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Home :: Cutaneous and Mucocutaneous Leishmaniasis

Cutaneous and Mucocutaneous Leishmaniasis

Leishmaniasis is a parasitic infection caused by many species of the protozoa Leishmania, manifested clinically as four major syndromes-cutaneous leishmaniasis (CL) of Old and New World types, mucocutaneous leishmaniasis (MCL), diffuse cutaneous leishmaniasis (DCL), and visceral leishmaniasis (VL). CL is characterized by development of single or multiple cutaneous papules at the site of a sandfly bite, often evolving into nodules and ulcers, which heal spontaneously with a depressed scar.

Causes of Cutaneous and Mucocutaneous Leishmaniasis

The clinical and immunologic spectrum of leishmaniasis parallels that of leprosy. CL occurs in a host with good protective immunity. MCL occurs in those with an intense inflammatory reaction. DCL occurs with extensive and widespread proliferation of the organism in the skin but without much inflammation or tendency for visceralization. VL occurs in the host with little immune response and/or in immunosuppression. Unlike leprosy, extent and pattern are strongly influenced by the specific species of Leishmania involved. Additional factors that affect the clinical picture: number of parasites inoculated, site of inoculation, nutritional status of host, nature of the last non-blood meal of vector. Infection and recovery are followed by lifelong immunity to reinfection by the same species of Leishmania. In some cases, interspecies immunity occurs.

Symptoms of Cutaneous and Mucocutaneous Leishmaniasis

  • Skin ulcer, forms at site of original lesion
  • Smaller lesions may form around the ulcer (satellite lesions)
  • Macule or papule, erythematous
  • Ulcer heals very slowly over a matter of months

Diagnosis

Clinical suspicion, confirmed by demonstrating amastigotes on smear or in skin biopsy specimen or promastigotes on culture of aspirates or tissue.

Treatment

Prophylaxis No chemoprophylaxis for travelers exists. OWCL: Delay specific treatment until ulceration occurs, allowing protective immunity to develop, unless lesions are disfiguring, disabling, persist ± 6 months.

Lesional Therapy Local injection of antimonials (Pentostam), usually at weekly intervals; up to 1 mg/kg may be injected in borders of lesions. Also cryosurgery, ultrasound-induced hyperthermia, excision, electrosurgery. Topical 15% paramomycin sulfate, 12% methylbenzethonium chloride in white paraffin twice daily for 10 days.

Systemic Therapy Depends on clinical form. OWCL is usually self-limited and in most cases does not require specific treatment. Treatment should be given for extensive lesions, especially involving face, or for those lesions that invade deeper tissues.

For selected CL, MCL, DCL Sodium antimony gluconate (Pentostam) IV or IM In single daily dose of 10 mg/kg for adults and 20 mg/kg for patients <18 years of age for 10 days. Meglumine antimonate (Glucantime) 20 mg/kg/d for 10 days, ECG control. Amphotericin B, pentamidine, or sodium antimony gluconate plus interferon gamma for resistant cases. Ketoconazole.

Indian VL Milfefosine PO 100 mg qd for 4 weeks.

Prevention
  • Avoid outdoor activities, especially from dusk to dawn when sandflies are the most active.
  • Infection can be prevented by avoidance of sandfly bites.
  • Wear long-sleeved shirts, long pants, and socks. Tuck shirt into pants.
  • Spray clothing, living and sleeping areas (including bed net) with permethrin-containing insecticides.
  • Apply insect repellent on uncovered skin and under the ends of sleeves and pant legs
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