AUTHOR AND EDITOR INFORMATION

Section 1 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

INTRODUCTION

Section 2 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Background

Leishmaniasis is a disease caused by the protozoa of the Leishmania species, which is transmitted by the bite of a female sandfly. While several ways to classify leishmaniasis (eg, by geography or taxonomy) are available, clinically, it can present itself in various ways, and is more easily classified as cutaneous, mucocutaneous, and visceral leishmaniasis.

The typical lesions of cutaneous leishmaniasis were described as early as 900 BC and have been referred to as the "Balkan sore" in the Balkans, the "Delhi boil" in India, the "Baghdad boil" in Iraq, and "saldana" in Afghanistan.

Pathophysiology

Leishmaniae spend part of their life cycle in the gut of the sandfly, but their life cycle is completed in a vertebrate host.

Within the sandfly gut, the protozoa are carried as extracellular promastigotes. Over the course of 4-25 days, these parasites multiply in the gut and migrate toward the pharynx. As the leishmaniae replicate, they create a blockage in the fly's esophagus. The feeding sandfly then clears out its esophagus by expelling leishmaniae into the skin of the host, from where they pass into the blood and tissues of the human host. Promastigotes are phagocytosed into macrophages of the reticuloendothelial system, where they shed their flagella and become amastigotes that multiply by binary fission. When the infected cells rupture, the infection spreads to other macrophages and is carried throughout the body. Temperature is an important factor that helps determine the localization of leishmanial lesions. Species causing visceral leishmaniasis are able to grow at core temperatures, while those responsible for cutaneous leishmaniasis grow best at lower temperatures.

Although the Leishmania species differ clinically and biologically, their characteristics overlap and each clinical syndrome can be produced by multiple species of Leishmania.

In cutaneous leishmaniasis, the hallmark of the disease is skin lesions, which can spontaneously heal in 2-10 months.

In mucocutaneous leishmaniasis, mucosal ulcerations usually develop by metastasis from disseminated protozoa rather than by local spread. Secondary infection plays a prominent role in the size and persistence of ulcers. Ulcer progression is slow and steady.

Typically, visceral leishmaniasis incubates for weeks to months before becoming clinically apparent. The disease can be subacute, acute, or chronic, and can manifest in patients who are immunocompromised years after they have left endemic regions.

Frequency

United States

Leishmaniasis is rare in the United States but has been reported in areas bordering Mexico such as rural southern Texas. Most of the cases found in the United States are acquired elsewhere such as in travelers to Latin America. More recently, more than 500 cases of leishmaniasis were diagnosed over an 18-month period in soldiers returning to the United States from the Middle East, especially from Iraq. A large portion of these was identified as cutaneous leishmaniasis.

International

The Centers for Disease Control and Prevention (CDC) estimates that approximately 1.5 million new cases of cutaneous leishmaniasis and 500,000 cases of visceral leishmaniasis occur worldwide each year. Mucocutaneous leishmaniasis is less common. The prevalence of the disease is increasing, with estimates of 12 million people currently infected worldwide. Once thought of only as a disease affecting rural areas, the disease remains common in the face of increasing urbanization.

Incidence is highest in tropical and subtropical regions where conditions are favorable for sandflies. Most cases of cutaneous leishmaniasis are seen in Afghanistan, Brazil, Iran, Iraq, Peru, and Saudi Arabia, while visceral leishmaniasis is most common in Bangladesh, Brazil, India, Nepal, and Sudan.

Leishmaniasis is found in some parts of 88 countries within Central America, South America, Africa, India, the Middle East, Asia, southern Europe, and the Mediterranean.

Australia and the South Pacific are not considered regions where leishmaniasis is present as an endemic illness.

Mortality/Morbidity

Poor nutrition, infection, and other stresses predispose patients to increased morbidity and mortality rates. Conditions such as complex emergencies, mass migration, and famine accelerate the development of the disease. Leishmaniasis is responsible for an estimated more than 80,000 deaths annually.

Co-infection with HIV is also increasingly recognized as an emerging threat. HIV has been implicated in cases of visceral leishmaniasis in areas previously untouched by this form of the disease. For example, visceral leishmaniasis has appeared in southern Europe among intravenous drug users.

• Untreated cutaneous leishmaniasis can progress to disseminated mucocutaneous leishmaniasis, and death can occur from secondary infection.
• Visceral leishmaniasis is progressive. Mortality rates in untreated cases range from 75-95% or as high as 100% within 2 years in developing countries.
• Of great importance is the social burden placed by the morbidity of the disease, which can cause severe deformities and disfigurement and lead to social isolation.

Sex

Males are more commonly infected than females, most likely because of their increased exposure to sandflies. Visceral leishmaniasis, in particular, has been shown to be twice as common in males than in females.

Age

A fatal type of visceral leishmaniasis, which is found along the Mediterranean, specifically affects infants. Although occurrence is proportional to sandfly exposure, children younger than 15 years represent a large proportion of cases in endemic areas.

• Untreated visceral leishmaniasis in a pregnant mother can also have consequences on the fetus or result in congenital visceral leishmaniasis.
• Certain types of visceral leishmaniasis affect certain pediatric age groups more than others (eg, visceral leishmaniasis in the Mediterranean Basin caused by Leishmania infantum mainly affects children aged 1-4 y).

CLINICAL

Section 3 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

History

In some endemic areas, natives have recognized that immunity occurs as a natural course of the disease. Some cultures deliberately inoculate their children on a part of the body that is not usually exposed to avoid later development of a disfiguring scar on an exposed part of the body.

• Cutaneous leishmaniasis
• • The broad spectrum of clinical manifestations of cutaneous leishmaniasis is often compared with that of leprosy. Cutaneous leishmaniasis can be simple or diffuse.
  • Different species, as well as host factors, can also affect the clinical picture, where some species cause "wet" ulcers and others "dry" ulcers.
  • After the bite of an infected sandfly, the incubation period is usually several weeks after inoculation, but this incubation period is variable. Initial lesions can appear immediately after a bite, or the incubation period may last for several months. These lesions are usually painless.
  • Skin trauma can result in activation of seemingly latent cutaneous infection long after the initial bite.
  • Over a period of weeks to years, some lesions may resolve spontaneously without pharmacotherapy.
• Mucocutaneous leishmaniasis
• • The incubation period is from 1-3 months. Mucocutaneous leishmaniasis can be the primary manifestation of the disease, but the primary lesions may also be limited to cutaneous manifestations, with mucosal lesions appearing only later in the course of disease when untreated cutaneous lesions progress to involve the oral and nasal surfaces. Cases in which the time between the primary lesion and the appearance of mucosal involvement is up to 2 decades have been reported.
  • Initial symptoms related to mucosal lesions may include nasal obstruction and bleeding.
  • Mucosal lesions become painful gradually and can become sites of infection, sometimes leading to sepsis.
• Visceral leishmaniasis
• • Kala azar is the Indian name for visceral leishmaniasis. The term means "black disease," which is a reference to the characteristic darkening of the skin that is seen in patients with the disease.
  • Many subclinical cases occur and go unrecognized for each clinically recognized case.
  • Malnutrition has been shown to contribute to the development of clinical disease.
  • Like cutaneous leishmaniasis, visceral leishmaniasis can take different forms ranging from asymptomatic or self-resolving disease to fulminant disease.
  • Onset can be insidious or sudden.
  • In endemic areas, kala azar may be suspected in a patient with persistent, irregular, or remittent fever; leukopenia; and splenomegaly. Other accompanying symptoms may be lymphadenopathy and weight loss.
  • Fever can be continuous, intermittent, or remittent, and it can recur at irregular intervals.

