eMedicine Specialties > Infectious Diseases > Parasitic Infections

Leishmaniasis

Author: Craig G Stark, MD, Regional Medical Director, Northern Europe and Russia Regions, Tricare Medical Director for Western Hemisphere, International SOS Assistance UK, Ltd
Contributor Information and Disclosures

Updated: Mar 27, 2008

Introduction

Background

Leishmaniasis is a protozoal disease capable of causing a spectrum of clinical syndromes ranging from cutaneous ulcerations to systemic infections. With the exception of Australia, the Pacific Islands, and Antarctica, the parasites have been identified throughout large portions of the world.

The protozoa are transmitted to mammals via the bite of the female sandfly of the genus Phlebotomus in the Old World and Lutzomyia in the New World. Humans are generally considered incidental hosts. For most species of Leishmania, an animal reservoir is required for endemic conditions to persist. Infections in wild animals are usually not pathogenic, with the exception of dogs, which may be severely affected.

Traditionally divided between Old World and New World parasites, more than 20 pathogenic species have been identified. Common Old World hosts are domestic and feral dogs, rodents, foxes, jackals, wolves, raccoon-dogs, and hyraxes. Common New World hosts include sloths, anteaters, opossums, and rodents.

Although uncommon in the United States, major epidemics currently exist in Afghanistan, Brazil, India, and Sudan. With the increase in international travel, immigration, overseas military exercises, and HIV co-infection, leishmaniasis is becoming more prevalent throughout the world.

Pathophysiology

Leishmaniasis can be divided into cutaneous, mucocutaneous, visceral, and viscerotropic forms. Cutaneous manifestations can be further subdivided into localized, diffuse, leishmaniasis recidivans, and post-kala-azar dermal leishmaniasis.

Parasites exist in the promastigote stage in sandflies and transform to the amastigote form in animal and human hosts. Rare cases of transmission through needle sharing, transfusions, pregnancy, and sexual intercourse have been reported.

Female sandflies can transmit the parasite 7-10 days after feeding on an infected host. The promastigotes migrate from the gut to the proboscis and are regurgitated during the next meal into the new host's tissue.

After inoculation, parasites infect the reticuloendothelial system and live in the intracellular lysosomal organelles of macrophages. Parasites may incubate for weeks to months before presenting as skin lesions or as a disseminated systemic infection involving the liver, spleen, and bone marrow. Pathogenesis appears related to T-cell cytotoxicity.

In India, visceral leishmaniasis caused by Leishmania donovani does not appear to have an animal reservoir and is thought to be transmitted via human-sandfly-human interaction. An animal reservoir for cutaneous leishmaniasis caused by Leishmania tropica has not been identified, although it has been found in some dogs in endemic areas.

The extent and presentation of disease depend on several factors, including the humoral and cell-mediated immune response of the host, the virulence of the infecting species, and the parasite burden. Infections may heal spontaneously or may progress to chronic disease, often resulting in death from secondary infection.

Frequency

United States

Endemic leishmaniasis is uncommon. Periodic cases of localized cutaneous and diffuse cutaneous leishmaniasis have been reported in southern Texas and Oklahoma.1 The usual reservoir is the wood rat of the Southern Plains, but parasites have been identified in coyotes and domesticated dogs and cats. Spread by the sandfly vector Lutzomyia anthophora, cases are usually associated with exposure to the habitat of the wood rat.

Travelers, government workers, and military personnel from the United States are at risk overseas. Since 2001, more than 700 US military personnel have been diagnosed with cutaneous leishmaniasis and 4 with visceral leishmaniasis after serving in Afghanistan and the Middle East. Up to 1% of US forces serving in the Southwest Asian Theater may have been infected. During the first Persian Gulf War, an estimated 400 cases of cutaneous leishmaniasis and 12 cases of viscerotropic leishmaniasis were reported.2 The etiological agent for most of these cutaneous leishmaniasis cases appears to have been Leishmania major.

