Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Leishmaniasis Treatment & Management

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

Approach Considerations

When to treat

Given the associated morbidity, always treat visceral, mucocutaneous, and severe forms of cutaneous leishmaniasis. Patients should receive treatment at facilities experienced in treating the disease as per latest guidelines.

Owing to its potential to progress into mucocutaneous leishmaniasis, definitively treat New World cutaneous leishmaniasis caused by members of the Leishmania Viannia subgenus. Cases due to L tropica (Old World) and some L major from certain regions of Afghanistan may have a more aggressive or chronic course (up to years); L tropica has been implicated in occasional cases of recidivans or viscerotropic leishmaniasis. As such, treatment may need to be more involved in cases caused by this species.

In New World leishmaniasis, estimates of recurrence range from less than 5% to as many as 10% of untreated individuals experiencing chronic ulcers, recidivans lesions, or mucocutaneous involvement. Because of this, treatment is very often the standard of care, and parenteral therapy is usually the treatment of choice.

New World cutaneous leishmaniasis due to L mexicana is not associated with mucocutaneous leishmaniasis and may not require systemic treatment. Cutaneous leishmaniasis acquired in the Old World tends to resolve spontaneously (eg, L major from Iraq), but patients with this infection should receive treatment if the lesions are disfiguring, painful, infected, over joints, or slow to heal.

Individualized management

Tailor treatment to the individual, because leishmaniasis is caused by many species or subspecies of the Leishmania protozoa, all of which have different degrees of virulence and clinical predilections. Consider the clinical pattern of disease, the geographic region in which the infection occurs, the immunologic status of the patient, and the previous attempts at treatment when therapy is started.

Treatment options

In general, if the case is not advanced with serious gastroenterologic, hematologic, or infectious issues, care can be accomplished on an outpatient basis. However, daily visits to a physician for medication may be required.

Multiple medical treatment options are used throughout the world for cutaneous disease. In addition to parenteral and oral medications (see Medication), local therapies for some forms of cutaneous leishmaniasis include (1) cryotherapy, (2) infiltration of sodium stibogluconate at 0.3-0.8 mL, (3) local heat therapy at 40-42°C, and (4) various topical paromomycin preparations, typically 15% with 10% urea.

Of primary importance in dealing with leishmaniasis is the treatment of malnutrition, concurrent systemic illness (eg, human immunodeficiency virus [HIV] infection, tuberculosis), or local infection (secondary bacterial). Malnourished individuals are at greater risk of acquiring leishmaniasis, have increase morbidity and mortality in mucocutaneous and visceral disease, and respond less well to treatment than those with adequate nutrition.

Other things to consider include the following:

  • At the onset of therapy, admit patients for laboratory and cardiac monitoring; alternate drug regimens require variable monitoring levels commensurate with their known adverse effects
  • Administer antibiotic therapy to treat superimposed bacterial wound infections, and consult an infectious disease specialist or a dermatologist for definitive diagnosis and treatment
  • Provide supportive care for patients with visceral and severe mucocutaneous leishmaniasis, as required; supportive treatment includes rest, a high-protein and high-calorie diet, blood transfusions, and wound care
  • The earliest sign of improvement is an improvement in symptoms; regression of splenomegaly takes a few months

Despite successful clinical outcomes, the question of whether the parasites are completely eradicated is unclear, because reactivation of leishmaniasis with immunosuppression has been reported.[26]

Immunization

In some areas of the world (eg, Russia, Middle East), live-attenuated L major promastigotes have been used preemptively to immunize against Old World cutaneous leishmaniasis. This practice produces a modified form of the disease and results in a scar at the injection site. Immunity to subsequent L major infections is usually good; however, as with natural infection, cross-reactive immunity to other Leishmania species does not occur.

Many more universally useful and cosmetically acceptable Leishmania vaccine formulations are under investigation. To date, no vaccines are commercially available.

Treatment guidelines

The guideline summary Guidelines for prevention and treatment of opportunistic infections in HIV-infected adults and adolescents. Recommendations from CDC, the National Institutes of Health, and the HIV Medicine Association of the Infectious Diseases Society of America may be of interest.[27] Recent updates to the guideline can be found at the AIDSinfo website[28] : http://aidsinfo.nih.gov/guidelines/html/4/adult-and-adolescent-oi-prevention-and-treatment-guidelines/0.

The Infectious Diseases Society of America is in the process of developing a new Clinical Practice Guidelines on Leishmaniasis. The projected date of publication is spring 2016.