Physical

• Cutaneous leishmaniasis
• • Systemic signs usually are absent.
  • Initially, the lesion is a small, red papule up to 2 cm in diameter. Over several weeks, the papule becomes darker and will crust in the center, eventually ulcerating to present a typical appearance of an ulcer with raised edges and surrounding dusky red skin. The ulcers can be moist or open with seropurulent exudate or dry with a crusted scab. After about 3-6 months, the ulcers heal, leaving a raised border.
  • Sores usually are found on exposed areas of skin, especially the extremities and face.
  • Regional adenopathy, satellite lesions, and subcutaneous nodules can be present.
  • Untreated sores can leave depigmented retracted scars.
• Mucocutaneous leishmaniasis
• • Cutaneous lesions can be single or multiple.
  • Secondary mucosal lesions often develop after the primary lesion has healed.
  • Mucosal lesions can progress to involve the entire nasal mucosa and the hard and soft palates. Without treatment, the entire nasal mucosa and palates become deformed with ulceration and erosion of the nasal septum, lips, and palate. The disease attacks cartilaginous areas but usually spares bony structures, and it can leave extreme disfigurement.
  • Signs include gingival edema, periodontitis, and adenopathy.
• Visceral leishmaniasis
• • Bouts of fever occur.
  • Hepatosplenomegaly occurs secondary to compensatory production of phagocytic blood cells.
  • Wasting and weakness are observed.
  • Darkening of the skin is characteristic (thus, the name kala azar or black fever).
  • Diarrhea may occur.
  • Lymphadenopathy is often present.
  • In visceral leishmaniasis, patients may die of hemorrhage (secondary to infiltration of the hematopoietic system), severe anemia, secondary bacterial infections of mucous membranes, bacterial pneumonia, septicemia, tuberculosis, dysentery, or measles.

Causes

• Cutaneous leishmaniasis
• • Americas - Leishmania tropica mexicana, Leishmania braziliensis, and Leishmania amazonensis
  • Old World - Leishmania tropica, Leishmania major, L infantum, and Leishmania aethiopica
• Mucocutaneous leishmaniasis
• • Americas - L braziliensis
  • Old World - L aethiopica
• Visceral leishmaniasis
• • India, Kenya - Leishmania donovani
  • South Europe and North Africa - L infantum
  • Americas - Leishmania chagasi
• Risk factors
• • Children are at greater risk than adults in endemic areas.
  • Malnutrition has been shown to contribute to the development of disease.
  • Persons with AIDS are at 100-1000 times greater risk of developing visceral leishmaniasis in certain areas.
  • Incomplete therapy of initial disease is a risk factor for recurrence of leishmaniasis.
  • Some studies have shown protection against cutaneous leishmaniasis with vaccination of killed Leishmania promastigotes and live bacillus Calmette-Guérin (BCG). However, this does not seem to be protective against visceral leishmaniasis.
  • Of note, the bite of one infected sandfly is sufficient to cause the disease, since a sandfly can egest more than 1000 parasites per bite.

DIFFERENTIALS

Section 4 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Other Problems to be Considered

Expanded differential diagnosis for cutaneous leishmaniasis includes syphilis and leprosy as well as sporotrichosis, blastomycosis, chromomycosis, lobomycosis, cutaneous tuberculosis, atypical mycobacterial infection, sarcoidosis, lupus vulgaris, yaws, and neoplasms.

Expanded differential diagnosis for mucocutaneous leishmaniasis includes syphilis and leprosy, blastomycosis, paracoccidioidomycosis, polymorphic reticulosis, Wegener granulomatosis, lymphoma, histoplasmosis, tuberculosis, nasopharyngeal carcinoma, and other destructive lesions.

Expanded differential diagnosis for visceral leishmaniasis includes malaria, syphilis, tuberculosis, systemic lupus erythematosus, typhoid fever, brucellosis, histoplasmosis, tropical splenomegaly syndrome, schistosomiasis, leukemia, and lymphoma. The differential for post kala azar dermal leishmaniasis includes syphilis, yaws, and leprosy.

