Leishmaniasis is caused by more than 20 species of the protozoan genus Leishmania, with a disease spectrum ranging from self-healing cutaneous lesions to debilitating mucocutaneous infections, subclinical viscerotropic dissemination, and fatal visceral involvement. Published disease burden estimates place leishmaniasis second in mortality and fourth in morbidity among all tropical diseases. Leishmaniasis is classified as one of the “most neglected diseases,” based on its association with poverty and on the limited resources invested in diagnosis, treatment, and control. The World Health Organization (WHO) estimates that 1.5 million cases of cutaneous leishmaniasis (CL) and 500,000 cases of visceral leishmaniasis (VL) occur every year in 88 countries. Estimates indicate that approximately 350 million people are at risk for acquiring leishmaniasis, with 12 million currently infected.

Cases of leishmaniasis are seen each year in the United States and can be attributed to immigrants from countries with endemic infection, military personnel, and American travelers. Another concern is the potential for more infections occurring in areas of endemic infection in Texas and Arizona.

GENERAL CHARACTERISTICS

The parasite has two distinct phases in its life cycle: amastigote and promastigote (Table 1, Figure 1). The amastigote form is an intracellular parasite in the cells of the reticuloendothelial system and is oval, measuring 1.5 to 5 µm, and contains a nucleus and kinetoplast. Leish mania spp. exist as the amastigote in humans and as the promastigote in the insect host. As the vector takes a blood meal, promastigotes are introduced into the human host. Depending on the species, the parasites then move from the bite site to the organs within the reticuloendothelial system (bone marrow, spleen, liver) or to the macro phages of the skin or mucous membranes.

Table1. Features of Human Leishmanial Infections ^a

Fig1. A, Leishmania donovani parasites in Küpffer cells of  liver (2000×). B, Leishmania sp. 

More than 90% of cutaneous leishmaniasis cases occur in Afghanistan, Algeria, Iran, Iraq, Saudi Arabia, Syria, Brazil, and Peru. There has been an increase in the number of cases among military personnel deployed in Afghanistan, Iraq, and Kuwait. Autochthonous (native to origin) human infections have been described in Texas. Most of the cases of mucocutaneous leishmaniasis occur in Bolivia, Brazil, and Peru. More than 90% of the cases of visceral leishmaniasis are found in Bangladesh, Brazil, India, Nepal, and Sudan.

Depending on the species involved, infection with Leishmania spp. can result in cutaneous, diffuse cutaneous, mucocutaneous, or visceral disease. In endemic areas with leishmaniasis, co-infection with human immunodeficiency virus (HIV)-positive patients is common. If co-infected patients are severely immunocompromised, up to 25% will die shortly after being diagnosed. The use of highly active antiretroviral therapy (HAART) has dramatically improved the prognosis of these co-infected patients.

PATHOGENESIS AND SPECTRUM OF DISEASE

The first sign of cutaneous disease is a lesion (generally a firm, painless papule) at the bite site. Although a single lesion may appear insignificant, multiple lesions or dis figuring facial lesions may be devastating for the patient. Usually, the lesions will have a similar appearance and will progress at the same speed. The original lesion may remain as a flattened plaque or may progress to a shallow ulcer. As the ulcer enlarges, it produces exudate and often becomes secondarily infected with bacteria or other organisms.

In mucocutaneous leishmaniasis, the primary lesions are similar to those found in cutaneous leishmaniasis. Untreated primary lesions may develop into the mucocutaneous form in up to 80% of the cases. Dissemination to the nasal or oral mucosa may occur from the active primary lesion or may occur years later after the original lesion has healed. These mucosal lesions do not heal spontaneously, and secondary bacterial infections are common and may be fatal. Also, untreated visceral leishmaniasis will lead to death; secondary bacterial and viral infections are also common in these patients.

The incubation period ranges from 10 days to 2 years, usually being 2 to 4 months. Common symptoms include fever, anorexia, malaise, weight loss, and, frequently, diarrhea. Clinical signs include nontender enlarged liver and spleen, swollen lymph nodes, and occasional acute abdominal pain. Darkening of facial, hand, foot, and abdominal skin (kala-azar) is often seen in light-skinned persons in India. Death may occur after a few weeks or after 2 to 3 years in chronic cases. The majority of infected individuals will be asymptomatic or have very few or minor symptoms that will resolve without therapy. Since 1990, an increase in leishmaniasis in organ transplant recipients has been documented. Most of these cases have been visceral leishmaniasis.

LABORATORY DIAGNOSIS

After the cutaneous lesion exudate is removed, these lesions should be thoroughly cleaned with 70% alcohol. Specimens can be collected from the margin of the lesion by aspiration, scraping, or punch biopsy or by making a slit with a scalpel blade. Smears can be pre pared from the material obtained and stained with any of the blood stains; biopsy specimens should also be submitted for routine histologic examination. Specimens for visceral disease include lymph node aspirates, liver biopsy specimens, bone marrow specimens, and buffy coat preparations of venous blood. Amastigotes with reticuloendothelial cells have been detected in a number of different specimens from HIV-positive patients.

Stained smears can be examined for the presence of the amastigotes. Although the specimens can be cultured using special techniques, these procedures are not routinely available. PCR methods have excellent sensitivity and specificity for direct detection, for identification of causative species, and for assessment of treatment efficacy; although not routinely available, they can be performed at some reference centers. A rapid immunochromatographic dipstick test using the recombinant K39 antigen has become available for the qualitative detection of total anti–Leishmania immunoglobulins.

In patients with severe visceral leishmaniasis (kala azar), there is a characteristic hypergammaglobulinemia, including both IgG and IgM. In highly suspect patients for the diagnosis of visceral leishmaniasis (assuming they are immunocompetent), if hypergammaglobulinemia is not present, this may be used to rule out the original diagnosis. Although serologic testing is available from some reference centers such as CDC, serologic assays are not very useful for the diagnosis of mucocutaneous and visceral leishmaniasis.

THERAPY

In simple cutaneous leishmaniasis, lesions usually heal spontaneously, although treatment options include cryotherapy, heat, photodynamic therapy, surgical excision of lesions, and chemotherapy. Standard therapy consists of injections of antimonial compounds; however, relapse is quite common and the patient response varies depending on the Leishmania species and type of disease.

Patients clinically cured of mucocutaneous infection continue to be PCR positive for many years following therapy; this disease is characterized by chronicity, latency, and metastasis with mucosal membrane involvement.

For many years, pentavalent antimony compounds have been the drugs of choice for the treatment of visceral leishmaniasis. However, with the first reports of primary treatment failures in the mid-1990s, additional drugs have been used and include lipid-associated amphotericin B for Mediterranean and Indian disease.

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