The Centers for Disease Control and Prevention (CDC) was notified of 129 cases between 1985 and 1990 involving travelers from the United States who acquired the disease abroad. During World War II, more than 1000 cases of cutaneous leishmaniasis were reported among US service members serving in the Persian Gulf. Illnesses now attributed to leishmaniasis have been identified throughout military campaigns from World War I back to antiquity.

International

Leishmaniasis can be found in 88 countries in the intertropical and temperate regions of the world. Visceral leishmaniasis is endemic in 62 countries. The World Health Organization reports an annual incidence of 600,000 cases but estimates up to 1.5 million new cases of cutaneous leishmaniasis and 500,000 cases of visceral leishmaniasis occur each year. An estimated 12 million people are infected from a population of 350 million people who are at risk. Of these infections, approximately 25% are of visceral leishmaniasis, most of which come from the Indian subcontinent, Sudan, and Brazil. As of July 2005, an outbreak of a rapidly fatal form of visceral leishmaniasis in Ethiopia is causing concerns for an epidemic in the Horn of Africa. In contrast, most cases of localized cutaneous leishmaniasis come from Afghanistan, Saudi Arabia, Syria, Iran, and the Americas. In Kabul alone, an estimated 67,500 people are thought to be infected with cutaneous leishmaniasis.3

Old World leishmaniasis can be found in the Middle East, Indian subcontinent, Asia, Mediterranean, East Africa, and republics of the former Soviet Union. New World leishmaniasis exists throughout the Americas, with the exception of Canada, Chile, and Uruguay.

Visceral and cutaneous leishmaniasis in patients with AIDS have been increasingly appreciated as a potential opportunistic infection. Co-infection with HIV has been reported in more than 35 countries throughout southern Europe, the Mediterranean Basin, Central and South America, and India. Disease occurs in conjunction with severe immunosuppression. The incidence of co-infection has decreased in developed countries because of the widespread use of antiretroviral therapy.

Mortality/Morbidity

  • Localized cutaneous leishmaniasis often spontaneously resolves in 3-6 months without therapy, although some infections persist indefinitely. Most cases of diffuse cutaneous leishmaniasis, post-kala-azar dermal leishmaniasis, and leishmaniasis recidivans are chronic and resistant to treatment and are associated with low mortality rates.
  • Mucocutaneous leishmaniasis is chronic and progressive. Death can occur from secondary infection and after respiratory tract mucosal invasion. Respiratory compromise and dysphagia may lead to malnutrition and pneumonia.
  • Visceral leishmaniasis is a progressive disease, with the mortality rate ranging from 75-95% if left untreated. With appropriate therapy and supportive care, the mortality rate is decreased to 5%. Death usually occurs from malnutrition and secondary infection. Tuberculosis, pneumonia, and dysentery are commonly implicated.

Sex

  • Males have an increased incidence of infection.
  • Male-to-female ratios of visceral leishmaniasis have been reported to be around 2:1.
  • Males appear to have higher rates of infection because of increased environmental exposure to the habitat of the sandfly through occupation and leisure activity.

Age

  • Leishmaniasis affects various age groups depending on the infecting species, geographic location, disease reservoir, and host immunocompetence.
  • Visceral leishmaniasis is found in all age groups in India and Brazil, where an animal reservoir has not been identified. In areas with animal reservoirs, such as the Mediterranean Basin, visceral leishmaniasis mainly affects children.
  • Cutaneous leishmaniasis affects all age groups. Reports from Afghanistan and Columbia show that adolescents and young adults are at risk the most. In Iran, most cases of the disease are found in infants.

