Cutaneous leishmaniasis (CL) of Old World (OWCL) and New World (NWCL) types, 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.
Mucosal leishmaniasis (ML)
Diffuse (anergic) cutaneous leishmaniasis (DCL)
Visceral leishmaniasis (VL); kala-azar; post–kala-azar dermal leishmaniasis (PKDL)
Life Cycle Leishmania dimorphic. In mammalian host: amastigote (leishmanial) form—2 to 3 m in length, oval/round, aflagellate; lives intracellularly in cells of reticuloendothelial system. In GI tract of sandfly/in culture: promastigote (leptomonad) form—10 to 15 m in length, spindle-shaped, flagellated; extracellular. Speciation: isoenzyme patterns, kinetoplast DNA buoyant densities, specific phlebotomine vectors, monoclonal antibodies, DNA hybridization, DNA restriction endonuclease fragment analysis.
Reservoir Varies with geography and leishmanial species. Zoonosis involves rodents/canines. Mediterranean littoral—dogs. Southern Russia—gerbils. For L. major, desert rodents. For L. tropica, rats. For L. infantum, wild canines, dogs; in endemic areas of Spain, up to 20% of dogs tested harbored parasites in skin and viscera.
Vector Female sandflies of genus Phlebotomus (Old World) and genera Lutzomyia (New World). Breed in cracks in buildings, rubbish, rubble; rodent burrows, termite hills, rotting vegetation. Weak fliers; remain close to ground near breeding site, Ingest amastigotes while feeding on infected mammals, converting to promastigotes in the gut of the sandfly; replicate in gut.
Transmission Promastigotes deposited on skin of host into a small pool of blood drawn by probing sandfly
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
OWCL
Asia, Africa, Europe in tropical and subtropical zones; Middle East (Iran, Iraq, eastern Saudi Arabia, Jordan Valley of Israel and Jordan, Sinai Peninsula). More common in rural areas. Begins as small erythematous papule, which may appear immediately after sandfly bite but usually 2 to 4 weeks later. Papule slowly enlarges to 2 cm over a period of several weeks and assumes a dusky violaceous hue (Fig. 26-29). Eventually, lesion becomes crusted in center with a shallow ulcer and raised indurated border = vulcano sign (Fig. 26-30). In some cases, the center of the nodule becomes hyperkeratotic, forming a cutaneous horn. Small satellite papules may develop at periphery of lesion, and occasionally subcutaneous nodules along the course of proximal lymphatics. Rarely, lesions become locally invasive and extend into subcutaneous tissue and muscle. Peripheral extension usually stops after 2 months, and ulcerated nodule persists for another 3 to 6 months, or longer. The lesion then heals with a slightly depressed scar. In some cases, CL remains active with positive smears for 24 months (nonhealing chronic cutaneous leishmaniasis). The number of lesions depends on the circumstances of the exposure and extent of infection within the sandfly vector. May result in multiple lesions, up to 100 or more (Figs. 26-30 and 26-31).
NWCL
Mexico, Central America, as far north as Texas, as far south as Brazil. Lesions develop in similar fashion to those caused by L. major. Small erythematous papule develops at sandfly bite site, evolving into ulcerated nodule (Fig. 26-32). Eventually lesion heals with a depressed scar. Enlarges 3 to 12 cm with raised border. Nonulcerating nodules may become verrucous. Lymphangitis, regional lymphadenopathy. Isolated lesions on hand or head usually do not ulcerate; heal spontaneously. Ear lesions may persist for years, destroying cartilage (chiclero ulcers)
L. braziliensis Complex
Clinical lesions similar to those of OWCL. Some strains can invade mucous membranes of mouth, nose, pharynx, larynx to cause MCL
Mucosal LeishmaniasisCharacterized by nasooropharyngeal mucosal involvement, a metastatic complication of CL. Caused by Viannia subgenus, typically L. (V.) braziliensis, L. (V.) panamensis, and L (V.) guyanensis. Mucosal disease usually becomes evident several years after healing of original cutaneous lesions; cutaneous and mucosal lesions can coexist or appear decades apart. Edema and inflammatory changes lead to epistaxis and coryzal symptoms. In time, nasal septum, floor of mouth, and tonsilar areas destroyed (Fig. 26-34). Results in marked disfigurement (referred to as espundia in South America). Death may occur due to superimposed bacterial infection, pharyngeal obstruction, or malnutrition.
Diffuse Cutaneous Leishmaniasis
Resembles lepromatous leprosy; large number of parasites in macrophages in dermis; no visceral involvement. In Old World, occurs in 20% of individuals with leishmaniasis in Ethiopia and Sudan. In South America, attributed to a member of L. braziliensis complex. Presents as a single nodule, which then spreads locally, often through extension from satellite lesions, and eventually by metastasis. In time, lesions become widespread with nonulcerating nodules appearing diffusely over face, trunk. Responds poorly to treatment.
Complication of L. tropica infection. Dusky-red plaques with active, spreading borders and healing centers, giving rise to gyrate and annular lesions. Most commonly affects face; can cause tissue destruction and severe deformity.
Post–kala-Azar Dermal Leishmaniasis (PKDL)
Sequel to VL that has resolved spontaneously or during/after adequate treatment. Lesions appear 1 y after course of therapy with macular, papular, nodular lesions, and hypopigmented macules/plaques on face, trunk, extremities. Resembles lepromatous leprosy when lesions are numerous. Develops in 20% of Indian patients treated for VL caused by L. donovani and in a small percentage of Ethiopian patients with VL caused by L. aethiopica.
Visceral Leishmaniasis
Can remain subclinical or become symptomatic, with acute, subacute, chronic course. Inapparent VL cases outnumber clinically apparent cases. Malnutrition is risk factor for clinically apparent VL. Bone marrow, liver, spleen are involved. Term kala-azar (Hindi for 'black fever,' some patients had gray color) refers to profoundly cachectic febrile patients with life-threatening disease. Patients present with fever, splenomegaly, pancytopenia, wasting.
Dermatopathology: Large macrophages filled with 2- to 4-m amastigotes (Leishman-Donovan bodies); mixed lymphocytic, plasmacytic infiltrate. In Wright- and Giemsa-stained preparations, the amastigote cytoplasm appears blue, nucleus relatively large and red; distinctive kinetoplast is rod-shaped and stains intensely red
Culture Novy-MacNeal-Nicolle medium at 22°C to 28°C for 21 days grows motile promastigotes – PCR
Course and Prognosis
Whether caused by L. tropica or L. mexicana, CL is self-limited. Scarring is increased by secondary bacterial infection.
May extend to secondary sites. Superinfection common. Death from pneumonia.
Progressive; refractory to treatment; cures rare
No chemoprophylaxis for travelers exists
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
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