Next

Pharmacotherapy

Leishmaniasis therapies available in the United States are limited and include the following[2] :

  • Antiparasitic pentavalent antimonial agents
  • Liposomal amphotericin B
  • Oral miltefosine
  • Pentamidine
  • Other agents
  • Antibiotics

Antiparasitic pentavalent antimonial agents

The treatment mainstays of leishmaniasis 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 only available from the CDC under an Investigational New Drug (IND) protocol. Military personnel may receive sodium stibogluconate from the Walter Reed Army Medical Center. This agent has been for the treatment of cutaneous and mucocutaneous leishmaniasis in the United States; it has also been the drug of choice in the treatment of visceral leishmaniasis, except for in Europe and regions in India with stibogluconate resistance.

In the United States, patients are sometimes monitored as inpatients when pentavalent antimony is administered, but more accepted is the use of infusion centers that complete full evaluations prior to use of the drug. Periodic evaluation of cardiac conduction with electroencephalographic (ECG) monitoring is prudent. Perform laboratory assessments of complete blood counts; renal function; and amylase, lipase, and serum transaminases levels.

Pentavalent antimony should be used according to CDC protocol. If marked variation from the protocol is being considered, CDC experts should be consulted.

A study in Guatemala that involved a combination of intravenous (IV) stibogluconate and allopurinol showed improved efficacy against cutaneous L (Viannia) panamensis infections compared with stibogluconate alone.[29] 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.

In a later study of IV sodium stibogluconate involving US military personnel with cutaneous leishmaniasis caused by L (Viannia) panamensis, the efficacy of a 10-day course was validated, with a significantly reduced side-effect profile over the standard 20-day course.[30] However, the results may not be applicable to infections caused by other species of Leishmania.

Unfortunately, resistance to this agent is on the rise. In the Bihar province of India, where visceral leishmaniasis is endemic, resistance is as high as 43%.

Amphotericin B

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 (amphotericin B lipid complex, liposomal amphotericin B, and amphotericin B colloidal dispersion) are more active, better tolerated, and are being used as first-line therapy against visceral leishmaniasis, but the response with cutaneous disease has been mixed, and treatment is costly.

Liposomal amphotericin B is the drug of choice for visceral leishmaniasis because of its shorter course and lower toxicity.

In an open-label comparative study, Sundar et al found that the efficacy of a single infusion of liposomal amphotericin B was equivalent to a conventional amphotericin B infusion (15 alternate-day infusions) for visceral leishmaniasis.[31] Additionally, the liposomal group was less expensive and exhibited fewer infusion-related adverse effects (eg, fever, rigors) compared with conventional amphotericin B.[31]

A separate study by Sundar et al suggested that varied combinations of drugs, including liposomal amphotericin B, miltefosine, and paromomycin (for durations as short as 7-10 days), provide effective, safer, and cheaper regimens compared with the conventional 30-day amphotericin B regimen for visceral leishmaniasis.[32]

A single-dose treatment with liposomal amphotericin B has shown a 91% cure rate in India.[33] In endemic areas of north India, liposomal amphotericin is used in combination with miltefosine.[34] A short-course regimen consisting of a single dose of liposomal amphotericin followed by 7-14 days of miltefosine has resulted in cure rates of over 90%.[34] The single-dose liposomal amphotericin B regimen has become affordable after its inclusion in India’s Kala-azar Programme, assisted by drug donations facilitated by the WHO.

Response to liposomal amphotericin B may be suboptimal in patients infected with human immunodeficiency virus (HIV).[35]

Oral miltefosine

The discovery of an affordable, orally administered, well-tolerated therapy for visceral leishmaniasis has made mass treatment of the disease in the developing world a reality. Miltefosine is the sole oral agent that has been shown to be effective against leishmaniasis. This drug is a phosphocholine analogue that was originally developed as an antineoplastic agent; it 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.[36] Oral treatment of 2.5 mg/kg/day lasting 4-6 weeks was generally well-tolerated. Common adverse effects included gastrointestinal distress and elevated creatinine levels, which resolved with cessation of therapy.

Another visceral leishmaniasis treatment study, which compared oral miltefosine with IV amphotericin B deoxycholate, showed a final cure rate after 6 months of 94% and 97%, respectively.[37, 38]

A 2011 phase IV trial from Bangladesh found monotherapy with oral miltefosine (2.5 mg/kg/d) for 28 days effective in the treatment of visceral leishmaniasis in children and adults.[39] This medication is approved in India for visceral leishmaniasis.

