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Leishmaniasis Medication

  • Author: Craig G Stark, MD; Chief Editor: Pranatharthi Haran Chandrasekar, MBBS, MD  more...
 
Updated: Apr 06, 2016
 

Medication Summary

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

Antiparasitic pentavalent antimonial agents

Antiparasitic pentavalent antimonials, such as sodium stibogluconate (Pentostam) or meglumine antimonate, have been the mainstays of therapy for all forms of the disease.[57] Until recently, sodium stibogluconate was the drug of choice in most areas and the only recommended treatment in the United States, but resistance is rising.

Pentavalent antimony is not marketed in the United States, but it can be obtained through the Centers for Disease Control and Prevention (CDC) Drug Service (404-639-3670), under an Investigational New Drug (IND) approved by the Food and Drug Administration (FDA), and by the CDC’S Institutional Review Board (IRB).[2]

Cure rates

Cure rates for pentavalent antimony are 90-97% with 1-3 full intravenous treatment courses; however, the drawbacks are considerable. These drugs are expensive and difficult to obtain. They must be delivered parenterally, they have numerous adverse effects, they may have lot-to-lot variability, and they are becoming increasingly less effective because of the emergence of drug-resistant parasites (especially in certain countries such as India). Interferon-gamma plus antimony may be an alternative option with an acceptable cure rate.

In other parts of the world, intralesional injections have shown promise with less toxicity (although with much lower patient tolerability owing to the pain associated with the intralesional injections).

Alternative treatment regimens with acceptable cure rates but that are not FDA approved for treating selected cases of leishmaniasis are parenteral agents pentamidine and amphotericin B deoxycholate, as well as oral agents ketoconazole, itraconazole, and fluconazole.[2]

However, although much has been made of the use of azoles for the Iraqi L major cutaneous disease, few practitioners in the field believe this is a prudent consideration for routine treatment of this disease. Liposomal amphotericin B has been used with good success in the treatment of cutaneous disease from many parts of the world and is gaining increased acceptance with many practitioners.

Although paromomycin also has acceptable cure rates, it is not available in the US or potentially available only through specific channels.[2]

Liposomal amphotericin B

Amphotericin B in its liposomal form (as opposed to amphotericin B deoxycholate) is now considered to be the drug of choice for visceral leishmaniasis because of its shorter course and lower toxicity. This agent is not approved for the cutaneous or mucosal forms of the disease.[2]

Cost issues prevent the use of liposomal drugs in most countries, where the mainstay of treatment is still prolonged intravenous treatment with antimonial agents, 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).

Oral miltefosine

Miltefosine is the sole oral agent that has been shown to be effective against leishmaniasis. This medication was developed first as an antineoplastic agent and later found to have considerable antiproliferative activity against leishmaniasis as well as against other trypanosome parasites. It is an attractive agent in areas, such as India, that have drug resistance against traditional chemotherapy.

In August 2013, the CDC made available an expanded access investigational new drug (IND) protocol for miltefosine for treatment of free-living amebae (FLA) in the United States.[40] In March 2014, the CDC approved miltefosine for the treatment of specific species that cutaneous, mucosal, and visceral leishmaniasis, in adults and adolescents who aged at least 12 years, weigh at least 66 lb, and are not pregnant or breastfeeding.[2]

This medication is approved in India for visceral leishmaniasis.

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Antifungals, Systemic

Class Summary

Antifungal and antiparasitic medications are used in resistant leishmaniasis in combination with other agents. The mechanisms of action may involve an alteration of RNA and DNA metabolism or an intracellular accumulation of peroxide that is toxic to the fungal cell. The major sterol in Leishmania organisms and fungi is ergosterol. Antiergosterol agents are marketed as antifungals.