WORKUP

Section 5 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Lab Studies

• Cutaneous leishmaniasis
• • Diagnosis usually is based on the appearance of the lesion.
  • In more than 70% of cutaneous leishmaniasis cases, microscopy of the parasite in Giemsa stains or histological section can reveal the parasite and should be attempted first. Culture of the organisms is an option but is unreliable because organisms are difficult to isolate from the lesion, especially as the lesion becomes older. The organism grows on Schneider Drosophila medium (positive results in 1 wk) and Novy-MacNeal-Nicolle (NNN) medium (media available from the CDC). Cultures can produce positive results in 1-3 weeks.
  • The leishmaniasis skin test (Montenegro test) produces positive results 3 months after the appearance of lesions. The Montenegro test is performed by injecting killed promastigotes intradermally and examining the skin 48 hours later to see if a delayed-type hypersensitivity response has formed. A positive result is defined as induration of 5 mm or more. The two main drawbacks are that acute infections cannot be identified (in endemic regions, more than 70% of the population will test positive) since it remains positive for life and those who are immunosuppressed may not mount a response.
  • Serologic tests such as isoenzyme or monoclonal antibody analysis are not well established. However, polymerase chain reaction (PCR) is being used more frequently and is more accurate in determining new-onset leishmaniasis than serum tests.
• Mucocutaneous leishmaniasis
• • Diagnosis preferably is made by culture of the organism, but organisms are often scant.
  • On biopsy, a nonspecific granulomatous reaction often is observed. Giemsa stain may show the organisms.
  • Results from the leishmanin skin test are positive after 2-3 months of infection. No skin tests currently are approved for use in the United States.
  • Serologic tests are available in some centers and, as in the cutaneous form, PCR is becoming more common as a method of diagnosing the disease.
  • Because the organisms often are scarce, the diagnosis often is epidemiologic (travel to endemic area, clinical picture coupled with laboratory data).
• Visceral leishmaniasis
• • Definitive diagnosis is made by observing the parasite (more specifically, amastigotes in tissue) on stained Giemsa smears or by observing the culture of bone marrow, splenic, hepatic, or lymph node aspirates. The most sensitive method is splenic puncture, although iatrogenic complications can be serious.
  • Cultures are grown on NNN medium (media available from the CDC), a biphasic medium, or liquid media with fetal calf serum (eg, Schneider Drosophila medium). Culture grows for 1-3 weeks.
  • Serologic testing is useful with the indirect fluorescent antibody test (IFAT), which is 80-100% sensitive in patients with visceral leishmaniasis who are not infected with HIV. IFAT may cross-react in patients who have leprosy, tuberculosis, malaria, schistosomiasis, Chagas disease, and African trypanosomiasis.
  • An enzyme-linked immunosorbent assay (ELISA) is now available and can be combined with IFAT and/or Western blot to increase sensitivity and specificity. If PCR is available, it is highly sensitive (between 92% and 99%) and specific (100%).
  • Obtain a complete blood count. Bone marrow infiltration may cause anemia, thrombocytopenia, and leukopenia with a relative monocytosis and lymphocytosis.
  • Perform liver function tests (LFTs).
  • Run a coagulation panel.

Other Tests

• Of note, very few of these diagnostic tests are available in developing countries, where most diagnoses are made clinically.
• Monoclonal antibodies (MoAb) or hybridization of tissue touch blots with labeled kinetoplast DNA probes are used for identification of different strains of Leishmania.
• An immunochromatographic strip test exists for rapid detection of antibodies to Leishmania antigen K39.
• New research is being performed using PCR to detect clinically occult visceral leishmaniasis.

TREATMENT

Section 6 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Emergency Department Care

• Cutaneous leishmaniasis
• • Treatment of cutaneous leishmaniasis differs according to the etiology and geographic location of the infection. For certain types of cutaneous leishmaniasis where the potential for mucosal spread is low, topical paromycin can be used.
  • For more invasive lesions (eg, those failing to respond to topical treatment; metastatic spread to the lymph nodes; or large, disfiguring, and multiple skin lesions, especially those on the face, near mucosal surfaces, or near joints), sodium stibogluconate, meglumine antimonate, or pentamidine can be used.
• Mucosal leishmaniasis
• • Pentavalent antimony for a course of 4 weeks has been recommended.
  • Amphotericin B deoxycholate may be first-line therapy for advanced mucosal disease.
• Visceral leishmaniasis
• • Be alert for complications related to reticuloendothelial system failure. Patients may have bleeding or neutropenia leading to infectious conditions such as pneumonia or diarrhea. Transfusions may be necessary for severe bleeding or anemia. Antibiotics are indicated to treat intercurrent infectious conditions.
  • Outside of India, treatment with a pentavalent antimonial compound usually is effective. The use of an alternative parenteral agent should be considered even for first-line therapy in areas where resistance to pentavalent antimony therapy is prevalent, as it is in India, or if nonantimonial therapy would be advantageous for other reasons (eg, toxicity profile, duration of therapy).
  • A major advance has been the advent of liposomal formulations of amphotericin B, in which various alternative lipids have replaced deoxycholate. These formulations, which passively target amphotericin to macrophage-rich organs, are much more costly than conventional amphotericin B (making them cost-prohibitive in poor countries) but are associated with less nephrotoxicity and can be given in considerably shorter courses.
  • Other parenteral alternatives that have merit include amphotericin B (not only in deoxycholate form but also in liposomal forms) and have generally replaced pentamidine. Miltefosine, a chemotherapeutic agent, is the first extremely effective oral agent for visceral leishmaniasis but is not currently available in the United States.