In August 2013, the Centers for Disease Control and Prevention (CDC) expanded access of the investigational new drug (IND) protocol in effect with the Food and Drug Administration (FDA) to make miltefosine available directly from the CDC for treatment of free-living amebae (FLA) in the United States (eg, primary amebic meningoencephalitis [PAM] caused by Naegleria fowleri and granulomatous amebic encephalitis caused by Balamuthia mandrillaris and Acanthamoeba species.[40]

In March 2014, the FDA approved oral miltefosine for visceral leishmaniasis due to L donovani; cutaneous leishmaniasis due to L braziliensis, L guyanensis, and L panamensis; and mucosal leishmaniasis due to L braziliensis.[37, 2] FDA approval was for patients who are aged 12 years or older, weigh at least 66 lb, and are not pregnant or breastfeeding.[2]

Intramuscular pentamidine

Intramuscular pentamidine is effective against visceral leishmaniasis, but this drug 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.[41]

Other agents

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.[42]

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.[29] Efficacy against L (Viannia) panamensis in Panama and L major in Iran and Israel has been demonstrated, whereas no effect was noted against L tropica in India and Turkey.[43]

Fluconazole was reportedly effective against 79% of patients infected with uncomplicated cutaneous leishmaniasis caused by L major in Saudi Arabia.[44]

Antibiotics

Patients with leishmaniasis may have concurrent systemic illness or local infection. Visceral leishmaniasis is an important opportunistic infection associated with acquired immunodeficiency syndrome (AIDS), and patients co-infected with human immunodeficiency virus (HIV) can develop unusual manifestations of leishmaniasis. Guidelines for prevention and treatment of opportunistic diseases in patients with HIV infection have been established.[27, 28]

Pentamidine is a first-line medication in cutaneous leishmaniasis except for L mexicana (ketoconazole 600 mg PO qd for 28 days). It is a treatment alternative in visceral leishmaniasis. Available antibiotic preparations include pentamidine isethionate (Pentam) and pentamidine dimethanesulfonate (Lomidine). Pentamidine dimethane sulphonate administered in the same dose schedule is more effective than pentamidine isethionate.

Previous
Next

Management of 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 paromomycin can be used. If only one or a few small lesions are present (excluding face or over a joint), careful follow-up without drug treatment may be appropriate.

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 or pentamidine can be used.

Oral miltefosine

Treatment of New World cutaneous leishmaniasis has met with variable levels of success. In a randomized controlled trial from Brazil, miltefosine used alone was significantly better than parenteral stibogluconate in older children and adults.[45] In Colombia, 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.[46] 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.

Topical paromomycin

Topical paromomycin has been shown to be effective against cutaneous leishmaniasis caused by L major and L mexicana. Because these species do not tend to cause visceral or mucocutaneous disease, topical paromomycin can spare the patient systemic adverse effects associated with parenteral medications. Topical therapy is not recommended for treatment of New World species that are known to progress to mucocutaneous disease.

In a randomized, double-blind, parallel group–controlled study in 375 patients from a region of Tunisia where leishmaniasis is endemic, Ben Salah et al demonstrated that paromomycin topical cream, with or without gentamicin, was effective against ulcerative cutaneous leishmaniasis.[47, 48] Study subjects received 15% paromomycin, 15% paromomycin plus 0.5% gentamicin, or vehicle control (containing neither gentamicin nor paromomycin). After 20 days of treatment, paromomycin alone achieved a cure rate of 82%, paromomycin-gentamicin achieved a cure rate of 81%, and vehicle control achieved a cure rate of 58%.[47, 48]

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.[49] Unfortunately, the performance of this cream with infections caused by L tropica has been disappointing.

Although topical paromomycin is not commercially available in the United States, this cream may be available from compounding pharmacies and is used in Israel for the treatment of L major lesions.

Other agents and therapeutic modalities

A short course of intramuscular pentamidine for 4 days was reported to be effective for cutaneous disease in Colombia.[50] A single report from Tunisia found doxycycline to be effective in cutaneous leishmaniasis.[51]

Other reported treatments include topical imiquimod cream, cryotherapy, thermotherapy, ketoconazole, photodynamic therapy, itraconazole, and allopurinol. However, these are effective only when used in combination with the first-line drugs

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 for the treatment of cutaneous leishmaniasis. This device heats the skin through radiofrequency waves directed to a specified area and depth. A study conducted in Afghanistan involving cutaneous disease caused by L tropica demonstrated a cure rate of 69% at 100 days after treatment.[52] However, the lesions treated in this study were small. Further studies may demonstrate this to be a useful therapy for mild disease.

Previous
Next

Management of Mucocutaneous Leishmaniasis

Mucocutaneous disease responds to a 20-day course of sodium antimony gluconate; amphotericin B may be used to treat advanced or resistant cases. Pentavalent antimony for a course of 4 weeks has also been recommended.

A single arm study in adults conducted to evaluate oral miltefosine efficacy for the treatment of mucocutaneous leishmaniasis showed that by 12 months after the end of therapy, 62% of patients had complete resolution of edema, erythema, infiltration, and erosion from the involved mucosal sites.[37] The study was conducted in Bolivia, where L braziliensis is epidemiologically the prevalent species.

