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General Reference

Nejm 1993;328:1383; Ann IM 1993;118:779 (cutaneous); 1990;113:934

Pathophys and Cause

Cause:Leishmania donovani(Kala-azar); L. tropica, L. major, and L. braziliensis(mucocutaneous)

Pathophys: Organisms in macrophages; suppressor T cells keep delayed hypersensitivity to leishmania antigens turned off (Nejm 1982;306:387). Cutaneous lesions often heal only to develop mucocutaneous disease years later

Epidemiology

Sandfly feeds in evening and ingests parasitized cell, ruptures, and becomes leptomonad stage, which reproduces in fly gut, then migrates to mouth parts where is injected with next bite and, as leptomonad stage, migrates to RES cells where becomes leishmania form, which bursts and invades other cells. Recurrent disease in immunocompromised host, eg, HIV pts

Animal reservoirs (eg, dogs, rodents, sloths); human-to-human contact transmission also possible, skin-to-skin in cutaneous types

Indigenous in Asia (90% of cases in India, also Nepal), Africa, Middle East (Gulf War regions), and tropical South America where there are 2000 cases/2 million/yr

Signs and Symptoms

Sx:

Kala-azar: long incubation period, weight loss, diarrhea

Mucosal/cutaneous: slow-healing skin ulcers, nasal mucosa, other areas of oropharynx in severe disease

Si:

Kala-azar: fever, hepatosplenomegaly

Mucosal/cutaneous: large ulcers, scars

Course

Kala-azar: chronic, fatal without rx

Complications

Kala-azar: gi and pulmonary superinfections; rarely amyloid and cirrhosis

Lab and Xray

Lab:

Bact:Culture all above

Hem:Depressed white counts

Path:Typical, 1-3 µ Leishmania-Donovan bodies in monocytes, lymph nodes, spleen, skin lesions, marrow, liver

Treatment

Rx: