Leishmaniasis and Other Protozoan Infections

Intracellular Pathogenesis and Life Cycle of Leishmania spp.

The Promastigote–Amastigote Cycle

• In the sandfly: when a sandfly feeds on an infected person, the non-flagellated amastigotes enter its gut and develop into motile, flagellated promastigotes.
• Entering the host: when the sandfly bites a person, promastigotes are injected into the dermis, where macrophages and monocytes quickly move in to engulf them.
• Multiplying inside cells (Leishman-Donovan bodies): instead of being destroyed in the phagolysosome, Leishmania transforms into amastigotes (round to oval, 2–4 µm, with a nucleus and a characteristic rod-shaped kinetoplast). Amastigotes keep dividing by binary fission until the macrophage bursts, releasing large numbers of new parasites that invade neighboring macrophages.

Granulomatous Inflammation and Tissue Destruction

• Infected macrophages pile up and, together with the cell-mediated (T-cell) immune response, form necrotizing granulomas in the dermis.
• Central necrosis and local loss of blood supply make the overlying epidermis break down, producing the typical raised-edge, volcano-like ulcer. In the mucocutaneous form (L. braziliensis), parasites travel through the blood or lymph to the junction of skin and mucosa in the nose and throat, setting off chronic inflammation that destroys the cartilage.

Clinical Forms and Other Protozoan Infections

Cutaneous Leishmaniasis (CL) – the Most Common Form:

• Incubation period: a few weeks to a few months after the sandfly bite.
• Lesions: it starts as a painless red bump at the bite site (usually on exposed skin such as the face, arms or legs). The bump grows into a granulomatous plaque whose center breaks down into a volcano-shaped ulcer: a firm, raised rim with a moist, velvety red base or a dry crust, and usually no pain (unless there is a bacterial infection on top).
• The ulcer persists for months to years and, when it heals, leaves a disfiguring, puckered, sunken scar.

Mucocutaneous Leishmaniasis (MCL / Espundia):

• Mainly caused by Leishmania braziliensis in South and Central America.
• It appears months to years after the skin ulcer has healed. Patients first notice a blocked nose and nosebleeds; necrotic ulcers then destroy the nasal septum, palate, lips and larynx ("tapir nose"), causing severe facial deformity and breathing difficulty.

Visceral Leishmaniasis (VL / Kala-azar):

• Caused by L. donovani or L. infantum. The parasites spread throughout the reticuloendothelial system (liver, spleen, bone marrow).
• Signs: prolonged, undulating fever, rapid weight loss, grade IV enlargement of the liver and spleen, low counts of all three blood cell lines, and gray-black darkening of the skin (hence the name kala-azar, "black fever").

Other Protozoan Skin Infections:

• Cutaneous amebiasis (Entamoeba histolytica): deep, ragged, intensely painful, foul-smelling ulcers around the anus or perineum, arising as a complication of intestinal amebic dysentery.
• Cutaneous acanthamebiasis (Acanthamoeba spp.): clusters of granulomatous nodules or chronic ulcers in people with weakened immunity (HIV/AIDS).

Diagnostic Workup at Haute-Derma

Giemsa/Wright-Stained Tissue Smear (Diagnostic Gold Standard):

• The doctor gently scrapes the inner raised edge of the ulcer or aspirates fluid from the margin of the lesion.
• The sample is Giemsa-stained and examined under a light microscope with oil immersion (×1000).
• Result: amastigotes (Leishman-Donovan or LD bodies) are seen inside macrophage cytoplasm or lying free. LD bodies are oval, with a large round purple nucleus and a small rod-shaped kinetoplast set at right angles to it.

Skin Biopsy: assesses the granulomatous infiltrate (macrophages, plasma cells, lymphocytes) and rules out malignancies such as squamous cell carcinoma and cutaneous lymphoma.

Real-Time PCR for Species Identification: PCR amplifying specific kDNA or 18S rRNA targets distinguishes the causative species (L. major, L. tropica or L. braziliensis). Identifying L. braziliensis is essential for judging the risk of progression to destructive mucocutaneous disease.

Treatment and Aesthetic Repair at Haute-Derma

Systemic Therapy

Indicated for ulcers larger than 4 cm, more than 4 ulcers, lesions near joints or on the face, suspected L. braziliensis, or immunocompromised patients:

• Pentavalent antimonials (CDC/WHO standard):
  • Meglumine antimoniate (Glucantime) OR sodium stibogluconate (Pentostam): 20 mg Sb5+/kg/day by intravenous (IV) or intramuscular (IM) injection for 20 consecutive days (CL) or 28 days (MCL/VL).
• Oral Systemic Treatment:
  • Miltefosine: 50 mg by mouth 2–3 times a day (2.5 mg/kg/day) for 28 consecutive days. (Note: contraindicated in pregnancy because it can cause birth defects.)
• Alternative Regimen for Resistant or Visceral Disease:
  • Liposomal amphotericin B: 3 mg/kg/day by IV infusion on days 1–5, 14 and 21 (total dose 18–24 mg/kg).

Local Therapy

Indicated for mild cutaneous disease: a single ulcer smaller than 4 cm, not on the face or near a joint:

• Intralesional injection: meglumine antimoniate (1–3 mL) injected directly into the raised edge of the ulcer until the whole rim blanches, 1–2 times a week, combined with liquid nitrogen cryotherapy, for 3–4 weeks.

Aesthetic Repair of Sunken Scars at Haute-Derma

Once the parasite has been cleared, Leishmania ulcers often leave sunken, puckered atrophic scars that are very disfiguring. Our doctors use a multi-layered approach:

• Superpulse fractional CO2 laser: microablation of the sunken scar stimulates new collagen and elastin and resurfaces the skin.
• Stem cell / PRP (platelet-rich plasma) injections: help fill the base of the scar faster, calm the skin and even out post-inflammatory hyperpigmentation.