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Infectious Diseases
Dermatology
Tropical Medicine

Leishmaniasis

High EvidenceUpdated: 2025-12-23

On This Page

Red Flags

  • Visceral Leishmaniasis (100% mortality within 2 years if untreated)
  • Mucocutaneous Leishmaniasis (Destructive facial disfigurement)
  • Pancytopenia with Massive Splenomegaly
Overview

Leishmaniasis

[!WARNING] Medical Disclaimer: This content is for educational and informational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional for diagnosis and treatment. Medical guidelines and best practices change rapidly; users should verify information with current local protocols.

1. Overview

Leishmaniasis is a vector-borne protozoal infection caused by Leishmania parasites and transmitted by the bite of infected female Phlebotomine Sandflies.

It is a "Neglected Tropical Disease" affecting the poorest populations.

The Three Forms

  1. Cutaneous (CL): Skin ulcers. Common. (95% of cases).
  2. Mucocutaneous (MCL): Destructive lesions of nose/mouth/throat.
  3. Visceral (VL) / Kala-Azar: Systemic infection of liver/spleen/marrow. Fatal.

Clinical Scenario: The Returning Soldier

A soldier returns from training in Belize. He has a non-healing, painless ulcer on his forearm with a raised 'pizza-like' edge. A few months later, he complains of a blocked nose and nosebleeds.

Key Teaching Points

  • The ulcer is typical of **Cutaneous Leishmaniasis** (New World).
  • The nasal symptoms suggest progression to **Mucocutaneous Leishmaniasis** (Espundia).
  • This is dangerous as it can destroy the nasal cartilage (Tapir Nose).
  • Systemic treatment is required (not just topical) to prevent facial destruction.

2. Visual Summary Panel

Image Integration Plan

Image TypeSourceStatus
Management AlgorithmAI-generatedPENDING
Vector (Sandfly)Web SourcePENDING
Clinical (Cutaneous Ulcer)Web SourcePENDING
Clinical (Hepatosplenomegaly)Web SourcePENDING

[!NOTE] Image Generation Status: Diagrams illustrating the Amastigote/Promastigote life cycle are queued.

Key Signs

  • Volcano Sign: Cutaneous ulcer with raised indurated edge and central crater.
  • Massive Splenomegaly: In Visceral Leishmaniasis, the spleen can cross the midline into the right iliac fossa (one of the biggest spleens in medicine).

3. Epidemiology
  • Vector: Sandfly (Phlebotomus - Old World; Lutzomyia - New World).
    • Tiny (1/3 size of mosquito). Silent fliers. Bite at night.
  • Geography:
    • CL: Middle East (Syria, Iraq, Afghanistan), Americas.
    • VL: India (Bihar), Sudan, Brazil.
  • Reservoir: Dogs (Zoonotic) or Humans (Anthroponotic).

4. Pathophysiology
  1. Bite: Sandfly injects Promastigotes.
  2. Phagocytosis: Macrophages eat them.
  3. Transformation: Inside the macrophage, they turn into Amastigotes (LD Bodies - Leishman-Donovan bodies).
  4. Replication: They survive/multiply in the acidic phagolysosome, burst the cell, and infect other macrophages.
  5. Spread:
    • CL: Stays in skin (cool temperature).
    • MCL: Migrates to nasopharynx.
    • VL: Migrates to Reticuloendothelial organs (Spleen, Liver, Bone Marrow) -> Hypertrophy of organs & Marrow suppression.

5. Clinical Presentation

1. Cutaneous Leishmaniasis (CL)

2. Mucocutaneous Leishmaniasis (MCL)

3. Visceral Leishmaniasis (Kala-Azar)


Incubation
Weeks to months.
Lesion
Papule -> Nodule -> Painless Ulcer (Oriental Sore).
Course
Heals spontaneously over months leaving a depressed scar.
6. Clinical Examination
  1. Skin: Inspect ulcers. Look for satellite lesions.
  2. ENT: Inspect nasal septum (MCL).
  3. Abdomen: Measure spleen size.
  4. General: Lymphadenopathy.