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

Amphotericin B liposomal (AmBisome)

 

Traditionally, amphotericin B, produced by a strain of Streptomyces nodosus, is a fungistatic or fungicidal agent that attacks the ergosterol wall of the Leishmania parasite, causing intracellular components to leak with subsequent fungal cell death. Its use has been 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. These formulations are taken up well by the reticuloendothelial system and poorly by the kidney, decreasing the risk of nephrotoxicity.

Liposomal amphotericin B has become the drug of choice in antimony-resistant infections (especially if contracted in India).

In addition to miltefosine, AmBisome is the only FDA-approved drug for the treatment of visceral leishmaniasis in the United States. This agent is available as a 100 mg/20 mL preparation.

Cure rates of 90% and higher have been observed in various studies, except possibly in patients with HIV infection. A short-course regimen consisting of a single dose of liposomal amphotericin followed by 7-14 days of miltefosine has resulted in cure rates greater than 90% in north India.

The high cost of liposomal amphotericin B is a disadvantage to its use in areas where visceral leishmaniasis is prevalent.

Ketoconazole

 

Ketoconazole is an imidazole broad-spectrum antifungal agent that inhibits synthesis of ergosterol, causing cellular components to leak and resulting in fungal cell death.

Itraconazole (Sporanox, Onmel)

 

Itraconazole is a synthetic triazole antifungal agent that slows fungal cell growth by inhibiting CYP-450–dependent synthesis of ergosterol, a vital component of fungal cell membranes.

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Xanthine Oxidase Inhibitors

Class Summary

Xanthine oxidase inhibitors may be added to first-line drugs for treatment against protozoal infections.

Allopurinol (Zyloprim, Aloprim)

 

Allopurinol inhibits xanthine oxidase, the enzyme that synthesizes uric acid from hypoxanthine. This reduces the synthesis of uric acid without disrupting the biosynthesis of vital purines.

Allopurinol is not effective as monotherapy for leishmaniasis.

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Antiprotozoal Agents

Class Summary

Antiprotozoan compounds are the drugs of choice in patients with visceral leishmaniasis. Parasite biochemical pathways are sufficiently different from the human host to allow selective interference by chemotherapeutic agents in relatively small doses.

Protozoal infections are typically more severe in immunocompromised patients than in immunocompetent patients. These infections occur throughout the world and are a major cause of morbidity and mortality in some regions. Primary immune deficiency is rare, whereas secondary deficiency is more common.

Immunosuppressive therapy, cancer and its treatment, infection with human immunodeficiency virus (HIV), and splenectomy all may increase vulnerability to infection. The infectious risk is proportional to neutropenia duration and severity.

Pentamidine (Pentam)

 

Pentamidine is a first-line medication in cutaneous leishmaniasis except for L mexicana (ketoconazole 600 mg PO qd for 28 d). It is a treatment alternative in visceral leishmaniasis.

This agent inhibits growth of protozoa by (1) interacting with trypanosomal kinetoplast DNA, (2) interfering with polyamine synthesis by a decrease in the activity of ornithine decarboxylase, and (3) and inhibiting incorporation of nucleic acids into RNA and DNA, causing inhibition of protein and phospholipid synthesis.

Pentamidine is well absorbed and highly tissue bound. This medication is formulated as a sterile powder and must be reconstituted and administered as slow IV infusion or via the IM route. Because patients receiving daily injections do not reach a steady-state plasma concentration and elimination half-life is 12 days, a great deal of accumulation of pentamidine can occur in tissues such as the liver, kidney, and spleen.

Resistance to pentamidine is common in India, with high relapse rates reported.

Paromomycin

 

Paromomycin is an oral orphan drug consisting of an amebicidal and antibacterial aminoglycoside obtained from a strain of Streptomyces rimosus that is active in intestinal amebiasis.

Paromomycin has a relatively favorable adverse effect profile, but it is not as effective as antimony or amphotericin B for visceral disease when used as monotherapy. Paromomycin can be used in combination with sodium antimony gluconate to reduce the total time of therapy, and it has better cure rates.