Clinical

History

  • Cutaneous leishmaniasis
    • Both New World and Old World species cause localized cutaneous leishmaniasis. Inoculation occurs after a sandfly bites an exposed part of the body (usually the legs, arms, neck, or face).
    • Incubation occurs over weeks to months followed by the appearance of an erythematous papule, which can evolve into a plaque or ulcer. New World disease usually presents with a solitary nodule, while Old World disease is associated with multiple lesions. Systemic symptoms are absent. Wound progression occurs over time and may exhibit localized lymphangitic spread.
    • Lesions are usually without pain or pruritus, although secondary bacterial infection may complicate the wound. Healing may occur spontaneously from 2-12 months and is followed by scarring and changes in pigmentation. New World disease may progress to mucocutaneous leishmaniasis.
    • Diffuse cutaneous leishmaniasis develops in an anergic host with poor immune response. Infection is characterized by a primary lesion, which spreads to involve multiple areas of the skin. Plaques, ulcers, and nodules may form over the entire body, resembling lepromatous leprosy. However, no neurologic or systemic invasion is involved. Infections are chronic and may recur after treatment. Although more common with New World species in Central and South America, Old World Leishmania aethiopica may progress to diffuse disease in east Africa.
    • Leishmaniasis recidivans may occur years after a localized cutaneous lesion has healed, commonly presenting on the face. New ulcers and papules form over the edge of the old scar and proceed inward to form a psoriasiform lesion. Infection may be from reactivation of dormant parasites or new infection from a different species. Infections tend to be resistant to treatment.
    • Post-kala-azar dermal leishmaniasis has predominantly been described in Africa and India. The Indian variant occurs several years after recovery from visceral leishmaniasis and is characterized by multiple, hypopigmented, erythematous macules. Over time, these can transform into large plaques and nodules that involve the face and trunk. The disease resembles lepromatous leprosy and requires intensive therapy. The African variant occurs shortly after treatment of visceral leishmaniasis and is characterized by an erythematous papular rash on the face, buttocks, and extremities. These lesions spontaneously resolve over the course of several months.
  • Mucocutaneous leishmaniasis
    • Mucocutaneous disease is most commonly caused by New World species, although Old World L aethiopica has been reported to cause this syndrome. Infection by Leishmania viannia braziliensis may lead to mucosal involvement in up to 10% of infections depending on the region in which it was acquired. Initial infection is characterized by a persistent cutaneous lesion that eventually heals, although as many as 30% of patients report no prior evidence of leishmaniasis. Several years later, oral and respiratory mucosal involvement occurs, causing inflammation and mutilation of the nose, mouth, oropharynx, and trachea.
    • Progressive disease is difficult to treat and often recurs. With prolonged infection, death occurs from respiratory compromise and malnutrition. Mucocutaneous leishmaniasis may arise after inadequate treatment of certain Leishmania species.
  • Visceral leishmaniasis
    • Visceral disease, the most devastating and fatal form, is classically known as kala-azar or black fever. It occurs with both New and Old World species and results from systemic infection of the liver, spleen, and bone marrow. The syndrome is characterized by the pentad of fever, weight loss, hepatosplenomegaly, pancytopenia, and hypergammaglobulinemia.
    • Patients may report night sweats, weakness, and anorexia. Melanocyte stimulation and xerosis can occur, causing characteristic skin hyperpigmentation.
    • The incubation period varies after infection and may depend on the patient's age and immune status and the species of Leishmania. If left untreated, death frequently occurs from immunosuppression and secondary infections.
  • Viscerotropic leishmaniasis
    • Viscerotropic disease caused by L tropica has been described in patients returning from the Middle East. These patients presented anywhere from 1 month to 2 years after exposure, with symptoms of malaise, fatigue, intermittent fever, cough, diarrhea, abdominal pain, and other gastrointestinal symptoms.
    • Viscerotropic leishmaniasis has an indolent but distinct clinical presentation and does not appear to progress to full visceral leishmaniasis. L tropica traditionally has been associated with cutaneous leishmaniasis, although several reports of visceral disease have been reported from Kenya, India, and Israel.