The protective effect against subsequent mucocutaneous disease is unknown at this time. One study showed a 1-year cure rate of 75% 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.

Previous
Next

Management of 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.

On the Indian subcontinent, the following treatment regimens are recommended for visceral leishmaniasis:

  • Liposomal amphotericin B alone, given as a single dose (currently recommended as the drug of choice by the Kala-Azar elimination programme of India)
  • Liposomal amphotericin B in a single dose, in combination with 7 days of oral miltefosine or 10 days of paromomycin
  • Miltefosine plus paromomycin for 10 days
  • Amphotericin B deoxycholate: 0.75-1 mg/kg/day via infusion, daily or on alternate days for 15-20 doses
  • Miltefosine orally for 28 days or paromomycin intramuscularly for 28 days
  • Pentavalent antimonials: 20 mg Sb5+/kg/day intramuscularly or intravenously for 30 days in areas where they remain effective: Bangladesh, Nepal, and the Indian states of Jharkhand, West Bengal, and Uttar Pradesh [13, 53]

Outside of India, treatment with a pentavalent antimonial compound is usually 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).

The advent of liposomal formulations of amphotericin B, which passively target amphotericin to macrophage-rich organs, have generally replaced the deoxycholate formulations. As noted earlier, liposomal amphotericin B is much more costly than conventional amphotericin B (making them cost-prohibitive in poor countries), but they are associated with less nephrotoxicity and can be given in considerably shorter courses. Although visceral leishmaniasis is traditionally treated with multiple doses of amphotericin B deoxycholate, it appears, based on a single randomized trial, that a single dose of liposomal amphotericin B may be just as effective and cheaper.[31]

Other parenteral alternatives that have merit include amphotericin B (not only in deoxycholate form but also in liposomal forms) and have generally replaced pentamidine. Injectable paromomycin has also been reported to be noninferior to amphotericin B.

Oral miltefosine is FDA approved for visceral, cutaneous, and mucocutaneous leishmaniasis. Sitamaquine is another oral therapy in the research pipeline for the treatment of visceral disease. Originally discovered by the Walter Reed Army Research Institute, this 8-aminoquinoline is currently undergoing phase 3 trials in Kenya and India.

Resistant visceral leishmaniasis

Drug resistance can be primary or secondary. Causes include (1) delayed diagnosis (prolonged duration of illness), (2) interrupted and low-dose treatment, (3) immunologic failure, (4) emergence of resistant strains of parasites, and (5) leishmaniasis associated with acquired immunodeficiency syndrome (AIDS).

Patients with stibogluconate-resistant disease should be treated with alternative agents, such as liposomal amphotericin (0.5-3 mg/kg) on alternate days until a dose of 20 mg/kg or pentamidine (2-4 mg/kg) on alternate days for 15 doses. Pentamidine is available in 2 preparations: pentamidine isethionate (Pentam 300) and pentamidine dimethane sulphonate (Lomidine). However, the effectiveness of pentamidine has recently declined.

Liposomal amphotericin has reported cure rates of more than 90% in various studies. However, the high cost of this drug is a disadvantage to its use in areas where visceral leishmaniasis is prevalent.

Another alternative agent is oral miltefosine. Miltefosine did not prevent visceral relapse in patients co-infected with human immunodeficiency virus (HIV) but remained effective with retreatment and over prolonged periods of therapy.[54]

A shift from monotherapy to multidrug combinations in short courses delivered at no or affordable cost, through directly observed therapy, appears to be the only way to effectively treat and prevent drug resistance. Combination therapy of stibogluconate with drugs such as aminosidine and interferon gamma has also produced good results in patients who with a poor response to stibogluconate therapy alone. Aminosidine, an aminoglycoside identical to paromomycin, has also been found to be effective in trials in India.

Guidelines for prevention and treatment of opportunistic diseases in patients with HIV infection have been established.[27, 28] Visceral leishmaniasis is an important opportunistic infection associated with AIDS, and patients co-infected with HIV can develop unusual manifestations of leishmaniasis. Research is being carried out on newer drug delivery systems for amphotericin, including the use of nanoparticles and cochleates, but these investigations have yet to enter human trials.[55]

Previous
Next

Surgical Intervention

Surgical excision to manage leishmaniasis is not usually recommended because of the following risks:

  • Relapse (exacerbation of quiescent disease)
  • Recurrence at the excision site
  • Cosmetic disfigurement

Surgical intervention may be necessary for adjunctive splenectomy in patients with treatment-resistant disease. Patients with severe mucocutaneous leishmaniasis may require orofacial surgery.

Previous
Next

Long-Term Monitoring

Carefully monitor patients with leishmaniasis for relapse or recrudescence for up to 6 months after successful treatment.

