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| Cutaneous Leishmaniasis |
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| Sangeeta B Kulkarni (Bhide)*, Ila M Vora**,
Rajiv Rajmohanan*** |
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| Leishmaniasis is a parasitic infection
caused by species leishmaniae, which can produce two types of
manifestations-visceral and cutaneous. In India visceral leishmaniasis
is more common than cutaneous leishmaniasis. A case of primary
cutaneous leishmaniasis from a veterinary doctor is presented
for its rarity. |
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| Introduction |
Leishmaniasis is a parasitic infection
caused by species leishmania which belongs to family Trypanosomatidae,
which can cause two types of manifestations- visceral
and cutaneous.1-3 In India more commonly visceral type
of Leishmaniasis caused by Leishmania Donovani is seen.2
Visceral Leishmaniasis (VC) also known as ‘Kala
azar’ is a systemic disease. Since Leishmania Donovani
infects and proliferates in the reticuloendothelial system,
organs like bone marrow, spleen, lymph node, liver etc.
are commonly evaluated for demonstration of parasite.1,3
A case of primary cutaneous leishmaniasis is presented
here due to its rarity.
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| Case History |
A 45-year-old male veterinarian doctor working in the
Middle East presented with a boil in the right shoulder
for more than six months duration. The boil was 1.0 X
1.0 cm in size, yellowish white in colour and was slowly
increasing in size. There was no history of pain and tenderness.
The boil did not discharge any secretions. The rest of
the skin was normal. He had no history of fever, weight
loss or weakness. There was no other systemic complaint.
On clinical examination, he had no significant abnormality.
On investigations, chest X-ray did not show any abnormality.
Routine investigations were within normal limits. An excision
biopsy of the lesion was done and routine histopathological
examination was done.
Gross examination showed two firm tissue bits measuring
1.0 X 1.0 cm covered by skin. Cut surface was grey-white.
Microscopically, sections studied showed skin with subcutaneous
tissue. Epidermis was lined by stratified squamous epithelium.
Dermis showed heavy lympho-histiocytic and plasmacytic
infiltration. There were few neutrophils and foci of lymphoid
follicles. There were extensive areas of granulomas consisting
of histiocytes or macrophages and occasional multinucleate
giant cells, resembling Langhan’s type of cells
(Fig. 1). At places some of them showed central area of
minimal necrosis. No typical epithelioid cells were seen.
The histiocytes showed round to oval organisms resembling
Leishmania intracellularly. Similar organisms were seen
extracellularly also.
Giemsa stain showed organisms having rounded bodies with
nucleus and a small kinetoplast resembling Leishmania.
(Fig. 2)
PAS and GMS were done and was negative ruling out Histoplasmosis.
Zeihl Neelsen stain was negative for Acid fast bacilli.
The diagnosis of cutaneous leishmaniasis was made. Bone
marrow examination was suggested, which did not show any
leishmania donovani bodies.
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Fig. 1 : Photomicrograph showing granulomatous reaction and lymphocytes at periphery. (Haematoxylin and Eosin - X 160)
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Fig. 2 : Photomicrograph showing lymphohistiocytic infiltration and Leishmania Donovani bodies intracellularly as well as extracellularly.
(Arrows) (Giemsa stain - X 400) |
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| Discussion |
The cutaneous leishmaniasis is divided into the OLD
WORLD and NEW WORLD cutaneous leishmaniasis.3,4
The old world cutaneous leishmania (OWCL) comprise three
species – Leishmania tropica, Leishmania major and
Leishmania aethiopica.3,4 The areas of disease are Middle
East, Northern Africa, Sub Saharan Africa, East Asia and
Southern Europe.3,4
The species of cutaneous leishmaniae of the NEW WORLD
are more numerous and more difficult to classify. They
produce disease that are more chronic than old world.
The species are – Leishmania braziliensis, Leishmania
Mexica, Leishmania guyanensis, Leishmania panamensis,
Leishmania peruviana. The areas of disease are South America
and the Carribean Islands where the preferred term is
‘Tegumentary’ or mucocutaneous leishmaniasis.
Morphologically and histologically the cutaneous leishmania
of the old and new world are similar.3 Transmission of
disease to humans occurs through the bite of an infected
sandfly.3,4, In general they produce a benign, limited
disease in the exposed parts of skin with a tendency to
heal spontaneously and leave the host with resistance
to reinfections by the same species.3 The infection begins
as a reddish papule at the site of the bite progressing
to induration and ulceration often called as tropical
sore.1-4 This patient presented with a boil on the right
shoulder.
In diffuse cutaneous leishmaniasis, which is rare form
of dermal infection begins as single skin nodule and spreads
until the entire body is covered by bizarre nodular lesions.4
The diagnosis of cutaneous leishmaniae is usually made
on clinical grounds like endemic area, clinical presentation
and origin of the patient.3 This disease is diagnosed
by demonstrating organisms from smears prepared from materials
aspirated with a syringe or scrapings from bottom of the
ulcer or biopsy of an ulcer.1,3,5,6
The smears are stained by Giemsa stain at pH –
7.2 which bring out the Leishnania Donovani (LD) bodies
prominently.1,3,5,6 In positive smears the amastigotes
are found intracellulary in macrophages.
The initial lesion is studded with the organisms with
no granulomatous reaction. As the lesion progresses to
chronicity for more than six months to 1–2 years,
it shows less or no organisms and may show granulomatous
reaction.1,4,7 In this case histopathological findings
were similar to chronic lesion.
Cultures are optional and are not required for diagnosis
unless species infecting the patient needs to be identified.3
Highly sensitive noninvasive molecular and antigen detection
methods are evaluated and made available routinely, still
tissue demonstration of Leishmaniae Donovani bodies remains
the method of choice.5,6,8
In summary, primary cutaneous Leishmaniasis is a rare
disease and the diagnosis can be made on clinical grounds,
characteristic appearance of Leishmania organism on histopathology
and Giemsa stain.
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| References |
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Indian J Pathol Microbiol 1998; 41(3) : 361–72.
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| 7. |
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| 8. |
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