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Section 2
Section 3
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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.

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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 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 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 virus (HIV) . . . [Go to Full Text]


Related text in Red Book:

Prevention of Mosquitoborne Infections

Red Book 2006: 197-199. [Extract] [Full Version]  

Drugs for Parasitic Infections

Red Book 2006: 790-820. [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]  
  • Singh, M. (2000). Health Care for Children in Afghanistan. Pediatrics 105: 160-160 [Full Version]