Intravenous and topical paromomycin products are not available in the United States.

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Immunomodulators

Class Summary

Interferons are naturally occurring cytokines that possess various biologic functions, which include immunosuppressive action. They are produced by cells in response to viruses, double-stranded RNA, antigens, or mitogens, and are classified in relation to biochemical properties and cell of origin. Interferons are commercially produced with recombinant DNA technology.

Interferon gamma-1b (Actimmune)

 

Interferon gamma-1b is a naturally occurring cytokine that possesses antiviral, immunomodulatory, and antiproliferative activity. This agent is commercially available as a protein product manufactured by recombinant DNA technology.

Interferon gamma-1b is administered with sodium antimony gluconate (probably ineffective alone).

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Antileishmaniasis Agents

Class Summary

Miltefosine is a new oral drug that is now approved in the United States to treat cutaneous, mucocutaneous, and visceral disease from specific Leishmania species. The antiprotozoal effect is poorly understood.

Sodium stibogluconate is a compound available in English-speaking countries, and meglumine antimonate is a compound available in Latin American countries.

Sodium stibogluconate (Pentostam)

 

Sodium stibogluconate has been the drug of choice for the treatment of cutaneous and mucocutaneous leishmaniasis in the United States. This agent is also effective against visceral leishmaniasis and is often the first-line treatment outside the United States. Patients with long-standing disease may require long-term therapy. Although not FDA approved, sodium stibogluconate is currently available from the Centers for Disease Control and Prevention (CDC) as an investigational new drug (404-639-3670).

Sodium stibogluconate acts by interfering with the metabolism of the parasite. This agent may be administered intravenously (IV) or intramuscularly (IM), with similar pharmacokinetic parameters. IV use is preferred, because large volumes are required. Sodium stibogluconate is available only from the CDC at 100 mg/mL. Dilute each mL in 10 mL of 5% dextrose water, and administer it over 15 minutes to prevent thrombophlebitis.

This agent can be administered at recommended dose for 30 days without toxicity. Children often tolerate adverse effects better than adults and may not require electrocardiographic (ECG) monitoring.

Primary unresponsiveness ranges from 2-8%. The relapse rate is usually below 10%, but it has been reported to be as high as 30% in Kenya. An increasing incidence of resistance is reported in India.

Miltefosine (Impavido)

 

Miltefosine is an alkylphosphocholine that was originally developed as an antineoplastic agent. The specific mode of action against Leishmania species is unknown but is likely to involve interaction with lipids (phospholipids and sterols), including membrane lipids, inhibition of cytochrome C oxidase (mitochondrial function), and apoptosis-like cell death.

In March 2014, the FDA approved miltefosine for visceral leishmaniasis caused by L donovani; cutaneous leishmaniasis due to L braziliensis, L guyanensis, and L panamensis; and mucosal leishmaniasis due to L braziliensis. FDA approval was for patients aged 12 years or older, those who weigh at least 66 lb, and those who aren't pregnant or breastfeeding.

Since 2002, this agent has rapidly become the drug of choice for visceral leishmaniasis in India. A short-course regimen consisting of a single dose of liposomal amphotericin followed by 7-14 days of miltefosine has resulted in cure rates greater than 90% in north India. Miltefosine is registered in India and Europe for the treatment of visceral leishmaniasis.

Its mechanism of action is likely due to inhibition of phospholipid and sterol biosynthesis via interference with cell signal transduction pathways. Resistance against miltefosine has been found.

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Contributor Information and Disclosures
Author

Craig G Stark, MD Regional Medical Director, International SOS

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, Society of US Army Flight Surgeons

Disclosure: Nothing to disclose.

Coauthor(s)

Conjivaram Vidyashankar, MD, MRCP Specialty Doctor in Pediatrics, Dumfries and Galloway Royal Infirmary, Scotland

Conjivaram Vidyashankar, MD, MRCP is a member of the following medical societies: International AIDS Society, Royal College of Paediatrics and Child Health, Indian Academy of Pediatrics, European Society for Paediatric Infectious Diseases

Disclosure: Nothing to disclose.

