocytic
system
The amastigote forms are circular, about 5 microns in diameter, having a
nucleus, kinetoplast and rudimentary flagellum.
It multiplies by binary fission, repeatedly until the host cell is destroyed.
Inside the gastrointestinal tract of the sandflies, the amastigote transforms
into paramastigotes and promastigotes - elongated, flagellated, motile forms,
which have a central nucleus and terminal kinetoplast
The transmission of the disease to vertebrate hosts occurs predominantly by
inoculation of the infective promastigote form during a bite of the sandfly.
However, other possible routes included direct contact, transplacental,
venereal and blood transfusions
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 After inoculation in mammalian hosts, the infective promastigote attaches to

macrophages through different cellular receptors, and it is then localized into
a vacuole which fuses with lysosomes
The parasite survives phagocytosis and undergoes different metabolic
transformations, becoming amastigote forms, which lyse the host cells and
then infect other phagocytic mononuclear cell

Main foci in Sudan:

Blue Nile (Sinnar, Singa, Damazine, Kurmuk). South: Upper Nile, Bahr el Gazal,
West: Darfur, Kordofan.
Recently, wide spread due to mass population movement on account of
urbanization settlement. In endemic areas, domestication of animals
increased rodents accumulation

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Pathophysiology
Promastigotes of leishmania are transmitted to human skin by the bite of a
sandfly. Leishmania then invades human macrophages and replicates
intracellularly.
A raised, red lesion develops at the site of the bite (often weeks or
sometimes years afterwards). The lesion then ulcerates and may become
secondarily infected with bacteria. In many species (for example, L. major)
the lesion often spontaneously heals with atrophic scarring.
In some species (for example, L. braziliensis) the lesion may spontaneously
heal with scarring, but then reappear elsewhere (especially as destructive
mucocutaneous lesions). Lesions of other leishmania species may
spontaneously heal and then reappear as satellite lesions around the site of
the original lesion, or along the route of lymphatic drainage.
Species that tend to cause CL (e.g., L. major and L.tropica

THE VECTOR
There are two hosts in leishmaniasis with the vertebrate and the specific fly.
The vector in cutaneous leismaniasis is the sand fly that belongs to the genus
phlebotomos
Sand flies breed in organic detritus in various sites that include; rodents burrows
human and animal manures and forest leaf litter.

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RESERVOIRS
Man, rodents, dogs, foxes and occasionally other animals have been
suggested to act as reservoir. When man is the only reservoir as in India,
infection is via sand fly from man to man, this creates a situation suitable for
epidemics particularly if the vector is an efficient one.
In Sudan, desert rodents, other rodents and dogs have been implicated in the
identification process of reservoirs in endemic zones
TYPES OF CUTANEOUS LEISHMANIASIS
The main varieties of cutaneous leishmaniasis are;
1. Cutaneous leishmaniasis of the old word (oriental sore)
2. Cutaneous leishmaniasis of the new world
CUTANEOUS LEISHMANIASIS OF THE OLD WORLD:
It is caused by L. tropica, L. major, L. aetiopica
It is found in the Mediterranean region, Europe, Middle East, Asia, Russia,
Africa and South of Sahara.
It is found in three types which includes;
I.

Rural or moist type, caused by leishmania tropica major. Its reservoir is

wild rodents and it is transmitted by the sand fly. Hunters, travelers into
desert and soldiers are those who are most vulnerable to the infection

Incubation period:
The incubation period of leishmania ranges from 2-8 weeks.
At the site of the bite, a granuloma reaction develops, and leads to the
formation of an ulcer, that may become secondarily infected. This may
remain for a whole year before it heals. It occurs in the exposed parts of
the body such as the hands, feet, legs and face. Metastasis may take place
to the regional lymph nodes but this is rather uncommon
The ulcers formed are usually single, although multiple ones have been
known to occur. It heals within 6 months by scarring and may lead to
such deformities as the eversion of the eyelid, eversion of the angle of the
mouth or deformity of the nose
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II.

