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leishmaniasis

 
Medical Encyclopedia: Leishmaniasis
 
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Definition

Leishmaniasis refers to several different illnesses caused by infection with an organism called a protozoan.

Description

Protozoa are considered to be the most simple organisms in the animal kingdom. They are all single-celled. The types of protozoa which cause leishmaniasis are carried by the blood-sucking sandfly. The sandfly is referred to as the disease vector, simply meaning that the infectious agent (the protozoan) is carried by the sandfly and passed on to other animals or humans in whom the protozoan will set up residence and cause disease. The animal or human in which the protozoan then resides is referred to as the host.

Once the protozoan is within the human host, the human's immune system is activated to try to combat the invader. Specialized immune cells called macrophages work to swallow up the protozoa. Usually, this technique kills a foreign invader, but these protozoa can survive and flourish within macrophages. The protozoa multiply within the macrophages, ultimately causing the macrophage to burst open. The protozoa are released, and take up residence within other neighboring cells.

At this point, the course of the disease caused by the protozoa is dependent on the specific type of protozoa, and on the type of reaction the protozoa elicits from the immune system. There are several types of protozoa which cause leishmaniasis, and they cause different patterns of disease progression.

At any one time, about 20 million people throughout the world are infected with leishmaniasis. While leishmaniasis exists as a disease in 88 countries around the globe, some countries are hit harder than others. These include Bangladesh, India, Nepal, Sudan, Afghanistan, Brazil, Iran, Peru, Saudi Arabia, and Syria. Other areas which harbor the causative protozoa include China, many countries throughout Africa, Mexico, Central and South America, Turkey, and Greece. Although less frequent, cases have occurred in the United States, in Texas.

In some areas of southern Europe, leishmaniasis is becoming an important disease which infects people with weakened immune systems. In particular, individuals with acquired immunodeficiency syndrome (AIDS) are at great risk of this infection.

— Rosalyn Carson-DeWitt, MD


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Dictionary: leish·man·i·a·sis   (lēsh'mə-nī'ə-sĭs) pronunciation
 
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n.
  1. An infection caused by any of the flagellate protozoans of the genus Leishmania, transmitted to humans and animals by bloodsucking sand flies.
  2. A disease, such as kala-azar or either of two clinically distinct ulcerative skin diseases, caused by flagellate protozoans of the genus Leishmania.

[From New Latin Leishmania, genus of protozoans, after Sir William Boog Leishman (1865–1926), British medical officer.]


 
Dental Dictionary: leishmaniasis
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n

An infection with any species of protozoan of the genus Leishmania.

 
Encyclopedia of Public Health: Leishmaniasis
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Leishmaniasis is caused by protozoan parasites of the genus Leishmania that are spread by the bite of female phlebotomine sand flies of the genus Phlebotomus in the Old World and Lutzomyia in the New World.

Approximately 350 million people in eighty-eight countries are thought to be at risk for leishmania infection. The true number of infected individuals is unknown, as it is not considered a reportable disease in many of the affected countries. The World Health Organization (WHO) estimates that twelve million people are infected and that there are between 1.5 and 2 million new cases each year.

Leishmania infection occurs in a variety of mammalian hosts, including the domestic dog, rodents, and sloths. When a sand fly, a night-biting insect, takes a blood meal from an infected mammal, it will ingest leishmania parasites, called amastigotes, along with the blood. Over seven days leishmania multiply in the flight muscles and develop into infective, flagellated promastigote forms. When the sand fly next takes a blood meal, these promastigotes are injected into a new mammalian host, where they transform back into the amastigote form and begin to divide. Leishmania species are obligate intracellular parasites that infect and replicate in mononuclear phagocytic cells such as macrophages. Infection can also occur via blood transfusion, shared intravenous needles, or, rarely, direct contact with skin lesions. The incubation period in humans is usually from three to eight months, but can be as short as two weeks or as long as several decades.

The spectrum of clinical manifestations caused by leishmania is divided into three broad categories: cutaneous, mucocutaneous, and visceral leishmaniasis. Cutaneous leishmaniasis is found worldwide and results in skin lesions ranging from a single, discrete, self-healing ulcer to diffuse progressive induration. The spectrum of disease is determined by the species of the parasite and the ability of the host to mount a cell-mediated response. A hyper-immune response causes destructive changes such as those seen in mucocutaneous disease, and a hypo-immune response results in visceral and diffuse cutaneous leishmaniasis. In Old World cutaneous leishmaniasis, the usual causative species are L. major, L. tropica, or L. aethiopica. In the Americas, cutaneous lesions are usually the result of infection with L. braziliensis, L. mexicana, L. amazonensis, or L. panamensis.

