Leishmaniasis

Aka: Leishmaniasis, Leishmania, Kala Azar, Leishmania donovani, Visceral Leishmaniasis

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II. History

  1. First reported in 1903 by both Leishman and Donovan

III. Epidemiology

  1. Incidence
    1. Worldwide: Up to 2 million new cases per year
    2. United States: Up to 100 cases/year (New World)
  2. Endemic Areas
    1. South-Central Texas
    2. Mexico and Central America
    3. South America (most common source for U.S. traveler)
      1. Most commonly contracted in Peru and Brazil
      2. No cases in Uruguay or Chile
    4. Middle East
    5. Africa
    6. Asia

IV. Pathophysiology

  1. Vector
    1. Transmitted by Sandflies
      1. Old World Genus: Phlebotomus
      2. New World Genus: Lutzomyia
    2. Sandfly is 2 mm long, hairy fly
      1. Not stopped by Mosquito netting
      2. Breeds in manure, rodent holes, leaf debris
    3. Natural reservoirs (Sandflies transmit between animals and humans)
      1. Rodents
      2. Dogs
      3. Foxes
  2. Leishmaniasis species
    1. Leishmania tropica
    2. Leishmania chagasi
    3. Leishmania major
    4. Leishmania brasiliensis
    5. Leishmania donovani
  3. Leishmaniasis Parasite
    1. Leishmania are blood borne flagellates
      1. Similar to Trypansoma (Chagas' Disease, African Sleeping Sickness)
    2. Promastigote (Infectious form)
      1. Motile form of Parasite with anterior flagellum
      2. Develops in sandfly over 10 days
      3. Transmitted to humans via sandfly bite
        1. Forms a Skin Ulcer at Insect Bite site (similar to Trypanososomiais)
      4. Macrophages ingest promastigote
        1. Promastigote transforms into non-motile amastigote form to endure acidic Lysosome
        2. Amastigote divides within Macrophage
        3. Spreads to liver, Spleen, Lymph Nodes and Bone Marrow
    3. Amastigote (Disease causing form)
      1. Non-motile (no flagella), round, obligate intracellular Parasite
      2. Diameter up to 7 microns
      3. Results in disease and decreased cellular Immunity
      4. Sandfly ingests amastigote form when feeding
  4. Severity of Leishmaniasis manifestations depends on a patient's cell mediated Immunity
    1. Specific inherited genetic deficiency against Leishmania results in more severe disease
    2. Broad spectrum of disease
      1. Simple Cutaneous Leishmaniasis (single ulcer at Insect Bite)
      2. Diffuse Cutaneous Leishmaniasis or Mucocutaneous Leishmaniasis
      3. Severe systemic infection involving the reticuloendothelial system (liver, Spleen)