Consultations

• Infectious disease consultation can offer the most effective antiprotozoal regimen.
• Although cutaneous leishmaniasis can heal on its own, early lesions can also be treated with physical measures, such as local cryotherapy, heat therapy, electrocoagulation, or surgical removal.
• Surgical consultation may be necessary for adjunctive splenectomy.

MEDICATION

Section 7 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Antiparasitic pentavalent antimonials, such as sodium stibogluconate (Pentostam) or meglumine antimoniate, are the mainstays of therapy. Until recently, sodium stibogluconate was the only recommended treatment in the United States and was available only through the CDC, but amphotericin B in its liposomal form (as opposed to amphotericin B deoxycholate) has recently been approved and is now considered to be the drug of choice for visceral leishmaniasis because of its shorter course and lower toxicity.

Cost issues prevent the use of liposomal drugs in most countries, where the mainstay of treatment is still prolonged intravenous treatment with antimonials, despite ever-increasing patterns of resistance and an increasing incidence of treatment failures. Alternative treatments, such as amphotericin B, should be used when resistance is endemic or when other reasons for using an alternative parenteral exist (eg, lower toxicity profile).

In terms of oral medications, miltefosine is the sole agent that has been shown to be effective. Miltefosine is currently approved in India for visceral leishmaniasis, but it is not yet available in the United States.

Drug Category: Antiparasitic

Therapy must cover all likely pathogens in the context of the clinical setting.

Drug Name	Amphotericin B (AmBisome)
Description	An evolving second-line drug to be used after failure of antimonials to treat mucocutaneous and visceral leishmaniasis. New lipid-associated formulations are taken up well by the reticuloendothelial system and poorly by the kidney. These formulations target the cells that host the parasite and have decreased nephrotoxicity.
Adult Dose	For cutaneous and mucosal leishmaniasis, no standard dose exists; in India, conventional amphotericin B deoxycholate is given as slow infusion (4-6 h) of 1 mg/kg qd for 20 d; alternatively, 0.5-1 mg/kg/d or qod intravenously for up to 8 wk can be used For visceral leishmaniasis, dose of amphotericin liposomal is 3 mg/kg/d on days 1-5, 14, and 21, which may be repeated, or for immunoincompetent persons, 4 mg/kg/d on days 1-5, 10, 17, 24, 31, and 38 (Recent studies show that similar results can be obtained with lower doses and shorter course: cumulative doses of 3.75 or 7.5 mg/kg given in 5 divided doses over 5 d)
Pediatric Dose	1 mg/kg IV qod
Contraindications	Documented hypersensitivity
Interactions	Antineoplastic agents may enhance the potential of amphotericin B for renal toxicity, bronchospasm, and hypotension; corticosteroids, digitalis, and thiazides may potentiate hypokalemia; risk of renal toxicity is increased with cyclosporine; concomitant use of nephrotoxic agents, such as aminoglycosides, can cause synergistic nephrotoxicity
Pregnancy	B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions	May cause fever, chills, nausea, vomiting, liver dysfunction, hypotension, rash, dyspnea, pruritus, and adrenal suppression Neutropenic patients receiving amphotericin B and leukocyte transfusions may experience pulmonary reactions characterized by hypoxemia, acute dyspnea, and interstitial infiltrates

Drug Category: Antiprotozoal

Protozoal infections occur throughout the world and are a major cause of morbidity and mortality in some regions. Immunocompromised patients are especially at risk. Primary immune deficiency is rare; whereas, secondary deficiency is more common. Immunosuppressive therapy, cancer and its treatment, HIV infection, and splenectomy all may increase vulnerability to infection. Infectious risk is proportional to neutropenia duration and severity. Protozoal infections are typically more severe in immunocompromised patients than in immunocompetent patients.

