Clinical Overview of Leishmaniasis

Key points

  • The term leishmaniasis encompasses multiple clinical syndromes.
  • Infection can range from asymptomatic to severe in all forms of leishmaniasis.
  • Cutaneous and mucosal leishmaniasis can cause substantial morbidity; visceral and mucosal leishmaniasis can be life threatening.


The term leishmaniasis encompasses multiple clinical syndromes, including the cutaneous, mucosal, and visceral forms, which result from infection of macrophages in the dermis, in the naso-orpharyngeal mucosa, and throughout the reticuloendothelial system, respectively. The infection can range from asymptomatic to severe in all of these forms. Cutaneous and mucosal leishmaniasis can cause severe morbidity; visceral and mucosal leishmaniasis can be life threatening.


Cutaneous leishmaniasis (CL)

CL is the most common form of leishmaniasis, both in general and in US travelers. Unless otherwise specified, CL refers to localized CL, rather than to much less common forms, such as diffuse CL and disseminated CL. Different Leishmania species cause different types of CL.

In the Eastern Hemisphere, the etiologic agents include

  • L. tropica
  • L. major
  • L. aethiopica
  • L. infantum
  • L. donovani

In the Western Hemisphere, the main species are

  • L. mexicana species complex
    • L. mexicana
    • L. amazonensis
    • L. venezuelensis
  • Viannia subgenus
    • L. [V.] braziliensis
    • L. [V.] guyanensis
    • L. [V.] panamensis
    • L [V.] peruviana

L. infantum can also cause CL in the Western Hemisphere although it is more commonly associated with VL.

Clinical features

Cutaneous leishmaniasis (CL)

In general, CL causes skin lesions, which can persist for months and sometimes years. The skin lesions usually develop within several weeks or months after the exposure, but occasionally first appear years later (e.g., in the context of trauma or immunosuppression). The lesions typically evolve from papules to nodular plaques to ulcerative lesions, with a raised border and central depression, which can be covered by scab or crust; some lesions persist as nodules. The lesions usually are painless but can be painful, especially if ulcerative lesions become infected with bacteria or if the lesions are near a joint. The healing process typically results in atrophic scarring.

Even patients with localized CL commonly develop more than one primary lesion (on the same or different parts of the body), satellite lesions, regional lymphadenopathy (occasionally bubonic), and/or nodular lymphangitis (sporotrichoid-like subcutaneous nodules). Sometimes lymphadenopathy is noticed before skin lesions develop.

Mucosal leishmaniasis (ML)

ML (also called espundia) refers to a metastatic sequela of cutaneous infection from specific Leishmania species in the Western Hemisphere. ML results from dissemination of parasites from the skin to the naso-oropharyngeal mucosa.

ML is caused by species in the Viannia subgenus (especially L. [V.] braziliensis but also L. [V.] panamensis and sometimes L. [V.] guyanensis). Fewer cases have been reported to be caused by other Leishmania species, such as L. (Leishmania) amazonensis, L. donovani, L. infantum, and L major. Adequate systemic treatment of CL caused by these species may reduce the risk for mucosal disease, but some risk may remain. The magnitude and determinants (parasite and host factors) of the risk for mucosal dissemination and for mucosal disease are poorly understood; even for the same species (for example, in L. [V.] braziliensis), the risk appears to vary among geographic regions in the Americas.

ML usually becomes clinically evident within several years (sometimes as long as decades) of the original cutaneous lesions, which typically were not treated at all or were treated sub optimally. However, mucosal and skin lesions may be noted concomitantly (mucocutaneous leishmaniasis), and some patients had subclinical cutaneous infection.

The initial manifestations of ML usually are persistent, unusual nasal symptoms (such as stuffiness or bleeding), although oral or pharyngeal symptoms sometimes are noticed first. If untreated, the disease can progress to ulcerative destruction of the naso-oropharyngeal mucosa (such as perforation of the nasal septum). ML may become life threatening if it involves the larynx because it can lead to airway obstruction.

Visceral Leishmaniasis (VL)

The general term VL encompasses a broad spectrum of severity and manifestations, usually caused by infection with one of two Leishmania species. Although the incubation period generally ranges from weeks to months, asymptomatic infection can become clinically manifest years to decades after the exposure in people who become immunocompromised for other medical reasons (such as HIV/AIDS). VL usually is caused by L. donovani and L. infantum in the Eastern Hemisphere and L. infantum chagasi (formerly called L. chagasi, but currently believed to be a subspecies to L. infantum) in the Western Hemisphere and affects internal organs (particularly, spleen, liver, and bone marrow).

The typical clinical manifestations of visceral infection include

  • Fever
  • Weight loss (cachexia; wasting)
  • Hepatosplenomegaly (usually, the spleen is more prominent than the liver)
  • Pancytopenia (i.e., anemia, leukopenia, and thrombocytopenia)
  • A high total protein level and a low albumin level, with hypergammaglobulinemia

Lymphadenopathy may be noted, particularly in some geographic regions (e.g., Sudan and South Sudan).

HIV-coinfected patients may have atypical manifestations, such as involvement of the gastrointestinal tract and other organ systems.

The term kala-azar,which means black (kala) fever (azar) in Hindi, is often reserved for severe (advanced) cases of VL, although the terms kala-azar and VL sometimes are used interchangeably. If untreated, severe cases of VL typically are fatal, either directly from the disease or indirectly from complications, such as secondary (myco)bacterial infection or hemorrhage.

Some patients who survive VL and who were inadequately treated develop post kala-azar dermal leishmaniasis (PKDL), a syndrome characterized by skin lesions. The lesions (often erythematous or hypopigmented macules, papules, nodules, and patches), may develop at variable intervals after (or during) therapy for VL, and are typically first noticed and most prominent on the face. Persons with chronic PKDL can serve as important reservoir hosts of infection.


There are no vaccines or drugs to prevent leishmaniasis infection. The best way people living in or visiting endemic areas can prevent infection is to protect themselves from sand fly bites. You can take personal protective measures such as

  • Minimizing nocturnal outdoor activities.
  • Wearing protective clothing.
  • Applying EPA-registered insect repellant to exposed skin.
  • Using a bet net and tucking it under your mattress if you are not sleeping in a well-screened or air-conditioned area. If possible, use a bed net that has been soaked in or sprayed with a pyrethroid-containing insecticide. The same treatment can be applied to screens, curtains, sheets, and clothing (clothing should be retreated after five washings.

Generally, prevention and control measures must be tailored to the local setting and typically are difficult to sustain. Control measures against sand fly vectors or animal reservoir hosts might be effective in some settings.

In many geographic areas where leishmaniasis is found in people, those infected are not needed to maintain the transmission cycle of the parasite in nature; animal reservoir hosts (such as rodents or dogs), along with sand flies, maintain the cycle. For example, in L. infantum-endemic regions, dogs serve as the main reservoir hosts; control strategies for such areas are being evaluated.

In some parts of the world, infected people are needed to maintain the cycle; this type of transmission (human-sand fly-human) is called anthroponotic. For example, in the Indian Subcontinent (South Asia), the transmission of L. donovani is anthroponotic. In such areas, early detection and effective treatment of infected persons can serve as a control measure; suboptimal treatment can lead to development and spread of drug resistance. Because the transmission is intra- and peridomiciliary (rather than sylvatic), spraying houses with residual-action insecticides and using small mesh bed nets treated with long-lasting insecticides may be protective.