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
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Date: 28/02/2016
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,
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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
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

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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

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

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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.

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
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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:

II.

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
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
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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
tissue-damaging 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

CUTANEOUS LEISHMANIASIS AND ESPUNDIA OF THE NEW

WORLD
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 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
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daily for two weeks. This being repeated after one weeks
rest. Folic acids and vitamin B should be given with it though
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
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 Splenomegaly in a few patients

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:
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 Sodium antimony gluconate 600mg/day for adult and

for children 3-14 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
C. Antifungal drugs:
Amphotericin B started at 0.25mg/kg and increased
gradually to 1mg/kg given in glucose solution IV over 36 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.

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 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, Ndiethylmetatoluamide).
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).
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 life-threatening
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.

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 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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