Perform a follow-up evaluation for patients 6 weeks after last dose of pentavalent antimony. Drug-resistant strains of leishmaniasis are appearing because of the unregulated use of these compounds. Improper dosing and shortened duration of therapy are contributing factors. Improvement in cutaneous disease is expected within the first couple of weeks of treatment. Patients with visceral disease should defervesce around 72 hours, with resolution of hepatosplenomegaly by 28 days.

Severe leishmaniasis recidivans, mucocutaneous leishmaniasis, diffuse cutaneous leishmaniasis, and post–kala-azar leishmaniasis are often difficult to treat and may require prolonged therapy.

Retreatment or second-line drugs may be required in patients with resistant disease.

Prescribe hematinics until the patient’s hemoglobin levels return to within the reference range.

Previous
Next

Prevention

Early diagnosis and treatment are the main measures for controlling leishmaniasis.

Postinfection immunity

After successful treatment, patients generally acquire immunity (97-98% effective) from the Leishmania species with which they were infected. Abortive infections due to therapy with effective agents are felt to reduce the protective immunity often seen with full course, self-resolving infections.

Vaccination

In some areas of the world, children are superficially inoculated with infected material in concealed areas to induce infection, to promote immunity, and to prevent facial scarring.

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.

Attempts to create a viable human vaccine along similar lines have been met with difficulty and have resulted in persistent cutaneous lesions. In May 2005, French researchers from the IRD Montpellier Research Centre successfully developed a novel vaccine against visceral leishmaniasis in dogs.[56] Using antigen proteins excreted by the parasite at the 100- and 200-mcg dose, 100% of the dogs (9 of 9) showed immunity over a period of 2 years after infection with L infantum.

Immunity appears to be related to activation of the Th1 lymphocytes, allowing macrophages to produce nitric oxide and to clear the Leishmania parasites. Researchers postulate that, by reducing the disease burden in dogs, the transmission cycle can be interrupted, indirectly reducing human infections. This new approach is currently being evaluated for incorporation into human vaccines.

Other measures

Reservoir eradication, vector control, and mass treatment of individuals who are infected have met with some success, but these are limited by cost and difficulty in coordinating efforts.

Insect repellent (eg, diethyltoluamide [DEET]), protective clothing, fans, and permethrin- or deltamethrin-impregnated mosquito nets offer some protection for visitors to endemic areas. The female sandfly makes no audible noise, is a relatively poor flyer, and is small enough to pass through standard mosquito nets; thus, specially designed, fine-mesh netting is required. Minimizing outdoor exposures at peak times (dawn to dusk) should also be used.

Because leishmaniasis can be transmitted through blood, infected patients should not donate blood or organs.

Previous
 
 
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.

References
  1. World Health Organization. Leishmaniasis: the disease and its epidemiology. Available at http://www.who.int/leishmaniasis/disease_epidemiology/en/. Accessed: April 10, 2014.

  2. Centers for Disease Control and Prevention. Parasites home: leishmaniasis. Epidemiology & risk factors. Available at http://www.cdc.gov/parasites/leishmaniasis/epi.html. Accessed: April 11, 2014.

  3. Cardo LJ, Rentas FJ, Ketchum L, Salata J, Harman R, Melvin W, et al. Pathogen inactivation of Leishmania donovani infantum in plasma and platelet concentrates using riboflavin and ultraviolet light. Vox Sang. 2006 Feb. 90(2):85-91. [Medline].

  4. Cardo LJ, Salata J, Harman R, Mendez J, Weina PJ. Leukodepletion filters reduce Leishmania in blood products when used at collection or at the bedside. Transfusion. 2006 Jun. 46(6):896-902. [Medline].

  5. McHugh CP, Melby PC, LaFon SG. Leishmaniasis in Texas: epidemiology and clinical aspects of human cases. Am J Trop Med Hyg. 1996 Nov. 55(5):547-55. [Medline].

  6. Centers for Disease Control and Prevention. Parasites home: leishmaniasis. Resources for health professionals. Available at http://www.cdc.gov/parasites/leishmaniasis/health_professionals/. Accessed: April 10, 2014.

  7. Magill AJ, Grogl M, Gasser RA Jr, Sun W, Oster CN. Visceral infection caused by Leishmania tropica in veterans of Operation Desert Storm. N Engl J Med. 1993 May 13. 328(19):1383-7. [Medline].

  8. Coleman RE, Burkett DA, Putnam JL, Sherwood V, Caci JB, Jennings BT, et al. Impact of phlebotomine sand flies on U.S. Military operations at Tallil Air Base, Iraq: 1. background, military situation, and development of a "Leishmaniasis Control Program". J Med Entomol. 2006 Jul. 43(4):647-62. [Medline].

