LEISHMANIASIS Fatih Kökdere

Leishmaniasis is a protozoan disease caused by any severeal species of Leishmania. It is transmitted to humans and other mammals by the blood sucking Phelebotomine sand fly. Parasite, host and other factors affect whether the infection symptomatic and whether cutaneous or visceral leishmaniasis results. Cutaneous Leishmaniasis appears in two forms: Old World and New World Old World Leishmaniasis New World Leishmaniasis Leishmania major Leishmania aethiopica Leishmania mexicana Leishmania braziliensis

Old World Leishmaniasis : Middle East, Asia, Africa, and Southern Europe New World Leishmaniais: Latin and Central America Most of the affected countries are in the tropics and subtropics. Cutaneous leishmaniasis is endemic in more than 70 countries, and 90% of cases occur in Saudi Arabia, Syria, Afghanistan, Algeria, Pakistan, Brazil, and Peru.

Leishmania Life Cycle

Clinical Features There are two forms of leishmaniasis disease: Cutaneous leishmaniasis and visceral leishmaniasis (kala-azar). The form of disease is determined by species, geographic distribution, and immune response

Cutenaous Leishmaniasis Lesions appear on exposed skin surfaces, especially on the extremities and face. The incubation period is variable. Lesions typically appear several weeks after a fly bite but lesions may appear days or months later. A painless papule forms at the bite site, enlarges to a nodule, crusts in the center, and ulcerates over 1 to 3 months. The ulcer has raised edges and the surrounding skin is dusky red. The lesion usually heals by involution within 6 months without treatment. On microscopic examination, the lesion is granulomatous, usually with many giant cells and few parasites.

Cutenaous Leishmaniasis Cutaneous leishmaniasis. A red papule eventually ulcerates and forms raised edges with surrounding dusky red skin.

Cutenaous Leishmaniasis

Cutenaous Leishmaniasis

Diffuse Cutenaous Leishmaniasis In diffuse cutaneous leishmaniasis, seen rarely in Ethiopia and adjacent East Africa and Latin America, parasite - laden nodules are widespread and do not ulcerate. Diffuse cutaneous leishmaniasis begins as a single skin nodule, which continues spreading until the entire body is covered by bizarre nodular lesions. Patients are usually immunologically unresponsive not only to leishmanin but also to other skin antigens, and the lesions often respond poorly to treatment.

Diffuse Cutenaous Leishmaniasis

Diffuse Cutenaous Leishmaniasis These lesions, which resemble keloids or large verrucae, are frequently confused with the nodules of lepromatous leprosy.

Mucocutaneous Leishmaniasis Mucosal dissemination occurs in 1% to 10% of infections, developing 1 to 5 years after cutaneous leishmaniasis lesions have healed, but sometimes coincident with active skin lesions. Mucocutaneous leishmaniasis is caused by L. brasiliensis in the Americas. L.aethiopica has been reported to cause this disease in the Old World.

Mucocutaneous Leishmaniasis Mucosal disease begins with erythema and ulcerations at the nares and progresses to nasal septum perforation with mutilation of the nose, mouth, oropharynx, and trachea

Mucocutaneous Leishmaniasis

Visceral Leishmaniasis (Kala – Azar) Visceral leishmaniasis is caused by L. donovani in India and Kenya, L. infantum in South Europe and North Africa, and L. chagasi in the Americas. The parasites invade macrophages throughout the mononuclear phagocyte system and cause severe systemic disease marked by hepatosplenomegaly, lymphadenopathy, pancytopenia, fever, night sweats, and weight loss. Untreated disease results in profound cachexia, bleeding from thrombocytopenia, susceptibility to secondary infections and death.

Visceral Leishmaniasis (Kala – Azar)

Diagnosis The diagnosis is made clinically and may be confirmed with smears and biopsy. Examination of Giemsa-stained slides of tissue is the most commonly used diagnostic technique. Polymerase chain reaction (PCR) techniques provide rapid diagnosis of Leishmania species. The test is becoming more widely available.

Treatment Cutaneous leishmaniasis is treated to accelerate cure, to reduce scarring, and to attempt to prevent dissemination (e.g., mucosal disease) or relapse. Treatment is given for persistent lesions (6 months), for lesions that are located over joints, or for multiple (5 to 10 or more) or large (4 to 5 cm in diameter) lesions.

Treatment The World Health Organization considers pentavalent antimony as the standard treatment. The two compounds used are sodium stibogluconate and meglumine antimoniate. CDC recommends a daily dose of 20 mg/kg body weight of sodium stibogluconate administered intravenously (IV) for 20 consecutive days. The advantages of intralesional administration are higher drug concentration at the site of infection, reduced systemic toxicity, faster time to healing, and reduced cost. Side effects are myalgias and arthralgias, cardiotoxicity, pancreatitis and renal failure. Most of these side effects are reversible.

Treatment Alternative treatments include amphotericin B, especially for mucosal leishmaniasis or for HIV coinfected patients, pentamidine, miltefosine, and thermotherapy. Other reported treatments include oral itraconazole and fluconazole, rifampicin, metronidazole and cotrimoxazole, IV or topical amphotericin B, oral dapsone, photodynamic therapy, and laser cryotherapy.

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