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Cutaneous leishmaniasis due to Leishmania aethiopica Clinical presentations & complications Mesfin Hunegnaw, MD July 2011, Addis Ababa
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Page 1: Leish clinicaldrmesfin

Cutaneous leishmaniasis due to

Leishmania aethiopicaClinical presentations & complications

Mesfin Hunegnaw, MD

July 2011, Addis Ababa

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Leishmania aethiopica

• It is the dominant species causing Cutaneous

leishmaniasis (CL) in Ethiopia

• Clinical subtypes:

- Localized CL

- Mucocutaneous

- Diffuse

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Localized cutaneous leishmaniasis

Incubation period variable, usually several weeks

Infection may be subclinical or clinical

Subclinical cases may manifest with immunosuppression

Primary lesion may be patch of erythematous induration at

site of sandfly bite

Progresses to papulonodular, plaque or ulcerative lesion

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Localized cutaneous leishmaniasis

When it ulcerates it forms central depression and

raised indurated border

Nodules plaques or ulcers may enlarge to assume a

diameter of several centimeters

May persist for months or years before eventually

healing with an atrophic scar

Many lesions do not ulcerate but persist as nodules or

plaques

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Localized cutaneous leishmaniasis

Some patients have more than one primary lesion

Lesions are not always well-defined

Because of lymphatic spread, may get:

Satellite lesions

Sporotichoid spread

Local lymphangitis

Local lymphadenopathy

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2 large lesions, both poorly defined. Only showed partial response to parenteral antimonial at end of 2nd cycle

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Inadequate treatment resulting in leishmaniasis recidivans: This will now be difficult to treat

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HIV co-infection

• As large as 5.6% co-infection rate (report from Tigray)

• Clinical presentations are

– Atypical

– Severe

– ↑ risk diffuse & mucocutaneous involvement

– Poor responses to standard therapy

– Higher relapse rate

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Diffuse cutaneous leishmaniasis

• L. aethiopica

• Initial lesion may be small and well-defined

• Then multiple nodular & infiltrative lesions may appear

• Resembles lepromatous leprosy

• Lesions occasionally ulcerate and scar causing deformity

• Diffuse CL may appear months/years after initial lesion healed

• Poor CMI: Lesions are laden with parasite

• Poor treatment responses & high relapse rate

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Diffuse CL very disfiguring and treatment unresponsive

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Ulcerative DCL

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Ulceration, Contracture and deformity of the fingers

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Extensive scaring, deformity & contractures

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Mucocutaneous leishmaniasis

• Causative agent is L. aethiopica• Occurs from lymphatic spread of amastigote • Mucosal infection can occur in the presence or absence of

the primary • Primary lesion may be adjacent to nostril or anywhere on

the face• Often significant facial lymphodema because of rich facial

lymphatic supply• The early symptoms of mucosal infection:

• nasal congestion • epistaxis

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Mucosal spread with lesions Naso-pharinigeal area

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Spread of facial lesion to lower lip mucosa with oedema

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Mucosal spread with severe facial lymphoedema developed one year after scar healed

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Scarring from previous lesions. Patient now complains of nasal stuffiness & epistaxis

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Untreated facial lesion self-healed. Patient now has mucosal disease affecting lips

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Although lesion is defined patient is c/o of nasal congestion

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Mucocutaneous leishmaniasis

• Lesions can be destructive: nasal septum & other cartilaginous

structures

• How great is the risk of inadequately treated CL progressing to

mucosal disease? Difficult to assess:

- Because of severe stigma, patients are isolated in home & villages and

do not seek treatment

- May be due to culture, the patients do not return to same clinician

when there is disease recurrence. They seek treatment elsewhere

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HIV -ve. Lesions still very active. c/o epistaxis

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HIV positive. Palate also affected

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HIV -ve. Previously healed facial lesions with scarring. Active mucosal disease

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Also has active lesions over hands associated with severe scarring and deformity

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Goals of therapy

• Accelerate healing• Minimize scarring• Prevent complications• Prevent disease progression• Decrease risk of relapse

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Antimonials

• Have efficacy against L. aethiopica

• Localized lesions respond well

• Established MCL or diffuse leish respond poorly

• Aim of treatment should be;

- Clinical & parasitological cure

- To prevent any risk of disease progressing to MCL or diffuse

leishmaniasis as cure will be difficult/ impossible

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Summary

• L. aethiopica is not a benign species

• Severe disease is probably underestimated as stigma might

cause social isolation

• We have seen cases of facial lesions which have

‘metastasized’ to mucosa

• Significantly associated lymphodema suggests lymphatic

spread

• DCL may manifest many years after single lesion has healed

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