  9. Myles O, Wortmann GW, Cummings JF, Barthel RV, Patel S, Crum-Cianflone NF, et al. Visceral leishmaniasis: clinical observations in 4 US army soldiers deployed to Afghanistan or Iraq, 2002-2004. Arch Intern Med. 2007 Sep 24. 167(17):1899-901. [Medline].

  10. Centers for Disease Control and Prevention. Update: Cutaneous leishmaniasis in U.S. military personnel--Southwest/Central Asia, 2002-2004. MMWR Morb Mortal Wkly Rep. 2004 Apr 2. 53(12):264-5. [Medline].

  11. Leishmaniasis Fact Sheet. World Health Organization. Available at http://www.who.int/mediacentre/factsheets/fs375/en/. 2016 Mar 01; Accessed: 2016 Mar 31.

  12. Leishmaniasis - Global Health Observatory Data. World Health Organization. Available at http://apps.who.int/gho/data/node.main.NTDLEISH?lang=en. 2016 Mar 01; Accessed: 2016 Mar 31.

  13. South-East Asia poised to defeat visceral leishmaniasis (kala-azar). WORLD HEALTH ORGANIZATION. Available at http://www.who.int/neglected_diseases/news/SEARO_poised_to_defeat_VL/en/. 2015 OCT 15; Accessed: 2016 MAR 31.

  14. World Health Organization. Essential leishmaniasis maps: visceral and mucocutaneous leishmaniasis. April 10, 2014. [Full Text].

  15. Martín-Ezquerra G, Fisa R, Riera C, Rocamora V, Fernández-Casado A, Barranco C, et al. Role of Leishmania spp. infestation in nondiagnostic cutaneous granulomatous lesions: report of a series of patients from a Western Mediterranean area. Br J Dermatol. 2009 Aug. 161(2):320-5. [Medline].

  16. Monno R, Giannelli G, Rizzo C, De Vito D, Fumarola L. Recombinant K39 immunochromatographic test for diagnosis of human leishmaniasis. Future Microbiol. 2009 Mar. 4(2):159-70. [Medline].

  17. Kubar J, Fragaki K. Recombinant DNA-derived leishmania proteins: from the laboratory to the field. Lancet Infect Dis. 2005 Feb. 5(2):107-14. [Medline].

  18. Zijlstra EE, Nur Y, Desjeux P, Khalil EA, El-Hassan AM, Groen J. Diagnosing visceral leishmaniasis with the recombinant K39 strip test: experience from the Sudan. Trop Med Int Health. 2001 Feb. 6(2):108-13. [Medline].

  19. Kumar R, Pai K, Pathak K, Sundar S. Enzyme-linked immunosorbent assay for recombinant K39 antigen in diagnosis and prognosis of Indian visceral leishmaniasis. Clin Diagn Lab Immunol. 2001 Nov. 8(6):1220-4. [Medline].

  20. Lemos EM, Carvalho SF, Corey R, Dietze R. [Evaluation of a rapid test using recombinant k39 antigen in the diagnosis of visceral leishmaniasis in Brazil]. Rev Soc Bras Med Trop. 2003. 36 Suppl 2:36-8. [Medline].

  21. Hartzell JD, Aronson NE, Weina PJ, Howard RS, Yadava A, Wortmann GW. Positive rK39 serologic assay results in US servicemen with cutaneous leishmaniasis. Am J Trop Med Hyg. 2008 Dec. 79(6):843-6. [Medline].

  22. Singh D, Pandey K, Das VN, Das S, Kumar S, Topno RK, et al. Novel noninvasive method for diagnosis of visceral leishmaniasis by rK39 testing of sputum samples. J Clin Microbiol. 2009 Aug. 47(8):2684-5. [Medline]. [Full Text].

  23. Alam MZ, Shamsuzzaman AK, Kuhls K, Schönian G. PCR diagnosis of visceral leishmaniasis in an endemic region, Mymensingh district, Bangladesh. Trop Med Int Health. 2009 May. 14(5):499-503. [Medline].

  24. Wortmann G, Hochberg L, Houng HH, Sweeney C, Zapor M, Aronson N, et al. Rapid identification of Leishmania complexes by a real-time PCR assay. Am J Trop Med Hyg. 2005 Dec. 73(6):999-1004. [Medline].

  25. Wall EC, Watson J, Armstrong M, Chiodini PL, Lockwood DN. Epidemiology of imported cutaneous leishmaniasis at the Hospital for Tropical Diseases, London, United Kingdom: use of polymerase chain reaction to identify the species. Am J Trop Med Hyg. 2012 Jan. 86(1):115-8. [Medline]. [Full Text].

  26. Ozcan D, Seçkin D, Allahverdiyev AM, Weina PJ, Aydin H, Ozçay F, et al. Liver transplant recipient with concomitant cutaneous and visceral leishmaniasis. Pediatr Transplant. 2007 Mar. 11(2):228-32. [Medline].