Drug Category: Antineoplastic

These agents inhibit cell growth and proliferation.

FOLLOW-UP

Section 8 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Further Inpatient Care

• If the case is not advanced with serious GI, hematologic, or infectious issues, care can be accomplished on an outpatient basis; however, daily visits to a physician for medication may be required.

Further Outpatient Care

• Response to treatment varies.
• Nonspecific measures, such as local heat and cleanliness, contribute to the spontaneous healing of the ulcers.
• Progression and resolution of the disease should be monitored carefully.
• Wound care is important.

In/Out Patient Meds

• The antimony sodium stibogluconate (known as Pentostam in the United States) is the current antiparasitic treatment of choice in the United States, although miltefosine holds a great deal of promise and is available in India.
• Antistaphylococcal antibiotic may be needed for secondary bacterial infection.
• Fluconazole has also been shown to have some effect against cutaneous leishmaniasis.

Deterrence/Prevention

• Protective immunity following medical treatment for infection is 97-98% effective for disease caused by the same species of Leishmania.
• Deliberate scarification (ie, making numerous superficial incisions) of the extremities with material from human lesions was once practiced to prevent facial scarring that might result from a later natural infection.
• The treatment of infected persons and elimination of diseased reservoir vertebrates can reduce the source of infection.
• Sandfly control (fine-mesh bed netting must be used, because sandflies are small enough to pass through ordinary mosquito netting) impregnated with an insecticide such as permethrin or deltamethrin, and use of insect repellent can prevent disease.
• Because leishmaniasis can be transmitted through blood, patients who have been infected should not donate blood or organs.
• General precautions, such as protective clothing, and minimizing outdoor exposures at peak times (eg, dusk) should also be used.
• Current efforts are being made by organizations such as the Tropical Disease Research branch of the World Health Organization and other vaccine initiatives to develop second-generation vaccines against leishmaniasis.

Complications

• Secondary bacterial infection
• Disfigurement of nose, lips, and palate
• Bleeding
• Splenic rupture
• Edema, cachexia, and hyperpigmentation in late stages
• Metastatic lesions in the nasopharynx with tissue destruction

Prognosis

• Prognosis depends on nutritional and overall immune status of the host and on the precise species of infection.
• With early treatment, the cure rate is higher than 90%.
• The mortality rate is 15-25% in untreated cases.
• If untreated, death occurs in 3-20 months.

Patient Education

• Education about sandfly control can reduce incidence of disease.

MISCELLANEOUS

Section 9 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Special Concerns

• Treatment of leishmaniasis requires expertise.
• The specific species should be identified, if possible.
• Pentostam should be used according to CDC protocol; if marked variation from the protocol is being considered, CDC experts should be consulted.

ACKNOWLEDGMENTS

Section 10 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, N Ewen Wang, MD, to the development and writing of this article.

MULTIMEDIA

Section 11 of 12  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

Media file 1:  Leishmaniasis. Photo courtesy of Robert Norris, MD, Stanford University Medical Center.
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Media file 2:  Leishmaniasis. Photo courtesy of Robert Norris, MD, Stanford University Medical Center.
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Media file 3:  Leishmaniasis. Image courtesy of the CDC Public Health Image Library.
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Media file 4:  Leishmaniasis. Image courtesy of the CDC Public Health Image Library.
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REFERENCES

Section 12 of 12

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Acknowledgments
• Multimedia
• References

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• Olliaro PL, Guerin PJ, Gerstl S, Haaskjold AA, Rottingen JA, Sundar S. Treatment options for visceral leishmaniasis: a systematic review of clinical studies done in India, 1980-2004. Lancet Infect Dis. Dec 2005;5(12):763-74. [Medline].
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Article Last Updated: Mar 31, 2008