In mucocutaneous leishmaniasis (also called espundia), the infection causes destruction of mucous membranes of the nose, mouth, and throat. This form of leishmania is found almost exclusively in the Americas and is seen predominantly in a subset of patients infected with L. braziliensis. Diffuse cutaneous leishmaniasisis, caused by L. aethiopica, is characterized by induration of skin without ulceration.

Visceral leishmaniasis, or kala-azar, is the most severe form of infection with parasites disseminated throughout the reticuloendothelial system. Patients experience fevers, night sweats, and weight loss. The spleen and liver become enlarged, sometimes massively. Blood work reveals anemia, leucopenia, thrombocytopenia, and a marked increase in gamma-globulin levels. If untreated, visceral leishmaniasis is virtually always fatal.

It used to be thought that each species of leishmania resulted in a particular clinical syndrome. However, it is now being recognized that there is considerable overlap in the clinical presentation of each species. Most people bitten by leishmania-infected sand flies will never manifest any evidence of the infection. After recovery from leishmaniasis, a person is immune for life from reinfection by that strain.

Conditions that impair cell-mediated immunity can result in more severe, disseminated leishmanial infections. This has been seen in organ transplant recipients and, most importantly, in persons infected with HIV (human immunodeficiency virus), in whom visceral leishmaniasis has become a frequent opportunistic infection in endemic regions.

Diagnosis is made by microscopic identification of the parasite in tissue samples, by growing the organisms in culture, or by polymerase chain reaction (PCR) of tissue. PCR is a test that will identify even trace amounts of leishmanial DNA in tissue. Samples are taken from the edge or base of a skin ulcer in cutaneous disease. Bone marrow or splenic aspirates are the best tissue samples in cases of visceral disease. Testing for serum antibodies against leishmania parasites may be helpful.

Cutaneous lesions often heal spontaneously. Treatment is undertaken when the lesions are in cosmetically disfiguring areas, when the infection is widespread, and for certain leishmania spp. that are less likely to heal (e.g., L. brasiliensis). Pentavalent antimony (sodium stibogluconate, Pentostam), given either systemically or intralesionally, is the drug of choice for cutaneous lesions. Mucocutaneous and visceral leishmaniasis always require intravenous treatment with a pentavalent antimonial. Other effective medications for some species include amphotericin B (HIV-infected individuals) and pentamidine (for L. panamensis).

As there are many animal reservoirs of infection, and as elimination of sand flies is unlikely, control of leishmaniasis depends on avoiding exposure to sand flies. This involves a combination of insect repellent, fine-meshed bed nets, and protective clothing, and avoiding areas known to harbor sand flies.

(SEE ALSO: Communicable Disease Control; Tropical Infectious Diseases)

Bibliography

Arias, J. R.; Monteiro, P. S.; and Zicker, F. (1996). "The Reemergence of Visceral Leishmaniasis in Brazil." Emerging Infectious Diseases 2(2):145–146.

Berman, J. D. (1997). "Human Leishmaniasis: Clinical, Diagnostic, and Chemotherapeutic Developments in the Last 10 Years." Clinical Infectious Diseases 24:684–703.

Desowitz, R. S. (1991). "Kala Azar: The Long Anguish of the Black Sickness." In The Malaria Capers. New York: W. W. Norton & Company.

Evans, T. G. (1993). "Leishmaniasis." Infectious Disease Clinics of North America 7(3):527–546.

Hernandez-Perez, J. et al. (1999). "Visceral Leishmaniasis (Kala-azar) in Solid Organ Transplantation: Report of Five Cases and Review." Clinical Infectious Diseases 29:918–921.

Herwaldt, B. (1999). "Leishmaniasis." Lancet 354:1191–1199.

World Health Organization (2000). "The Leishmaniases and Leishmania/HIV Co-Infections—Fact Sheet No.116." WHO Information Fact Sheets. Geneva: Author.

— MARTHA FULFORD; JAY KEYSTONE


 
Britannica Concise Encyclopedia: leishmaniasis
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Human protozoal infection spread by the bite of a bloodsucking sand fly. It occurs worldwide but is especially prevalent in tropical areas. It is caused by various species of the flagellate protozoan Leishmania, which infect rodents and canines. Visceral leishmaniasis, or kala-azar, occurs throughout the world but is especially prevalent in the Mediterranean area, Africa, Asia, and Latin America; it affects the liver, spleen, and bone marrow and is usually fatal if not treated. Cutaneous leishmaniasis is endemic in areas around the Mediterranean, in central and northern Africa, and in southern and western Asia; it is also found in Central and South America and parts of the southern U.S. It is characterized by lesions on the skin of the legs, feet, hands, and face, most of which heal spontaneously after many months.