Chief Editor

Pranatharthi Haran Chandrasekar, MBBS, MD Professor, Chief of Infectious Disease, Program Director of Infectious Disease Fellowship, Department of Internal Medicine, Wayne State University School of Medicine

Pranatharthi Haran Chandrasekar, MBBS, MD is a member of the following medical societies: American College of Physicians, American Society for Microbiology, International Immunocompromised Host Society, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Acknowledgements

Ruchir Agrawal, MD Chief, Allergy and Immunology, Aurora Sheboygan Clinic

Ruchir Agrawal, MD, is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American Academy of Pediatrics, American College of Allergy, Asthma and Immunology, and American Medical Association

Disclosure: Nothing to disclose.

Pranatharthi Haran Chandrasekar, MBBS, MD Professor, Department of Internal Medicine, Director of Infectious Disease Fellowship, Harper Hospital, Wayne State University School of Medicine

Pranatharthi Haran Chandrasekar, MBBS, MD is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Dirk M Elston, MD Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

John Halpern, DO, FACEP Clinical Assistant Professor, Department of Family Medicine, Nova Southeastern University College of Osteopathic Medicine; Medical Director, Health Career Institute; Medical Director Emergency Department, Palms West Hospital

John Halpern, DO, FACEP is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Edmond A Hooker II, MD, DrPH, FAAEM Associate Professor, Department of Health Services Administration, Xavier University, Cincinnati, Ohio; Assistant Professor, Department of Emergency Medicine, University of Cincinnati College of Medicine

Edmond A Hooker II, MD, DrPH, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American Public Health Association, Society for Academic Emergency Medicine, and Southern Medical Association

Disclosure: Nothing to disclose.

Renee Y Hsia, MD, MSc Clinical Instructor, Division of Emergency Medicine, University of California at San Francisco School of Medicine; Attending Physician, Department of Emergency Medicine, San Francisco General Hospital

Disclosure: Nothing to disclose.

Julie R Kenner, MD, PhD Private Practice, Kenner Dermatology Center

Julie R Kenner, MD, PhD is a member of the following medical societies: American Academy of Dermatology and American Society for Dermatologic Surgery

Disclosure: Nothing to disclose.

Thomas M Kerkering, MD Chief of Infectious Diseases, Virginia Tech Carilion School of Medicine

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.

Abdul-Ghani Kibbi, MD Professor and Chair, Department of Dermatology, American University of Beirut Medical Center, Lebanon

Disclosure: Nothing to disclose.

Jennifer J Lee MD, Assistant Professor, Division of Dermatology, Department of Medicine, Vanderbilt University Medical Center

Jennifer J Lee is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Lester F Libow, MD Dermatopathologist, South Texas Dermatopathology Laboratory

Lester F Libow, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, and Texas Medical Association

Disclosure: Nothing to disclose.

Gary J Noel, MD Professor, Department of Pediatrics, Weill Cornell Medical College; Attending Pediatrician, New York-Presbyterian Hospital

Gary J Noel, MD is a member of the following medical societies: Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

William G Stebbins, MD Assistant Professor of Medicine, Division of Dermatology, Vanderbilt University

William G Stebbins, MD is a member of the following medical societies: American Academy of Dermatology, American Society for Dermatologic Surgery, and Dermatology Foundation

Disclosure: Nothing to disclose.

Russell W Steele, MD Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Jeter (Jay) Pritchard Taylor III, MD Compliance Officer, Attending Physician, Emergency Medicine Residency, Department of Emergency Medicine, Palmetto Health Richland, University of South Carolina School of Medicine; Medical Director, Department of Emergency Medicine, Palmetto Health Baptist

Jeter (Jay) Pritchard Taylor III, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

N Ewen Wang, MD Consulting Staff, Department of Surgery, Division of Emergency Medicine, Stanford University Hospital

Disclosure: Nothing to disclose.

