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Section 3. Summaries of Infectious Diseases
Leishmaniasis
Clinical Manifestations|
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CLINICAL MANIFESTATIONS
The 3 major clinical syndromes are as follows:
Cutaneous leishmaniasis. After inoculation by the bite of an infected female phlebotomine sand fly (approximately 2–3 mm long), parasites proliferate locally in mononuclear phagocytes, leading to an erythematous papule, which typically evolves to become a nodule and then a shallow ulcerative lesion with raised borders. Lesions can, however, persist as nodules or papules. Lesions commonly are located on exposed areas of the body (eg, face and extremities) and may be accompanied by satellite lesions, which appear as sporotrichoid-like nodules, and regional adenopathy. Clinical manifestations of Old World and New World (American) cutaneous leishmaniasis are similar. Spontaneous resolution of lesions may take weeks to years and usually results in a flat atrophic (cigarette paper) scar.
Mucosal leishmaniasis (espundia). Mucosal infection may become clinically evident from months to years after the cutaneous lesions heal; sometimes mucosal and cutaneous lesions are noted simultaneously. Parasites may disseminate to the naso-oropharyngeal mucosa. In some patients, granulomatous ulceration and necrosis follows, leading to facial disfigurement, secondary infection, and mucosal perforation, which may occur months to years after the initial cutaneous lesion heals.
Visceral leishmaniasis (kala-azar). After cutaneous inoculation of parasites, organisms spread throughout the mononuclear macrophage system to the spleen, liver, and bone marrow. The resulting clinical illness typically manifests as fever, anorexia, weight loss, splenomegaly, hepatomegaly, lymphadenopathy (in some geographic areas), anemia, leukopenia, thrombocytopenia sometimes associated with hemorrhage, hypoalbuminemia, and hypergammaglobulinemia. Secondary gram-negative enteric and mycobacterial infections are common (eg, tuberculosis). Untreated clinically manifested visceral infection (ie, visceral leishmaniasis) nearly always is fatal. Reactivation of latent visceral infection can occur in patients who become immunocompromised, including people with concurrent human immunodeficiency
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