Physical

  • Cutaneous leishmaniasis
    • The presentation varies depending on the stage of disease. Lesions are usually found in exposed areas. The skin lesion begins as a nontender, firm, red papule several centimeters in size at the site of the sandfly bite. In time, the lesion widens with central ulceration, serous crusting, and granuloma formation. The border often has a raised erythematous rim known as the volcano sign.
    • Lesions may be wet or dry and become fibrotic or hyperkeratotic with healing. Other findings include eczematous, psoriasiform, varicelliform, and verrucous lesions. The area surrounding the primary lesion may exhibit lymphangitic spread with palpable cords and subcutaneous nodules. This is common in New World lesions caused by L viannia braziliensis infections. Satellite lesions may be present. The lesions are generally painless and without pruritus. A generalized inflammatory reaction to migrating parasites may be present in the skin surrounding the sore. Overlying bacterial infection may complicate the natural history. Healing occurs over months to years, leaving a characteristic retracted hypopigmented scar.
    • Diffuse cutaneous leishmaniasis presents with disseminated, nontender, nonulcerating plaques and nodules covering the body similar in presentation to lepromatous leprosy. Generally a chronic disease, it may be resistant to therapy.
    • Leishmaniasis recidivans presents with lesions in the center or periphery of an old healed leishmaniasis scar. New ulcers may form years after the initial infection and often involve the cheek. Over years, these sores advance toward the center of the scar and form a psoriasiform plaque. It is often resistant to treatment.
    • Post-kala-azar leishmaniasis is initially characterized by a malar erythematous rash in conjunction with hypopigmented or reddish macules, following treatment for visceral leishmaniasis. Usually involving the face or trunk, the lesions progress to nontender plaques and nodules. Over time, these lesions join to form large raised growths similar to those of lepromatous leprosy. In Sudan, patients often present with a facial rash consisting of small papules resembling measles that spreads to involve other parts of the body. This syndrome may heal spontaneously, but relapse is common. Established disease is generally difficult to treat.
    • No systemic symptoms are evident.
  • Mucocutaneous leishmaniasis
    • The initial skin lesion is often notable for its prolonged healing time and large size. In most cases, a healed scar can be identified based on careful examination. Months to years after the initial infection, patients may have rhinorrhea, epistaxis, and nasal congestion.
    • Examination reveals excessive tissue obstructing the nares, septal granulation, and perforation. Nose cartilage may be involved, giving rise to external changes known as parrot's beak or camel's nose.
    • The palate, uvula, lips, pharynx, and larynx may exhibit granulation, erosion, and ulceration with sparing of the bony structures. Hoarseness may be a sign of laryngeal involvement.
    • Other physical signs include gingivitis, periodontitis, and localized lymphadenopathy. In time, disfiguring facial deformities may occur, requiring plastic surgery. Optical and genital mucosal involvement have been reported in severe cases.
    • Death occurs from suffocation secondary to airway obstruction, respiratory infection, and aspiration pneumonia.
  • Visceral leishmaniasis
    • In endemic areas, the diagnosis often is made based on the history and physical examination. Patients present with recurrent high fevers, wasting, anorexia, night sweats, diarrhea, and malaise. Physical examination reveals a patient who is thin and cachetic with abdominal distension and protuberance due to massive hepatosplenomegaly. The liver and spleen are usually soft and easily palpated, and the patient may experience intermittent abdominal distress. Epistaxis and petechiae from severe thrombocytopenia may occur. Lymphadenopathy and hair changes, such as alopecia and eyelash elongation, may be present. Characteristic patchy darkening of the face and trunk has been described. Although uncommon, xerosis may occur. Complications of visceral leishmaniasis include amyloidosis, glomerulonephritis, and cirrhosis.
    • In patients with HIV and visceral leishmaniasis co-infection, other atypical findings include gastrointestinal and respiratory involvement. Patients have presented with gastrointestinal ulcerations, masses, pleural effusions, and odynophagia. Spread outside of the reticuloendothelial system appears more common.
  • Viscerotropic leishmaniasis
    • Patients have presented with an array of symptoms months to years after infection, including fever, rigors, fatigue, malaise, nonproductive cough, intermittent diarrhea, headache, arthralgias, myalgias, nausea, adenopathy, transient hepatosplenomegaly, and abdominal pain.
    • This disease does not appear to progress to visceral leishmaniasis.