For more information on leishmaniasis, visit Britannica.com.

 
Columbia Encyclopedia: leishmaniasis
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leishmaniasis (lēsh'mənī'əsĭs) , any of a group of tropical diseases caused by parasitic protozoans of the genus Leishmania. The parasites live in dogs, foxes, rodents, and humans; they are transmitted by the bites of sand flies. There they infect the very white blood cells that normally would defend the body from such invaders. There are two forms of leishmaniasis. The more serious, called kala-azar or visceral leishmaniasis, affects the internal organs, causing fever, anemia, splenomegaly, and discoloration of the skin. Untreated, it can be fatal. The second, or cutaneous form, leaves deep, disfiguring sores at the site of the bite. Treatment is with amphotericin B and other drugs. Leishmaniasis is rarely seen in the United States, but is prevalent in South Asia, the Middle East, North Africa, and parts of the Mediterranean.

 
Wikipedia: Leishmaniasis
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Leishmaniasis
Classification and external resources
Cutaneous leishmaniasis in the hand of a Central American adult
ICD-10 B55.
ICD-9 085
DiseasesDB 3266 29171 3266 7070
MedlinePlus 001386
eMedicine emerg/296 
MeSH D007896

Leishmaniasis is a disease caused by protozoan parasites that belong to the genus Leishmania and is transmitted by the bite of certain species of sand fly (subfamily Phlebotominae). Two genera transmit Leishmania to humans: Lutzomyia in the New World and Phlebotomus in the Old World.[1]

Most forms of the disease are transmissible only from animals (zoonosis), but some can be spread between humans. Human infection is caused by about 21 of 30 species that infect mammals. These include the L. donovani complex with three species (L. donovani, L. infantum, and L. chagasi); the L. mexicana complex with 3 main species (L. mexicana, L. amazonensis, and L. venezuelensis); L. tropica; L. major; L. aethiopica; and the subgenus Viannia with four main species (L. (V.) braziliensis, L. (V.) guyanensis, L. (V.) panamensis, and L. (V.) peruviana). The different species are morphologically indistinguishable, but they can be differentiated by isoenzyme analysis, DNA sequence analysis, or monoclonal antibodies.

Cutaneous leishmaniasis is the most common form of leishmaniasis. Visceral leishmaniasis is a severe form in which the parasites have migrated to the vital organs.

Contents

Classification

Leishmaniasis may be divided into the following types:[2]:422–428

Geography and epidemiology

A 1917 case of Cutaneous Leishmaniasis in the Middle East, known then locally as "Jericho Buttons" for the frequency of cases near the ancient city of Jericho

Leishmaniasis can be transmitted in many tropical and sub-tropical countries, and is found in parts of about 88 countries. Approximately 350 million people live in these areas. The settings in which leishmaniasis is found range from rainforests in Central and South America to deserts in West Asia and the Middle East. It affects as many as 12 million people worldwide, with 1.5–2 million new cases each year.[3] The visceral form of leishmaniasis has an estimated incidence of 500,000 new cases and 60,000 deaths each year.[4] More than 90 percent of the world's cases of visceral leishmaniasis are in India, Bangladesh, Nepal, Sudan, and Brazil.

Leishmaniasis is found through much of the Americas from northern Argentina to southern Texas, though not in Uruguay or Chile, and has recently been shown to be spreading to North Texas.[5] During 2004, it is calculated that some 3,400 troops from the Colombian army, operating in the jungles near the south of the country (in particular around the Meta and Guaviare departments), were infected with Leishmaniasis. Apparently, a contributing factor was that many of the affected soldiers did not use the officially provided insect repellent, because of its allegedly disturbing odor. It is estimated that nearly 13,000 cases of the disease were recorded in all of Colombia throughout 2004, and about 360 new instances of the disease among soldiers had been reported in February 2005.[6][7][8]

The disease is found across much of Asia, though not Southeast Asia, and in the Middle East. Within Afghanistan, leishmaniasis occurs commonly in Kabul- partly due to bad sanitation and waste left uncollected in streets, allowing parasite-spreading sand flies an environment they find favorable.[9][10] In Kabul the number of people infected is estimated at at least 200,000, and in three other towns (Herat, Kandahar and Mazar-i-Sharif) there may be about 70,000 more, according to WHO figures from 2002.[11]

Africa, in particular the East and North, is home to cases of Leishamaniasis. The disease is spreading to Southern Europe but is not found in Australia or Oceania.

