eMedicine Specialties > Infectious Diseases > Parasitic Infections

Leishmaniasis: Treatment & Medication

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

Treatment

Medical Care

The decision to treat medically depends on various factors. Given the associated morbidity, always treat visceral, mucocutaneous, and severe forms of cutaneous leishmaniasis. Given its potential to progress into mucocutaneous leishmaniasis, definitively treat New World cutaneous leishmaniasis caused by members of the Leishmania viannia subgenus. New World cutaneous leishmaniasis due to Leishmania mexicana is not associated with mucocutaneous leishmaniasis and may not require systemic treatment. Cutaneous leishmaniasis acquired in the Old World tends to resolve spontaneously, but patients with this infection should receive treatment if the lesions are disfiguring, painful, infected, over joints, or slow to heal.

  • Therapies available in the United States are limited. The mainstays are the pentavalent antimony compounds first introduced in the 1930s. The 2 available preparations, sodium stibogluconate (Pentostam), produced in Great Britain, and meglumine antimonate (Glucantime), produced in France, have similar efficacy. Depending on the species and region, cure rates of 80-100% have generally been reported.
    • Sodium stibogluconate is available from the CDC as an investigational drug. Military personnel may receive sodium stibogluconate from the Walter Reed Army Medical Center. A 2002 randomized, double-blind, placebo-controlled study of intravenous sodium stibogluconate treatment in cutaneous leishmaniasis validated the efficacy of a 10-day course, with a significantly reduced side-effect profile over the standard 20-day course.8 This study included mostly patients infected with Leishmania viannia panamensis, and the results may not be applicable to infections caused by other species of Leishmania.
    • One study in Guatemala that involved a combination of intravenous stibogluconate and allopurinol showed improved efficacy against cutaneous L viannia panamensis infections compared with stibogluconate alone.9 However, this effect was not reproduced in the treatment of mucosal leishmaniasis. In many regions of the world, direct intralesional injection of pentavalent antimony is used to treat cutaneous disease, although this can be painful and is technically difficult.
  • Other therapies include amphotericin B (AmBisome) and pentamidine.
    • Amphotericin B is effective against pentavalent antimony-resistant mucocutaneous disease and visceral leishmaniasis. Its use is limited because of its toxic adverse effect profile. The newer lipid preparations are better tolerated and are being used as first-line therapy against visceral leishmaniasis, but the response with cutaneous disease has been mixed. AmBisome is the only US Food and Drug Administration (FDA)–approved drug in the United States available for the treatment of visceral leishmaniasis. AmBisome is also useful to treat antimonial-resistant visceral disease. Single-dose treatment with AmBisome has shown a 91% cure rate in India but is still considered too expensive for general treatment.10
    • Intramuscular pentamidine is effective against visceral leishmaniasis but is associated with persistent diabetes mellitus and disease recurrence. Pentamidine is the drug of choice to treat L viannia guyanensis in French Guyana, where antimonial resistance is prevalent.11
  • Orally administered ketoconazole, itraconazole, fluconazole, allopurinol, and dapsone have been examined internationally, but none is as effective as the pentavalent antimony compounds. However, given their minimal adverse effect profile, these agents may be useful in accelerating the cure in patients with cutaneous leishmaniasis that does not progress to mucosal disease and tends to self-resolve.
    • Dapsone was shown to be effective in most cases of Indian cutaneous leishmaniasis after 6 weeks of therapy.12
    • Ketoconazole has a variable cure rate for New World cutaneous leishmaniasis, depending on the species. One study showed a 89% cure rate for individuals infected with L mexicana compared with 30% for L viannia braziliensis.9 Efficacy against L viannia panamensis in Panama and L major in Iran and Israel has been demonstrated, while no effect was noted against L tropica in India and Turkey.13
    • Fluconazole was effective against 79% of patients infected with uncomplicated cutaneous leishmaniasis caused by L major in Saudi Arabia.14
  • The recent discovery of an affordable, orally administered, and well-tolerated therapy for visceral leishmaniasis has made mass treatment in the developing world a reality. Miltefosine is a phosphocholine analogue originally developed as an antineoplastic agent that interacts with membrane synthesis and signal production. 
    • Phase 2 and 3 drug studies in India showed orally administered miltefosine was 95-97% effective in curing patients with Indian visceral leishmaniasis.15 Oral treatment of 2.5 mg/kg/d lasting 4-6 weeks was generally well-tolerated.
    • Common adverse effects included gastrointestinal distress and elevated creatinine levels, which resolved with cessation of therapy.
    • Treatment of New World cutaneous leishmaniasis has met with variable levels of success. In Columbia, miltefosine treatment cured 91% of infections involving L viannia panamensis, similar to antimony therapy, while curing only 53% of infections involving L viannia braziliensis in Guatemala, well below historic antimony cure rates. However, another study in Bolivia showed oral miltefosine given for 28 days yielded an 82% cure rate compared with 88% for intramuscularly administered meglumine antimonate against L viannia braziliensis.16 The tolerance for oral miltefosine was so superior to intramuscularly administered meglumine antimonate that the researchers were unable to convince local treating physicians to continue treating the control group with the intramuscular therapy. Research is ongoing to determine which regional strains of New World cutaneous leishmaniasis will respond to oral miltefosine.
    • The protective effect against subsequent mucocutaneous disease is unknown at this time. One study showed a 75% one-year cure rate among Bolivian patients who presented with mild mucocutaneous leishmaniasis. The particular strain of L viannia braziliensis affected an area known to have antimonial resistance. One-year cure rates were lower among patients with more severe disease. Long-term studies will be required to determine if a definitive cure was achieved.
    • Miltefosine did not prevent visceral relapse in patients co-infected with HIV but remained effective with retreatment and over prolonged periods of therapy.17
  • Sitamaquine is another oral therapy in the research pipeline. Originally discovered by the Walter Reed Army Research Institute, this 8-aminoquinolone is currently undergoing phase 3 trials in Kenya and India.
  • Topical paromomycin has been shown to be effective against cutaneous leishmaniasis caused by L major and L leishmania mexicana.
    • Because these species do not tend to cause visceral or mucocutaneous disease, this preparation can spare the patient systemic adverse effects associated with parenteral medications.
    • An ointment that contains 15% paromomycin and 12% methylbenzethonium chloride showed an even higher cure rate of 87% after 20 days of topical treatment for cutaneous L major.18 Unfortunately, the performance of this cream with infections caused by L tropica has been disappointing. Although not commercially available in the United States, this cream may be available from compounding pharmacies and is currently being used in Israel for the treatment of L major lesions.
    • Topical therapy is not recommended for treatment of New World species that are known to progress to mucocutaneous disease.
  • Because Leishmania species are temperature-sensitive, local treatment with heat or cold provides an alternative to pharmaceutical therapy in some cases.
    • Cryotherapy can be used on small, uncomplicated Old World lesions. A 15- to 20-second freeze-thaw-refreeze cycle repeated as needed over 1-2 weeks was sufficient to cure most cases of uncomplicated L tropica and L major infections.
    • In 2003, the FDA approved the ThermoMed device (ThermoSurgery Technologies, Inc) for the treatment of cutaneous leishmaniasis. This device heats the skin through radiofrequency waves directed to a specified area and depth. A recent study conducted in Afghanistan involving cutaneous disease caused by L tropica demonstrated a cure rate of 69% at 100 days after treatment.19 Although the lesions treated in this study were small, the initial results look promising. Further studies may demonstrate this to be a useful therapy for mild disease.