7. Investigations

Diagnosis

  1. Skin Slit Smear / Biopsy (for CL/MCL):
    • Microscopy: Identification of Amastigotes (LD bodies) inside macrophages. Giemsa stain.
  2. Serology:
    • rK39 Dipstick: Rapid field test for Visceral Leishmaniasis. High sensitivity.
  3. Bone Marrow / Splenic Aspirate (for VL):
    • Splenic aspirate is Gold Standard (>95% sensitive) but risky (bleeding). Marrow is safer but less sensitive.
  4. PCR: Most sensitive.

8. Management

Consult ID specialist. Treatment depends on species and geography.

A. Cutaneous

  • Mild: Watch and wait OR Cryotherapy / Intralesional Antimonials.
  • Complex: Systemic treatment (see below).

B. Visceral / Mucocutaneous (Systemic Rx)

  1. Liposomal Amphotericin B (AmBisome):
    • Gold Standard.
    • Single dose in India; multi-dose elsewhere.
    • Safe and effective (>90% cure). Expensive.
  2. Miltefosine:
    • First effective oral drug.
    • Teratogenic (Avoid in pregnancy).
  3. Sodium Stibogluconate (Pentostam):
    • Pentavalent Antimonial. Old standard.
    • Toxic (Cardiotoxic, Pancreatitis). Increasing resistance in India.

9. Complications

Post-Kala-Azar Dermal Leishmaniasis (PKDL)

  • A skin rash (hypopigmented macules/nodules on face/trunk) appearing months/years after cure of Visceral Leishmaniasis.
  • These patients are infectious reservoirs.
  • Requires prolonged treatment.

10. Prognosis & Outcomes
  • CL: Good. Scarring is main issue.
  • VL: Mortality > 95% if untreated. Cure rate > 90% with Amphotericin.

11. Evidence & Guidelines
  • WHO Guidelines for the treatment of Leishmaniasis.
  • IDSA Guidelines.

12. Patient & Layperson Explanation

What is Leishmaniasis? A disease caused by a tiny parasite passed on by the bite of a Sandfly.

Where do you catch it? Mostly in tropical and sub-tropical countries (Middle East, South America, India). Sandflies are tiny hairy flies that bite silently at night.

What does it do?

  • Skin form: Causes a nasty sore on the skin where you were bitten. It looks like a volcano. It usually heals on its own but leaves a scar.
  • Internal form (Kala-Azar): The parasite travels to your liver and spleen. This makes you very sick with intermittent fever, growing tummy (big spleen), and weight loss. This type is fatal if not treated.

How is it treated? We use strong antiparasitic medicines.

  • For simple sores, we might freeze them or inject them.
  • For the internal type, we use a drip called Amphotericin B which kills the parasite effectively.

13. References
  1. WHO. Control of the leishmaniases: report of a meeting of the WHO Expert Committee. 2010.
  2. Alvar J, et al. Leishmaniasis worldwide and global estimates of its incidence. PLoS One. 2012.
  3. Sundar S, Chakravarty J. An update on pharmacotherapy for leishmaniasis. Expert Opin Pharmacother. 2013.

Last updated: 2025-12-23

At a Glance

EvidenceHigh
Last Updated2025-12-23

Red Flags

  • Visceral Leishmaniasis (100% mortality within 2 years if untreated)
  • Mucocutaneous Leishmaniasis (Destructive facial disfigurement)
  • Pancytopenia with Massive Splenomegaly

Clinical Pearls

  • **Image Generation Status**: Diagrams illustrating the Amastigote/Promastigote life cycle are queued.
  • Hypertrophy of organs & Marrow suppression.
  • Painless Ulcer (**Oriental Sore**).

Guidelines

  • NICE Guidelines
  • BTS Guidelines
  • RCUK Guidelines