Peter J Weina, MD, PhD Colonel, US Army; Deputy Commander/Deputy Director, Medical Director of the Leishmania Diagnostics Laboratory, Walter Reed Army Institute of Research

Peter J Weina, MD, PhD is a member of the following medical societies: American College of Physicians, American Society of Tropical Medicine and Hygiene, Association of Military Surgeons of the US, and International Society of Travel Medicine

Disclosure: Nothing to disclose.

Michael J Wells, MD Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Acknowledgments

The opinions or assertions contained herein are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of the Army or the Department of Defense.

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Classic Leishmania major lesion from a case in Iraq shows a volcanic appearance with rolled edges.
Atypical appearance of Leishmania major lesion with local spread beyond the borders of the primary lesion. Many of the lesions in cases from Iraq show an atypical appearance.
Old World localized cutaneous leishmaniasis located on the trunk of a soldier stationed in Kuwait. This lesion was a 3-cm by 4-cm nontender ulceration that developed over the course of 6 months at the site of a sandfly bite. The patient reported seeing several rats around his encampment.
Old World cutaneous leishmaniasis located on the right arm of the same soldier stationed in Kuwait. This 2-cm by 3-cm lesion was located at the exposed area where the sleeve ended. Note the satellite lesions.
Active cutaneous leishmaniasis lesion with likely secondary infection in a soldier.
Cutaneous leishmaniasis with keloid formation in a black soldier.
Taxonomy of some of the medically important protozoans showing the relative relationship of the Kinetoplastida parasites generally, and Leishmania specifically.
Leishmania donovani is one of the main Leishmania species that infects humans.
Life cycles of the medically important Kinetoplastida illustrating the similarities and differences between the trypanosomes and Leishmania.
Distribution map of cutaneous leishmaniasis.
Geographical distribution of Old World cutaneous leishmaniasis due to L tropica and related species and L aethiopica. Source: World Health Organization, Department of Control of Neglected Tropical Diseases, Innovative and Intensified Disease Management (WHO/NTD/IDM) Human Immunodeficiency Virus/Acquired Immunodeficiency Syndrome (HIV/AIDS), Tuberculosis and Malaria (HTM) WHO, October 2010: http://www.who.int/leishmaniasis/leishmaniasis_maps/en/index1.html
Geographical distribution of Old World cutaneous leishmaniasis due to L major. Source: World Health Organization, Department of Control of Neglected Tropical Diseases, Innovative and Intensified Disease Management (WHO/NTD/IDM) Human Immunodeficiency Virus/Acquired Immunodeficiency Syndrome (HIV/AIDS), Tuberculosis and Malaria (HTM) WHO, October 2010: http://www.who.int/leishmaniasis/leishmaniasis_maps/en/index1.html.
Geographical distribution of cutaneous and mucocutaneous leishmaniasis in the New World. Source: World Health Organization, Department of Control of Neglected Tropical Diseases, Innovative and Intensified Disease Management (WHO/NTD/IDM) Human Immunodeficiency Virus/Acquired Immunodeficiency Syndrome (HIV/AIDS), Tuberculosis and Malaria (HTM) WHO, October 2010: http://www.who.int/leishmaniasis/leishmaniasis_maps/en/
Geographical distribution of visceral leishmaniasis in the Old and New world. Source: World Health Organization, Department of Control of Neglected Tropical Diseases, Innovative and Intensified Disease Management (WHO/NTD/IDM) Human Immunodeficiency Virus/Acquired Immunodeficiency Syndrome (HIV/AIDS), Tuberculosis and Malaria (HTM) WHO, October 2010: http://www.who.int/leishmaniasis/leishmaniasis_maps/en/.
Distribution map of visceral leishmaniasis.
