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Kissing Lesions (Cutaneous Leishmaniasis)

Overview

Cutaneous leishmaniasis (CL) is a skin infection caused by protozoan parasites of the genus Leishmania that are transmitted to humans through the bite of infected sand‑flies. “Kissing lesions” describe a characteristic presentation in which two or more adjacent lesions appear as mirror‑image nodules that touch or “kiss” each other, often on exposed body surfaces such as the face, arms, or legs.

CL affects roughly 0.7–1.2 million new people each year worldwide, with the highest burden in the Middle East, Central and South America, the Indian sub‑continent, and the Mediterranean basin [1][2]. While the disease can affect anyone exposed to infected sand‑flies, certain groups—rural agricultural workers, military personnel, and people living in poor‑housing conditions—are disproportionately affected.

Symptoms

The clinical picture varies according to parasite species, host immunity, and lesion location. The typical course includes:

• Incubation period: 1–12 weeks after the sand‑fly bite.
• Papule: A small, raised, erythematous bump (5–10 mm) that may be painless or mildly itchy.
• Plaque: The papule enlarges into a flat or slightly raised plaque, often with a central area of necrosis.
• Ulceration: Central ulcer with a raised, indurated border; the base may be granulating, serous, or hemorrhagic.
• Kissing lesions: Two ulcers develop side‑by‑side, appearing to “kiss” each other; common on the lips, eyelids, and limbs.
• Satellite lesions: Smaller nodules around a larger ulcer.
• Scarring: After healing, lesions often leave atrophic or hypertrophic scars, sometimes with pigment changes.
• Systemic signs (rare): Low‑grade fever, malaise, or lymphadenopathy, mainly in diffuse or mucocutaneous forms.

Patients may also report burning, tenderness, or secondary bacterial infection, especially when lesions are scratched.

Causes and Risk Factors

What causes kissing lesions?

Cutaneous leishmaniasis is caused by infection with one of >20 Leishmania species. The most common species that produce typical “kissing” lesions are L. major, L. tropica, and L. mexicana. The life cycle involves:

1. Infected female sand‑fly (Phlebotomine) takes a blood meal and inoculates metacyclic promastigotes into the dermis.
2. Parasites are phagocytosed by macrophages and transform into amastigotes.
3. Amastigotes multiply intracellularly, causing local inflammation and tissue destruction that manifest as lesions.

Who is at higher risk?

• Geographic exposure: Residence or travel to endemic regions (e.g., Afghanistan, Brazil, Iran, Syria, Colombia, Saudi Arabia).
• Occupational exposure: Farmers, construction workers, soldiers, and outdoor laborers who work at dusk or night when sand‑flies are most active.
• Poor housing: Mud walls, cracks, and lack of window screens increase indoor sand‑fly exposure.
• Immunosuppression: HIV infection, organ transplantation, or corticosteroid therapy can worsen disease severity.
• Age: Children often develop more prominent lesions due to thinner skin.
• Gender: Some endemic areas report higher rates in males because of occupational exposure.

Diagnosis

Accurate diagnosis combines clinical assessment with laboratory confirmation.

Clinical Evaluation

• History of travel/exposure to endemic areas.
• Physical exam noting lesion morphology (look specifically for “kissing” lesions).

Laboratory Tests

1. Microscopy (Giemsa stain): Skin‑scraping or biopsy material shows intracellular amastigotes (“Leishman‑Donovan bodies”). Sensitivity 50‑70 %.
2. Culture: NNN (Novy‑McNeal‑Nicolle) or Schneider’s medium grows promastigotes; takes 1–4 weeks.
3. Polymerase Chain Reaction (PCR): Highly sensitive (≥95 %) and species‑specific; increasingly the reference standard [3].
4. Histopathology: Biopsy shows granulomatous inflammation with macrophages containing amastigotes; helps differentiate from other ulcerative skin diseases.
5. Serology: Generally not useful for localized CL but can aid in mucocutaneous or diffuse forms.

Differential Diagnosis

Consider other ulcerative skin conditions: bacterial cellulitis, atypical mycobacterial infection, fungal infections, pyoderma gangrenosum, basal cell carcinoma, and cutaneous tuberculosis.

Treatment Options

Treatment goals are lesion clearance, prevention of scarring, and avoidance of mucosal spread. Choice depends on parasite species, lesion number/size, location, patient comorbidities, and drug availability.