  27. [Guideline] Kaplan JE, Benson C, Holmes KK, Brooks JT, Pau A, Masur H. Guidelines for prevention and treatment of opportunistic infections in HIV-infected adults and adolescents: recommendations from CDC, the National Institutes of Health, and the HIV Medicine Association of the Infectious Diseases Society of America. MMWR Recomm Rep. 2009 Apr 10. 58:1-207; quiz CE1-4. [Medline].

  28. [Guideline] AIDSinfo.com. Clinical guidelines portal. Guidelines for the prevention and treatment of opportunistic infections in HIV-infected adults and adolescents: what’s new in the guidelines. July 8, 2013. Available at http://aidsinfo.nih.gov/contentfiles/lvguidelines/adult_oi.pdf. Accessed: April 14, 2014.

  29. Navin TR, Arana BA, Arana FE, Berman JD, Chajon JF. Placebo-controlled clinical trial of sodium stibogluconate (Pentostam) versus ketoconazole for treating cutaneous leishmaniasis in Guatemala. J Infect Dis. 1992 Mar. 165(3):528-34. [Medline].

  30. Wortmann G, Miller RS, Oster C, Jackson J, Aronson N. A randomized, double-blind study of the efficacy of a 10- or 20-day course of sodium stibogluconate for treatment of cutaneous leishmaniasis in United States military personnel. Clin Infect Dis. 2002 Aug 1. 35(3):261-7. [Medline].

  31. Sundar S, Chakravarty J, Agarwal D, Rai M, Murray HW. Single-dose liposomal amphotericin B for visceral leishmaniasis in India. N Engl J Med. 2010 Feb 11. 362(6):504-12. [Medline].

  32. Sundar S, Sinha PK, Rai M, et al. Comparison of short-course multidrug treatment with standard therapy for visceral leishmaniasis in India: an open-label, non-inferiority, randomised controlled trial. Lancet. 2011 Feb 5. 377(9764):477-86. [Medline].

  33. Sundar S, Agrawal G, Rai M, Makharia MK, Murray HW. Treatment of Indian visceral leishmaniasis with single or daily infusions of low dose liposomal amphotericin B: randomised trial. BMJ. 2001 Aug 25. 323(7310):419-22. [Medline].

  34. Avasthi R, Chaudhary SC, Khanna S. Visceral leishmaniasis simulating chronic liver disease: successful treatment with miltefosine. Indian J Med Microbiol. 2009 Jan-Mar. 27(1):85-6. [Medline].

  35. Ritmeijer K, Ter Horst R, Chane S, Aderie EM, Piening T, Collin SM, et al. Limited Effectiveness of High-Dose Liposomal Amphotericin B (AmBisome) for Treatment of Visceral Leishmaniasis in an Ethiopian Population With High HIV Prevalence. Clin Infect Dis. 2011 Oct 19. [Medline].

  36. Prasad R, Kumar R, Jaiswal BP, Singh UK. Miltefosine: an oral drug for visceral leishmaniasis. Indian J Pediatr. 2004 Feb. 71(2):143-4. [Medline].

  37. Impavido (miltefosine) prescribing information. [package insert]. Wilmington, DE: Paladin Therapeutics, Inc. 2014.

  38. Sundar S, Jha TK, Thakur CP, et al. Oral miltefosine for the treatment of Indian visceral leishmaniasis. Trans R Soc Trop Med Hyg. 2006 Dec. 100 Suppl 1:S26-33. [Medline].

  39. Rahman M, Ahmed BN, Faiz MA, Chowdhury MZ, Islam QT, Sayeedur R, et al. Phase IV trial of miltefosine in adults and children for treatment of visceral leishmaniasis (kala-azar) in Bangladesh. Am J Trop Med Hyg. 2011 Jul. 85(1):66-9. [Medline]. [Full Text].

  40. Investigational Drug Available Directly from CDC for the Treatment of Infections with Free-Living Amebae. MMWR Morb Mortal Wkly Rep. 2013 Aug 23. 62(33):666. [Medline].

  41. Nacher M, Carme B, Sainte Marie D, Couppie P, Clyti E, Guibert P, et al. Influence of clinical presentation on the efficacy of a short course of pentamidine in the treatment of cutaneous leishmaniasis in French Guiana. Ann Trop Med Parasitol. 2001 Jun. 95(4):331-6. [Medline].

  42. Dogra J. Current therapies for treatment of cutaneous leishmaniasis in India. Infection. 1992 Jul-Aug. 20(4):189-91. [Medline].

  43. Ozgoztasi O, Baydar I. A randomized clinical trial of topical paromomycin versus oral ketoconazole for treating cutaneous leishmaniasis in Turkey. Int J Dermatol. 1997 Jan. 36(1):61-3. [Medline].

