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
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
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
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
Rx: