Parasite
Leishmaniasis
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Leishmaniasis
, Leishmania, Kala Azar, Leishmania donovani, Visceral Leishmaniasis
See Also
Protozoa
History
First reported in 1903 by both Leishman and Donovan
Epidemiology
Incidence
Worldwide: Up to 2 million new cases per year
United States: Up to 100 cases/year (New World)
Endemic Areas
South-Central Texas
Mexico and Central America
South America (most common source for U.S. traveler)
Most commonly contracted in Peru and Brazil
No cases in Uruguay or Chile
Middle East
Africa
Asia
Pathophysiology
Vector
Transmitted by Sandflies
Old World Genus:
Phlebotomus
New World Genus: Lutzomyia
Sandfly is 2 mm long, hairy fly
Not stopped by
Mosquito
netting
Breeds in manure, rodent holes, leaf debris
Natural reservoirs (Sandflies transmit between animals and humans)
Rodents
Dogs
Foxes
Leishmaniasis species
Leishmania tropica
Leishmania chagasi
Leishmania major
Leishmania brasiliensis
Leishmania donovani
Leishmaniasis
Parasite
Leishmania are blood borne flagellates
Similar to Trypansoma (Chagas' Disease,
African Sleeping Sickness
)
Promastigote (Infectious form)
Motile form of
Parasite
with anterior flagellum
Develops in sandfly over 10 days
Transmitted to humans via sandfly bite
Forms a
Skin Ulcer
at
Insect Bite
site (similar to Trypanososomiais)
Macrophage
s ingest promastigote
Promastigote transforms into non-motile amastigote form to endure acidic
Lysosome
Amastigote divides within
Macrophage
Spreads to liver,
Spleen
,
Lymph Node
s and
Bone Marrow
Amastigote (Disease causing form)
Non-motile (no flagella), round, obligate intracellular
Parasite
Diameter up to 7 microns
Results in disease and decreased cellular
Immunity
Sandfly ingests amastigote form when feeding
Severity of Leishmaniasis manifestations depends on a patient's cell mediated
Immunity
Specific inherited genetic deficiency against Leishmania results in more severe disease
Broad spectrum of disease
Simple
Cutaneous Leishmaniasis
(single ulcer at
Insect Bite
)
Diffuse Cutaneous Leishmaniasis
or
Mucocutaneous Leishmaniasis
Severe systemic infection involving the reticuloendothelial system (liver,
Spleen
)
Types
Some species cause visceral and
Cutaneous Leishmaniasis
Cutaneous Leishmaniasis
See
Cutaneous Leishmaniasis
Simple
Cutaneous Leishmaniasis
Single ulcer ("oriental sore") forms at sandfly bite site
Leishmania can be seen in ulcer bed scrapings under microscopy
Cell mediated
Immunity
limits infection to localized skin lesion
Future delayed
Hypersensitivity
to Leishmania
Leishmanin Skin Test
Intradermal injection of Leishmania
Antigen
results in PPD-like reaction at 48-72 hours
Ulcer heals over the course of the year
Hypopigmented scar remains at bite site
Diffuse Cutaneous Leishmaniasis
Less common than other forms of Leishmaniasis
Associated with specific Leishmania species (e.g. L. amazonensis, L. mexicana, L. aethiopica)
Most severe cases reported in Brazil, Ethiopia, Sudan, South Sudan, India, and Bangladesh
Chronic form of
Cutaneous Leishmaniasis
in
Immunocompromised
patients
Cell mediated
Immunity
deficiency allows for chronic smoldering infection
Promastigotes persist in the skin and spread systemically
Leishmanin Skin Test is negative due to deficient cell mediated
Immunity
Nodular skin lesion forms at sandfly bite but does not ulcerate
Diffuse skin
Nodule
s develop over time, distant from the initial bite site
Predisposition for perinasal lesions
Infection persists for decades in untreated patients
Mucocutaneous Leishmaniasis
Begins with
Skin Ulcer
at sandfly bite (as with simple
Cutaneous Leishmaniasis
)
Mucous membrane ulcers form on mouth and nose, months to years after
Skin Ulcer
heals
Lesion scrapings demonstrate Leishmania under microscopy
Chronic infections in untreated patients leads to erosions of the nasal septum,
Palate
and lips
Lesions develop over decades in untreated patients
Complications (esp. secondary
Bacterial Infection
s) may be lethal
Visceral Leishmaniasis (Kala Azar, described on this page)
Most common in poorly nourished, young children
Caused by Leishmania donovani or Leishmania chagasi transmitted by sandfly bite
Fatal in 90% of untreated patients
Gastrointestinal symptoms follow a 3 month incubation (from time of sandfly bite)
Abdominal Pain
and distention
Hepatomegaly
and severe
Splenomegaly
(due to Leishmania invasion of reticuloendothelial system)
Anorexia
and weight loss
Other findings
Low grade fever
Anemia
and
Leukopenia
Symptoms
Visceral Leishmaniasis
See
Cutaneous Leishmaniasis
Irregular
Recurrent Fever
Weakness
Sweating
Cough
Nausea
or
Vomiting
Diarrhea
Weight loss
Abdominal Pain
Signs
Visceral Leishmaniasis
See
Cutaneous Leishmaniasis
Abdominal Distention
Massive
Splenomegaly
Hepatomegaly
Lymphadenopathy
Labs
Visceral Leishmaniasis
Complete Blood Count
Leukopenia
Anemia
Pancytopenia
Liver Function Test
s
Hypoalbuminemia
Diagnosis
Visceral Leishmaniasis
Culture, Biopsy, or buffy coat stain
Skin lesion
Bone Marrow
Lymph Node
Anti-Leishmanial IgG
High titers in Visceral Leishmaniasis
Leishmanin Skin Test
Negative in active Visceral Leishmaniasis (deficient cell-mediated
Immunity
)
Complications
Cirrhosis
develops in 10% of Visceral Leishmaniasis
Visceral Leishmaniasis is fatal without treatment in 90% of cases
Management
Visceral Leishmaniasis
See
Cutaneous Leishmaniasis
Immunocompetent Patients in Non-East African Region
Liposomal Amphotericin B
3 mg/kg IV daily on days 1-5, 14 and 21
Total cummulative dose of 21 mg/kg is required
Alternative agents
Miltefosine
Meglumine Antimoniate
(
Glucantime
)
Immunocompetent Patients in East Africa with high resistance rates
Meglumine Antimoniate
(
Glucantime
) AND
Paromomycin
for 17 days (preferred) OR
Liposomal Amphotericin B
with extended course to cummulative total dose 40 mg/kg (instead of 21 mg/kg)
HIV/
AIDS
See other references
Prevention
See
Prevention of Vector-borne Infection
Insect
Repellant
References
Freedman (2025) Sanford Guide, accessed 7/13/2025 on IOS
Gladwin, Trattler and Mahan (2014) Clinical Microbiology, Medmaster, Fl, p. 348-9
Pearson (1996) Clin Infect Dis 22:1-13 [PubMed]
Scarpini (2022) Microorganisms 10(10):1887 +PMID: 36296164 [PubMed]
Tobin (2001) Am Fam Physician 63(2):326-32 [PubMed]
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