  44. Alrajhi AA, Ibrahim EA, De Vol EB, Khairat M, Faris RM, Maguire JH. Fluconazole for the treatment of cutaneous leishmaniasis caused by Leishmania major. N Engl J Med. 2002 Mar 21. 346(12):891-5. [Medline].

  45. Machado PR, Ampuero J, Guimarães LH, Villasboas L, Rocha AT, Schriefer A, et al. Miltefosine in the treatment of cutaneous leishmaniasis caused by Leishmania braziliensis in Brazil: a randomized and controlled trial. PLoS Negl Trop Dis. 2010 Dec 21. 4(12):e912. [Medline]. [Full Text].

  46. Soto J, Toledo JT. Oral miltefosine to treat new world cutaneous leishmaniasis. Lancet Infect Dis. 2007 Jan. 7(1):7. [Medline].

  47. Ben Salah A, Ben Massaoud N, Guedri E, et al. Topical paromomycin with or without gentamicin for cutaneous leishmaniasis. N Engl J Med. 2013. 368:524-32.

  48. Keller DM. Novel noninvasive method for diagnosis of visceral leishmaniasis by rK39 testing of sputum samples. Medscape Medical News. February 7, 2013. Available at http://www.medscape.com/viewarticle/778974. Accessed: February 18, 2013.

  49. El-On J, Livshin R, Even-Paz Z, Hamburger D, Weinrauch L. Topical treatment of cutaneous leishmaniasis. J Invest Dermatol. 1986 Aug. 87(2):284-8. [Medline].

  50. Braunwald E, Fauci AS, Hauser SL, et al. Leishmaniasis. 15th ed. Harrison's Manual of Medicine. 2001: McGraw-Hill;

  51. Masmoudi A, Dammak A, Chaaben H, Maalej N, Akrout F, Turki H. Doxycycline for the treatment of cutaneous leishmaniasis. Dermatol Online J. 2008 Aug 15. 14(8):22. [Medline].

  52. Reithinger R, Mohsen M, Wahid M, Bismullah M, Quinnell RJ, Davies CR, et al. Efficacy of thermotherapy to treat cutaneous leishmaniasis caused by Leishmania tropica in Kabul, Afghanistan: a randomized, controlled trial. Clin Infect Dis. 2005 Apr 15. 40(8):1148-55. [Medline].

  53. Singh OP, Singh B, Chakravarty J, Sundar S. Current challenges in treatment options for visceral leishmaniasis in India: a public health perspective. Infect Dis Poverty. 2016 Mar 8. 5 (1):19. [Medline].

  54. Sindermann H, Engel KR, Fischer C, Bommer W; Miltefosine Compassionate Use Program. Oral miltefosine for leishmaniasis in immunocompromised patients: compassionate use in 39 patients with HIV infection. Clin Infect Dis. 2004 Nov 15. 39(10):1520-3. [Medline].

  55. Tiuman TS, Santos AO, Ueda-Nakamura T, Filho BP, Nakamura CV. Recent advances in leishmaniasis treatment. Int J Infect Dis. 2011 Aug. 15(8):e525-32. [Medline].

  56. Lemesre JL, Holzmuller P, Cavaleyra M, Gonçalves RB, Hottin G, Papierok G. Protection against experimental visceral leishmaniasis infection in dogs immunized with purified excreted secreted antigens of Leishmania infantum promastigotes. Vaccine. 2005 Apr 22. 23(22):2825-40. [Medline].

  57. Rubiano LC, Miranda MC, Muvdi Arenas S, Montero LM, Rodríguez-Barraquer I, Garcerant D, et al. Noninferiority of miltefosine versus meglumine antimoniate for cutaneous leishmaniasis in children. J Infect Dis. 2012 Feb 15. 205(4):684-92. [Medline]. [Full Text].

  58. Brooks M. FDA Clears Miltefosine (Impavido) for Leishmaniasis. Medscape Medical News. Mar 20 2014. [Full Text].

  59. Alvar J, Cañavate C, Gutiérrez-Solar B, Jiménez M, Laguna F, López-Vélez R, et al. Leishmania and human immunodeficiency virus coinfection: the first 10 years. Clin Microbiol Rev. 1997 Apr. 10(2):298-319. [Medline].

  60. World Health Organization. Essential leishmaniasis maps: cutaneous leishmaniasis. Available at http://www.who.int/leishmaniasis/leishmaniasis_maps/en/index1.html. Accessed: April 10, 2014.

  61. Zijlstra EE. Visceral leishmaniasis: a forgotten epidemic. Arch Dis Child. 2016 Feb 19. [Medline]. [Full Text].

 
Previous
Next
 
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.
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.