Urban or dry type, caused by leishmania tropica minor. Its reservoirs are
dogs and man, and it is transmitted by the sand fly. It is common in the
Middle East, where 80% of the affected individuals living in the big cities
The lesion occurs on the exposed parts of the body, and begins as a small
itchy nodule, which grows very slowly. Ulceration is not commonly seen,
and the lesions, which are mainly single heals with little scarring.
Disfiguration therefore hardly ever results

III.

Leishmania Recidiva (Lupoid leishmaniasis): is a chronic form of the

disease that is seen mainly in the Middle East. It consist of a lesion that heals
at the center, but ulcerates at the peripherals to involve large areas of the
skin.
Leishmanin test is positive for it
They should be differentiated from tropical ulcers, tertiary syphilis, T.B of
the skin or fungal infection

Diffuse cutaneous leishmaniasis

There are nodules that are multiple, but do not ulcerate. It resembles
lepromatous leprosy, and is diagnosed by demonstrating the organism in the
nodules. The entire skin may be involved. This form has been described in
Sudan, Ethiopia and Venezuela
The spectrum of cutaneous leishmaniasis has been compared to that of
leprosy. Persons with diffuse cutaneous leishmaniasis are similar to those
with lepromatous leprosy, in whom large numbers of mycobacteria are
observed within macrophages, while those with leishmaniasis recidiva are
similar to those with tuberculoid leprosy, in whom there is a tissuedamaging granulomatous response but few parasites. In leprosy the
histopathological findings are predictive of the clinical syndrome, while in
simple cutaneous leishmaniasis the histopathology evolves from a
predominance of Amastigote-filled macrophages early in infection to a
granulomatous response with lymphocyte predominance as the lesions age.
Its diagnosis is by demonstrating the organisms in the nodules. The entire
skin maybe involved

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CUTANEOUS LEISHMANIASIS AND ESPUNDIA OF THE NEW WORLD

It is caused by;
L. braziliensis
L. panamenensis
L. guyanesis
L. Mexicana
L. amazonensis
L. Peruvian
The cutaneous leishmaniasis caused by L. Mexicana complex is usually
called chiclero ulcer. The parasite is zoonotic of forest rodents and man is
only an accidental host (when he interferes or disturbs the lutzomiya
sandfly). The lesions formed are single and self-limited.
Healing being spontaneous and without treatment unless there is secondary
bacterial infections result which may result in the formation of disfiguring
scars
The L. braziliensis complex is responsible for mucocutaneous leishamaniasis
which is greatly disfiguring form. This begins with infections of
reticuloendothelial cells of the skin and then moves on to the mucosa of the
mouth and nose.
The infection is transmitted from man to man by the sandfly and is
characterized by variety of skin and metastatic lesions which erode adjacent
soft tissue resulting in sepsis and mutilation

Diagnosis
Is by the recovery and identification of the parasite in aspirates of tissue
juice from lesions, biopsy of the lesion and scrapings from nasal mucosa.
No serological tests are distinct for this form
It is usually resistant to pentavalent antimonys although at times it could
respond to them when given in maximum dosage
Sodium antimony tartrate as used in schistosomiasis has been of some effect
or even pyrimethamine given as 25mg daily for two weeks. This being
repeated after one weeks rest. Folic acids and vitamin B should be given
with it though

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TRANSMISSION:
Through the following routes
Intentional scarification as a form of immunization
Suckling through the bites of sandfly
CLINICAL FEATURES:

Starts as erythematous papule at the site of inoculation

Becomes a nodule after increasing gradually, it ends as a wet ulcer
It contain a covering exudates
Develop raised borders
Other lesions may be dry with central crust
They can get secondarily infected by bacteria or fungi
Cutaneous lesions last for months or in some for years
Spontaneous recovery occurs
The areas of lesions after healing becomes flat, hypopigmented scars
Occasionally CL may give rise to nodule formation, which may stimulate
skin cancer
Local lymphatics may become involved by cutaneous leishmaniasis

Disseminated cutaneous leishmaniasis may be seen in patients with;

Apparently intact immunity
Diabetes
HIV
With L. braziliensis, a form of prodromal symptoms before the appearance
of the lesions include;
Regional lymph node involvement
Fever
Other constitutional symptoms
Splenomegaly in a few patients