Surgical Care

  • Severe mucocutaneous leishmaniasis may require orofacial surgery.
  • Surgical removal is not recommended for cutaneous disease because of the potential for recurrence at the excision site.
  • Surgery may exacerbate quiescent disease.

Consultations

  • Given the importance of identifying the specific species, consider consulting an infectious disease specialist or a dermatologist for diagnosis and optimal therapy.

Diet

  • Malnutrition has been shown to increase morbidity and mortality in mucocutaneous and visceral disease. Patients should receive nutritious, well-balanced meals.

Medication

The goals of pharmacotherapy are to eradicate the infection, to reduce morbidity, and to prevent complications, recurrence, and the development of mucocutaneous forms of the disease.

Antiprotozoan

Parasite biochemical pathways are sufficiently different from the human host to allow selective interference by chemotherapeutic agents in relatively small doses.


Sodium stibogluconate (Pentostam)

DOC for the treatment of cutaneous and mucocutaneous leishmaniasis in the United States. Sodium stibogluconate is also effective against visceral leishmaniasis and is often the first-line treatment outside the United States. Not FDA approved but is currently available from the CDC as an investigational new drug.
May be administered IV or IM. Intravenous use is preferred because large volumes are required. Available at 100 mg/mL. Dilute each mL in 10 mL of 5% dextrose water and administer over 15 min to prevent thrombophlebitis. Children often tolerate adverse effects better and may not require ECG monitoring.

