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Section 2
Section 3
Section 4
Section 5
Appendices

The following text is from an archived Red Book® edition and may not reflect current recommendations or information. To view the current edition, click here.

Section 3. Summaries of Infectious Diseases

Leishmaniasis

Clinical Manifestations
Etiology
Epidemiology
Diagnostic Tests
Treatment
Isolation of the Hospitalized Patient
Control Measures

CLINICAL MANIFESTATIONS:
The 3 major clinical syndromes are as follows:

  • Cutaneous leishmaniasis. After inoculation by the bite of an infected sandfly, parasites proliferate locally in mononuclear phagocytes, leading to an erythematous macula or nodule that typically evolves to form a shallow ulcer with raised borders. Lesions commonly are located on exposed areas of the face and extremities and may be accompanied by satellite lesions and regional adenopathy. The clinical manifestations of Old World and New World cutaneous leishmaniasis are similar. Spontaneous resolution of lesions may take weeks to years and usually results in a flat atrophic (cigarette paper) scar.

  • Mucocutaneous leishmaniasis (espundia). From the initial cutaneous infection caused by Leishmania braziliensis or related New World species, parasites may disseminate to the oral and nasopharyngeal mucosa. In some patients, granulomatous ulceration follows, leading to facial disfigurement, secondary infection, and mucosal perforation months to years after the cutaneous lesion heals.

  • Visceral leishmaniasis (kala-azar). After cutaneous inoculation of parasites, organisms spread throughout the mononuclear macrophage system and are concentrated in the spleen, liver, and bone marrow. The resulting clinical illness is marked by fever, anorexia, weight loss, splenomegaly, hepatomegaly, lymphadenopathy (in some geographic areas), anemia, leukopenia, thrombocytopenia with hemorrhage, hypoalbuminemia, and hypergammaglobulinemia. Secondary pyogenic, gram-negative enteric, and mycobacterial infections are common. Active untreated visceral disease nearly always is fatal. Reactivation of latent visceral leishmaniasis is common in patients with concurrent human immunodeficiency virus (HIV) infection or other immunocompromising conditions.


ETIOLOGY:
In the human host, Leishmania species are obligate intracellular parasites of mononuclear phagocytes. A single Leishmania species can produce different clinical syndromes, and each syndrome . . . [Go to Full Text]


Related text in Red Book:

Drugs for Parasitic Infections

Red Book 2003: 744-770. [Extract] [Full Version]  

Directory of Resources

Red Book 2003: 789-794. [Extract] [Full Version]  




This topic has been referenced by these articles:

  • Cascio, A., Calattini, S., Colomba, C., Scalamogna, C., Galazzi, M., Pizzuto, M., Camilli, R., Gramiccia, M., Titone, L., Corbellino, M., Antinori, S. (2002). Polymerase Chain Reaction in the Diagnosis and Prognosis of Mediterranean Visceral Leishmaniasis in Immunocompetent Children. Pediatrics 109: e27-27 [Abstract] [Full Version]  
  • Gagnaire, M.-H., Galambrun, C., Stéphan, J. L. (2000). Hemophagocytic Syndrome: A Misleading Complication of Visceral Leishmaniasis in Children---A Series of 12 Cases. Pediatrics 106: 58e-58 [Abstract] [Full Version]