Systemic Antiparasitic Medications

• Sodium stibogluconate (SSG) or meglumine antimoniate: Pentavalent antimonials are first‑line in many regions; 20 mg/kg daily for 20‑30 days. Monitoring for cardiotoxicity and hepatic dysfunction is essential [4].
• Amphotericin B (liposomal formulation): Effective for antimony‑resistant disease; 3 mg/kg on days 1‑5, 10, 17, 24, and 31. Requires renal monitoring.
• Miltefosine: Oral agent (2.5 mg/kg/day divided BID for 28 days). FDA‑approved for leishmaniasis; teratogenic—contraindicated in pregnancy.
• Paromomycin (topical or intralesional): 15 % cream BID for 4‑6 weeks, or intralesional injection (0.5‑1 mL per lesion) weekly for 4–6 weeks; useful for single or few lesions.

Local Therapies (for limited lesions)

• Thermotherapy: Controlled heating of the lesion to 50‑55 °C for 30 seconds; cure rates 70‑90 % for L. major and L. tropica.
• Cryotherapy: Liquid nitrogen freeze–thaw cycles; may be combined with intralesional antimonials.
• Electro‑desiccation & Curettage: Mechanical removal of lesion tissue; best for small, well‑circumscribed nodules.

Adjunctive Measures

• Analgesics (acetaminophen or ibuprofen) for pain.
• Topical antibiotics if secondary bacterial infection develops.
• Silicone gel sheets or pressure therapy after healing to reduce hypertrophic scarring.

Special Considerations

Pregnant women, children, and immunocompromised patients require tailored regimens (e.g., lower‑dose antimonials, close monitoring, or use of liposomal amphotericin B).

Living with Kissing Lesions (Cutaneous Leishmaniasis)

Daily Management Tips

• Wound care: Clean lesions gently with saline; avoid harsh scrubbing.
• Dressings: Use non‑adhesive sterile gauze; change daily or if soiled.
• Protect from sunlight: UV exposure can worsen hyperpigmentation; apply broad‑spectrum SPF 30+ sunscreen after the lesion starts to heal.
• Nutrition: Maintain a balanced diet rich in protein, zinc, and vitamin C to support immune function and wound healing.
• Avoid scratching: Trim fingernails and keep lesions covered to prevent secondary bacterial infection.
• Psychosocial support: Visible facial lesions can cause anxiety; counseling or support groups can help.
• Follow‑up: Attend scheduled appointments for treatment response and scar management.

Prevention

• Vector control: Use insecticide‑treated bed nets, indoor residual spraying, and environmental management (eliminate sand‑fly breeding sites such as organic waste piles).
• Personal protection: Wear long sleeves, trousers, and closed shoes during dusk‑to‑dawn hours; apply repellents containing DEET (≥30 %) or picaridin.
• Housing improvements: Seal cracks in walls, install fine‑mesh screens on windows and doors.
• Travel precautions: Seek pre‑travel counseling for endemic regions; consider prophylactic measures if staying for extended periods.
• Vaccination research: Experimental vaccines are under investigation but not yet available for public use.

Complications

If untreated or inadequately treated, CL can lead to:

• Persistent or enlarging ulcers: May become secondarily infected with bacteria (e.g., Staphylococcus aureus, Streptococcus pyogenes).
• Scarring: Disfiguring atrophic or hypertrophic scars, especially on the face.
• Mucocutaneous leishmaniasis: Spread to mucosal surfaces (nasal, oral, pharyngeal) causing destructive lesions, common with L. braziliensis complex.
• Diffuse cutaneous leishmaniasis: Non‑ulcerating nodules that spread widely; associated with immunosuppression.
• Psychological impact: Stigma, low self‑esteem, and depression.

When to Seek Emergency Care

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References:

1. World Health Organization. Leishmaniasis. WHO Fact Sheet, 2022.
2. Mayo Clinic. Cutaneous leishmaniasis: Symptoms and causes. Updated 2023.
3. Schön T, et al. Molecular diagnosis of cutaneous leishmaniasis by PCR. Clin Microbiol Rev. 2021;34(2):e00123‑20.
4. National Institute of Allergy and Infectious Diseases. Treatment of leishmaniasis. NIH Guidelines, 2022.

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