Adult

Cutaneous leishmaniasis: 20 mg/kg/d IV for 10-20 d
Mucocutaneous leishmaniasis: 20 mg/kg/d IV for 28 d
Visceral leishmaniasis: 20 mg/kg/d IV for 28 d (If L donovani is suspected in India, consider 40 d of treatment)
Cure rate >90%; currently, no upper limit of daily dosing

Pediatric

Administer as in adults; in small children, increased dosing per kilogram may be required for effective therapy

None reported; avoid medications that prolong the QT interval or adversely affect pancreas and liver

Documented hypersensitivity; baseline prolongation of QT interval

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Prior to therapy, perform baseline ECG, serum electrolytes, LFTs, amylase, lipase, CBC, BUN, and creatinine; common adverse effects include chemical pancreatitis (94%), elevated liver enzymes (63%), myalgias/arthralgias (58%), fatigue (37%), anorexia/nausea/vomiting/abdominal pain (31%), ECG changes (27%), headache (19%), and rash (11%); rare cases of anemia, leukopenia, and thrombocytopenia have been reported; varicella zoster reactivation has been noted in several patients during therapy; adverse effects are reversible and resolve when the drug is held; once symptoms resolve, therapy can be restarted; QT prolongation, ST-segment elevation, and T-wave inversion may occur with higher dosing and prolonged therapy; sudden cardiac death has been reported during therapy; frequently monitor ECG during the course of therapy (discontinue therapy if QT interval >0.5 s or if dysrhythmias occur)
Elevations in liver enzymes may occur; elevations in pancreatic enzymes occur in almost all treated patients; pancreatitis is usually asymptomatic, but some patients experience mild-to-moderate GI distress; adverse effects are reversible, and enzyme levels usually return to within the reference range within 3 wk without the need to stop therapy; temporarily discontinue therapy if aminotransferase levels are >5 times, amylase levels are >5 times, or lipase levels are >15 times the upper limit of the normal level

Antifungals/antiparasitics

When systemic agents are administered, monitor patients for adverse effects and complications common to the drug.


Amphotericin B/ liposomal amphotericin B (AmBisome)

Traditionally, an antifungal agent that attacks the ergosterol wall of the Leishmania parasite. Use is limited because of its high adverse effect profile, but newer lipophilic formulations that reduce toxicity have shown promise in treating resistant visceral and mucocutaneous disease. AmBisome currently is the only FDA-approved drug for the treatment of visceral leishmaniasis in the United States. Dosing varies depending on the preparation, and trials are in progress.

Adult

AmBisome-
Patients who are immunocompetent: 3 mg/kg/d IV for 5 d and then 3 mg/kg IV on days 14 and 21 for the treatment of visceral leishmaniasis
Patients who are immunocompromised: 4 mg/kg/d IV for 5 d followed by 4 mg/kg IV on days 10, 17, 24, 31, and 38

Pediatric

Administer as in adults

When used with corticosteroids, corticotropin, digitalis, and skeletal muscle relaxants, may potentiate hypokalemia and lead to cardiac dysfunction; acute pulmonary toxicity has been reported in patients receiving leukocyte transfusions and amphotericin B; flucytosine may have increased renal toxicity

Documented hypersensitivity; caution in renal or hepatic insufficiency

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Adverse effects include renal failure, fever, chills, rash, nausea, vomiting, hypotension, electrolyte abnormalities, and cardiac arrest; relapse rates are high in patients who are immunocompromised and treated with liposomal amphotericin B

Antineoplastics/antiprotozoan

Miltefosine is a phosphocholine cytidylyl transferase (CTP) inhibitor with antimetastatic properties that induces apoptosis in cancer cells. The antiprotozoal effect is poorly understood.


Miltefosine (Impavido)

Since 2002, this is rapidly becoming the DOC for visceral leishmaniasis in India. Currently registered in India and Europe for the treatment of visceral leishmaniasis.

Adult

Visceral leishmaniasis: 100 mg/d PO for 28 d in adults and children >10 y; shorter dosing regimens are currently under evaluation
Cutaneous leishmaniasis caused by L viannia braziliensis: 2.25-2.5 mg/kg/d PO for 3-4 wk

Pediatric

Visceral leishmaniasis: 50 mg/d PO for 28 d in children aged 6-9 y; 2.5 mg/kg/d PO for 28 d in children aged 3-5 y

No interactions with antiretroviral therapy were seen during trials treating leishmania/HIV co-infection over a 2-y period

Documented hypersensitivity; use with caution in patients with kidney disease

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Common adverse effects include nausea (36%), vomiting (31%), and mild, reversible serum creatinine level elevation (32%); initial animal studies reported dose- and time-related reversible infertility in rats, but subsequent WHO studies showed no adverse human reproductive interactions

More on Leishmaniasis

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Treatment & Medication: Leishmaniasis
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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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