V. Types

  1. Some species cause visceral and Cutaneous Leishmaniasis
  2. Cutaneous Leishmaniasis
    1. See Cutaneous Leishmaniasis
    2. Simple Cutaneous Leishmaniasis
      1. Single ulcer ("oriental sore") forms at sandfly bite site
        1. Leishmania can be seen in ulcer bed scrapings under microscopy
      2. Cell mediated Immunity limits infection to localized skin lesion
        1. Future delayed Hypersensitivity to Leishmania
        2. Leishmanin Skin Test
          1. Intradermal injection of Leishmania Antigen results in PPD-like reaction at 48-72 hours
      3. Ulcer heals over the course of the year
        1. Hypopigmented scar remains at bite site
    3. Diffuse Cutaneous Leishmaniasis
      1. Less common than other forms of Leishmaniasis
        1. Associated with specific Leishmania species (e.g. L. amazonensis, L. mexicana, L. aethiopica)
        2. Most severe cases reported in Brazil, Ethiopia, Sudan, South Sudan, India, and Bangladesh
      2. Chronic form of Cutaneous Leishmaniasis in Immunocompromised patients
        1. Cell mediated Immunity deficiency allows for chronic smoldering infection
        2. Promastigotes persist in the skin and spread systemically
        3. Leishmanin Skin Test is negative due to deficient cell mediated Immunity
      3. Nodular skin lesion forms at sandfly bite but does not ulcerate
      4. Diffuse skin Nodules develop over time, distant from the initial bite site
        1. Predisposition for perinasal lesions
      5. Infection persists for decades in untreated patients
  3. Mucocutaneous Leishmaniasis
    1. Begins with Skin Ulcer at sandfly bite (as with simple Cutaneous Leishmaniasis)
    2. Mucous membrane ulcers form on mouth and nose, months to years after Skin Ulcer heals
      1. Lesion scrapings demonstrate Leishmania under microscopy
    3. Chronic infections in untreated patients leads to erosions of the nasal septum, Palate and lips
      1. Lesions develop over decades in untreated patients
      2. Complications (esp. secondary Bacterial Infections) may be lethal
  4. Visceral Leishmaniasis (Kala Azar, described on this page)
    1. Most common in poorly nourished, young children
    2. Caused by Leishmania donovani or Leishmania chagasi transmitted by sandfly bite
    3. Fatal in 90% of untreated patients
    4. Gastrointestinal symptoms follow a 3 month incubation (from time of sandfly bite)
      1. Abdominal Pain and distention
      2. Hepatomegaly and severe Splenomegaly (due to Leishmania invasion of reticuloendothelial system)
      3. Anorexia and weight loss
    5. Other findings
      1. Low grade fever
      2. Anemia and Leukopenia

VI. Symptoms: Visceral Leishmaniasis

  1. See Cutaneous Leishmaniasis
  2. Irregular Recurrent Fever
  3. Weakness
  4. Sweating
  5. Cough
  6. Nausea or Vomiting
  7. Diarrhea
  8. Weight loss
  9. Abdominal Pain

VII. Signs: Visceral Leishmaniasis

  1. See Cutaneous Leishmaniasis
  2. Abdominal Distention
  3. Massive Splenomegaly
  4. Hepatomegaly
  5. Lymphadenopathy

VIII. Labs: Visceral Leishmaniasis

  1. Complete Blood Count
    1. Leukopenia
    2. Anemia
    3. Pancytopenia
  2. Liver Function Tests
    1. Hypoalbuminemia

IX. Diagnosis: Visceral Leishmaniasis

  1. Culture, Biopsy, or buffy coat stain
    1. Skin lesion
    2. Bone Marrow
    3. Lymph Node
  2. Anti-Leishmanial IgG
    1. High titers in Visceral Leishmaniasis
  3. Leishmanin Skin Test
    1. Negative in active Visceral Leishmaniasis (deficient cell-mediated Immunity)

X. Complications

  1. Cirrhosis develops in 10% of Visceral Leishmaniasis
  2. Visceral Leishmaniasis is fatal without treatment in 90% of cases

XI. Management: Visceral Leishmaniasis

  1. See Cutaneous Leishmaniasis
  2. Immunocompetent Patients in Non-East African Region
    1. Liposomal Amphotericin B 3 mg/kg IV daily on days 1-5, 14 and 21
      1. Total cummulative dose of 21 mg/kg is required
    2. Alternative agents
      1. Miltefosine
      2. Meglumine Antimoniate (Glucantime)
  3. Immunocompetent Patients in East Africa with high resistance rates
    1. Meglumine Antimoniate (Glucantime) AND Paromomycin for 17 days (preferred) OR
    2. Liposomal Amphotericin B with extended course to cummulative total dose 40 mg/kg (instead of 21 mg/kg)
  4. HIV/AIDS
    1. See other references

XII. Prevention

  1. See Prevention of Vector-borne Infection
  2. Insect Repellant

XIII. References

  1. Freedman (2025) Sanford Guide, accessed 7/13/2025 on IOS
  2. Gladwin, Trattler and Mahan (2014) Clinical Microbiology, Medmaster, Fl, p. 348-9
  3. Pearson (1996) Clin Infect Dis 22:1-13 [PubMed]
  4. Scarpini (2022) Microorganisms 10(10):1887 +PMID: 36296164 [PubMed]
  5. Tobin (2001) Am Fam Physician 63(2):326-32 [PubMed]

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