Causes

  • Localized cutaneous leishmaniasis
    • Old World
      • L donovan i - China, India, Bangladesh, Sudan
      • L tropica - Middle East, China, India, Mediterranean
      • L major - Middle East, Africa, India, Asia
      • L aethiopica - Ethiopia, Kenya, Namibia
      • Leishmania infantum - Asia, Africa, Europe
    • New World
      • Leishmania leishmania mexicana - Central and South America, North America
      • L leishmania amazonensis - Dominican Republic, Central America, South America
      • L leishmania venezuelensis - Venezuela
      • L viannia braziliensis - Central America, South America
      • L viannia guyanensis - Guyana, French Guyana, Surinam, Brazil
      • L viannia panamensis - Costa Rica, Panama, Colombia, Ecuador
      • L viannia peruviana - Peru, Argentina
      • Leishmania donovani chagasi - Texas, Caribbean, Central America, South America
  • Diffuse cutaneous leishmaniasis
    • Old World
      • L aethiopica - Ethiopia, Kenya, Namibia
    • New World
      • L leishmania mexicana - Central, South America, North America
      • L leishmania amazonensis - Dominican Republic, Central America, South America
  • Leishmaniasis recidivans
    • Old World
      • L tropica - Middle East, China, India, Mediterranean
    • New World
      • L viannia braziliensis - Central America, South America
  • Post-kala-azar leishmaniasis
    • Old World
      • L donovani - China, India, Bangladesh
      • L infantum - Asia, Africa, Europe
    • New World
      • L donovani chagasi - Central America, South America
  • Mucocutaneous leishmaniasis
    • Old World
      • L aethiopica - Ethiopia, Kenya, Namibia
    • New World
      • L viannia braziliensis - Central America, South America
      • L viannia panamensis - Central America, South America
      • L viannia guyanensis - Guyana, French Guyana, Surinam, Brazil
      • Less often seen with L leishmania mexicana - Central America, South America, North America
      • Less often seen with L leishmania amazonensis - Brazil, Panama
  • Visceral leishmaniasis
    • Old World
      • L donovani - China, India, Bangladesh, Sudan
      • L infantum - Asia, Africa, Europe
    • New World
      • L donovani chagasi - Central America, South America
  • Viscerotropic leishmaniasis
    • Old World
      • L tropica - Middle East

More on Leishmaniasis

Overview: Leishmaniasis
Differential Diagnoses & Workup: Leishmaniasis
Treatment & Medication: Leishmaniasis
Follow-up: Leishmaniasis
Multimedia: Leishmaniasis
References
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Further Reading

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Keywords

leishmaniasis, cutaneous leishmaniasis, mucosal leishmaniasis, visceral leishmaniasis, dermal leishmaniasis, post-kala-azar dermal leishmaniasis, leishmaniasis recidivans, mucocutaneous leishmaniasis, viscerotropic leishmaniasis, black fever, kala-azar, forest yaws, Aleppo evil, Baghdad sore, Biskra button, Chiclero ulcer, Delhi boil, Oriental sore, Rose of Jericho, Uta, dumdum fever, Assam fever, infantile splenomegaly

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Contributor Information and Disclosures

Author

Craig G Stark, MD, Regional Medical Director, Northern Europe and Russia Regions, Tricare Medical Director for Western Hemisphere, International SOS Assistance UK, Ltd
Craig G Stark, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, International Society of Travel Medicine, Phi Beta Kappa, and Society of US Army Flight Surgeons
Disclosure: Nothing to disclose.

Medical Editor

Pranatharthi Haran Chandrasekar, MD, Director of Infectious Disease Fellowship, Professor, Department of Internal Medicine, Harper Hospital, Wayne State University School of Medicine
Pranatharthi Haran Chandrasekar, MD is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Thomas M Kerkering, MD, Chief of Infectious Diseases, Virginia Tech, Carilion School of Medicine, Roanoke, Virginia
Thomas M Kerkering, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Public Health Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Medical Society of Virginia, and Wilderness Medical Society
Disclosure: Nothing to disclose.

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD, Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital
Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America
Disclosure: Nothing to disclose.

 
 
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