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DIAGNOSIS:
This is based mainly on the identification of the parasites in the smears taken
from the edge of the ulcers and not the center.
These are stained by the leishman stain and examined under the microscope
for the amastigotes (intracellular or extracellular). As only the amastigote
form is found, it cannot be differentiatiated from visceral leishmaniasis
If the smear examination is negative, then culture in the NNN medium will
show the promastigotes in positive cases

Differential diagnosis:

Insect bite
Impetigo
Furende
Basal cell carcinoma
Syphilitic gumma
Tropical ulcer
Anthrax

TREATMENT:
If the lesions are multiple and metastatic, the treatment include:
1. Admission is essential with absolute bed rest
2. General management of fever, anemia, infection and pneumonia
3. Pharmacological treatment include
A. Antimony compounds:
Sodium antimony gluconate 600mg/day for adult and for children 314 years, it is 400 mg/day. Those less than 2 years are given
200mg/day
Urea stibamine if sodium antimony gluconate is not available
250mg/day IV for 30 injections
Ethyl stibamine started at 100mg IV, then increased daily at 100mg to
a max. of 300mg/day
B. Diamidines:
Hydroxylstilbamidine isoethionate slow IV 250mg/day
Pentamidine isoethionate 10 injections at 4mg/kg body weight/day
repeated with interval of 10-14 days
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C. Antifungal drugs:
Amphotericin B started at 0.25mg/kg and increased gradually to
1mg/kg given in glucose solution IV over 3-6 hours especially for old
world type
Most physicians advise not to prescribe treatment for the old world if
the lesion is single, non-ulcerating and non-metastasizing.

CONTROL AND PREVENTION:

No vaccines or drugs to prevent infection are available. The best way for travelers
to prevent infection is to protect themselves from sand fly bites. To decrease the
risk of being bitten, follow these preventive measures:
Avoid outdoor activities, especially from dusk to dawn, when sand flies generally
are the most active.
Educate people explaining the life cycle of the parasite, mode of infection
and means of protection
When outdoors (or in unprotected quarters):
Minimize the amount of exposed (uncovered) skin. To the extent that is
tolerable in the climate, wear long-sleeved shirts, long pants, and socks; and
tuck your shirt into your pants.
Apply insect repellent to exposed skin and under the ends of sleeves and
pant legs. Follow the instructions on the label of the repellent. The most
effective repellents generally are those that contain the chemical DEET (N,
N-diethylmetatoluamide).
When indoors:
Stay in well-screened or air-conditioned areas.
Keep in mind that sand flies are much smaller than mosquitoes and therefore
can get through smaller holes.
Spray living/sleeping areas with an insecticide to kill insects.
If you are not sleeping in a well-screened or air-conditioned area, use a bed
net and tuck it under your mattress. If possible, use a bed net that has been
soaked in or sprayed with a pyrethroid-containing insecticide. The same
treatment can be applied to screens, curtains, sheets, and clothing (clothing
should be retreated after five washings).
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 Avoiding regions where the sandfly is known to live and breed

Vaccination. The vaccine is live L. tropica form which provides a long term
immunity although it may take 6 months for full protection to occur

Complication:
Bleeding
Other infections due to a weakened immune system, which can be lifethreatening
Disfigurement
Summary of cutaneous leishmaniasis
Cutaneous leishmaniasis is one of the most common tropical dermatoses
worldwide and is of major public health importance. It is caused by
numerous Leishmania protozoa species, which are responsible for its clinical
diversity.
With changes in vector (sandfly) habitat and increased travel among human
populations, its incidence is rising, and in nonendemic countries, including
the UK, it is increasingly diagnosed in migrants, returned travellers, and
military personnel.
Diagnostic tests have not always been sufficiently sensitive, and despite a
wide range of treatments, poor therapeutic responses and adverse effects are
common.
In the past decade, there have been notable advances in molecular
diagnostics, in the understanding of host immune responses to infection, and
in new therapeutic interventions and vaccine development.
References:
Preventive and social medicine text book
Cutaneous leishmaniasis in Kenya: Trans R Soc Trop med hyg 1984
Studies on leishmaniasis in the Sudan. Clinical and parasitological studies of
cutaneous leishmaniasis; Trans R Soc Trop med hyg 1991

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