Distribution map of human immunodeficiency virus (HIV) and leishmaniasis coinfection.
The predominant mode of leishmaniasis transmission is a sandfly's bite.
Sandfly. Courtesy of Kenneth F. Wagner, MD.
Comparison of a sandfly (left) and a mosquito (right). The sandfly's small size affects the efficacy of bed nets when used without permethrin treatment.
Cutaneous leishmaniasis. Courtesy of Kenneth F. Wagner, MD.
Cutaneous leishmaniasis lesion. Image courtesy of the Centers for Disease Control and Prevention Public Health Image Library.
Cutaneous leishmaniasis with sporotrichotic spread.
Cutaneous leishmaniasis lesion. Image courtesy of the Centers for Disease Control and Prevention Public Health Image Library.
Cutaneous leishmaniasis is generally considered to be an innocuous disease; however, in some parts of the world, especially in tribal areas, even cutaneous disease can have a life altering effect on a person's life. Minimal facial disfiguring can condemn young girls to life without the prospect of marriage or acceptance in society.
Leishmaniasis in an Ethiopian woman with a 1-year history of asymptomatic pink-erythematous infiltrative plaque with overlying scale and central crust.
Healed cutaneous leishmaniasis lesions. Photo courtesy of Robert Norris, MD, Stanford University Medical Center.
Cutaneous leishmaniasis lesions. Photo courtesy of Robert Norris, MD, Stanford University Medical Center.
Diffuse (disseminated) cutaneous leishmaniasis. Courtesy of Jacinto Convit, National Institute of Dermatology in Caracas, Venezuela.
Leishmaniasis recidivans. Courtesy of Kenneth F. Wagner, MD.
Post–kala-azar dermal leishmaniasis. Courtesy of R. E. Kuntz and R. H. Watten, Naval Medical Research Unit, Taipei, Taiwan.
Mucocutaneous leishmaniasis. Courtesy of Kenneth F. Wagner, MD.
Mucocutaneous leishmaniasis. Courtesy of Kenneth F. Wagner, MD.
Visceral leishmaniasis. Courtesy of Kenneth F. Wagner, MD.
Marked splenomegaly (enlargement/swelling of the spleen) in a patient in lowland Nepal who has visceral leishmaniasis. (Credit: C. Bern, CDC) Source: Centers for Disease Control and Prevention. Parasites home: leishmaniasis. Resources for health professionals: http://www.cdc.gov/parasites/leishmaniasis/health_professionals/.
Amastigotes in a macrophage at 1000× magnification. Inset shows the cell membrane and points out the nucleus and kinetoplast, which are required to confirm that the inclusion seen in a macrophage is indeed an amastigote.
Free amastigotes near a disrupted macrophage. On touch preparations like this (Giemsa stain, original magnification × 1000), the amastigotes are easier to identify than on other preparations. These stains clearly demonstrate the cell membrane, nucleus, and kinetoplast; all 3 are required for definitive diagnosis.
Free amastigote in a touch preparation (Giemsa stain, original magnification × 1000).
Light-microscopic examination of a stained bone marrow specimen from a patient with visceral leishmaniasis—showing a macrophage (a special type of white blood cell) containing multiple Leishmania amastigotes (the tissue stage of the parasite). Note that each amastigote has a nucleus (red arrow) and a rod-shaped kinetoplast (black arrow). Visualization of the kinetoplast is important for diagnostic purposes, to be confident the patient has leishmaniasis. (Credit: CDC/DPDx) Source: Centers for Disease Control and Prevention. Parasites home: leishmaniasis. Resources for health professionals: http://www.cdc.gov/parasites/leishmaniasis/health_professionals/
Illustration of one form of the rK39 test for the serologic diagnosis of visceral leishmaniasis. It is an easy, very sensitive, and specific test for visceral disease. In this case, the dipstick second from the left shows a positive result and all the rest show reaction only at the control line.
 
 
 
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