Leishmaniasis is mostly a disease of the Developing World, and is rarely known in the developed world outside a small number of cases, mostly in instances where troops are stationed away from their home countries. Leishmaniasis has been reported by U.S. troops stationed in Saudi Arabia and Iraq since the Gulf War of 1990, including visceral leishmaniasis.[12][13][14] In September 2005 the disease was contracted by at least four Dutch marines who were stationed in Mazari Sharif, Afghanistan, and subsequently repatriated for treatment.

Life cycle

Life cycle of Leishmania

Leishmaniasis is transmitted by the bite of female phlebotomine sandflies. The sandflies inject the infective stage, metacyclic promastigotes, during blood meals (1). Metacyclic promastigotes that reach the puncture wound are phagocytized by macrophages (2) and transform into amastigotes (3). Amastigotes multiply in infected cells and affect different tissues, depending in part on which Leishmania species is involved (4). These differing tissue specificities cause the differing clinical manifestations of the various forms of leishmaniasis. Sandflies become infected during blood meals on an infected host when they ingest macrophages infected with amastigotes (5,6). In the sandfly's midgut, the parasites differentiate into promastigotes (7), which multiply, differentiate into metacyclic promastigotes and migrate to the proboscis (8)

Signs and symptoms

The symptoms of leishmaniasis are skin sores which erupt weeks to months after the person affected is bitten by sand flies. Other consequences, which can become manifest anywhere from a few months to years after infection, include fever, damage to the spleen and liver, and anaemia.

In the medical field, leishmaniasis is one of the famous causes of a markedly enlarged spleen, which may become larger even than the liver. There are four main forms of leishmaniasis:

  • Visceral leishmaniasis – the most serious form and potentially fatal if untreated.
  • Cutaneous leishmaniasis – the most common form which causes a sore at the bite site, which heal in a few months to a year, leaving an unpleasant looking scar. This form can progress to any of the other three forms.
  • Diffuse cutaneous leishmaniasis – this form produces widespread skin lesions which resemble leprosy and is particularly difficult to treat.
  • Mucocutaneous leishmaniasis – commences with skin ulcers which spread causing tissue damage to (particularly) nose and mouth
Cutaneous leishmaniasis ulcer on left forearm

Diagnosis

Leishmaniasis is diagnosed in the haematology laboratory by direct visualization of the amastigotes (Leishman-Donovan bodies). Buffy-coat preparations of peripheral blood or aspirates from marrow, spleen, lymph nodes or skin lesions should be spread on a slide to make a thin smear, and stained with Leishman's or Giemsa's stain (pH 7.2) for 20 minutes. Amastigotes are seen with monocytes or, less commonly in neutrophil in peripheral blood and in macrophages in aspirates. They are small, round bodies 2-4μm in diameter with indistinct cytoplasm, a nucleus and a small rod-shaped kinetoplast. Occasionally amastigotes may be seen lying free between cells.[15]

Treatment

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There are two common therapies containing antimony (known as pentavalent antimonials), meglumine antimoniate (Glucantime) and sodium stibogluconate (Pentostam). It is not completely understood how these drugs act against the parasite; they may disrupt its energy production or trypanothione metabolism. Unfortunately, in many parts of the world, the parasite has become resistant to antimony and for visceral or mucocutaneous leishmaniasis,[16] but the level of resistance varies according to species.[17] Amphotericin is now the treatment of choice;[18] failure of AmBisome to treat visceral leishmaniasis (Leishmania donovani) has been reported in Sudan,[19] but this failure may be related to host factors such as co-infection with HIV or tuberculosis rather than parasite resistance.

Miltefosine (Impavido), is a new drug for visceral and cutaneous leishmaniasis. The cure rate of miltefosine in phase III clinical trials is 95%; Studies in Ethiopia show that it is also effective in Africa. In HIV immunosuppressed people who are coinfected with leishmaniasis it has shown that even in resistant cases 2/3 of the people responded to this new treatment. Clinical trials in Colombia showed a high efficacy for cutaneous leishmaniasis. In mucocutaneous cases caused by L.brasiliensis it has shown to be more effective than other drugs. Miltefosine received approval by the Indian regulatory authorities in 2002 and in Germany in 2004. In 2005 it received the first approval for cutaneous leishmaniasis in Colombia. Miltefosine is also currently being investigated as treatment for mucocutaneous leishmaniasis caused by Leishmania braziliensis in Colombia,[16] and preliminary results are very promising. It is now registered in many countries and is the first orally administered breakthrough therapy for visceral and cutaneous leishmaniasis.[20](More, et al., 2003). In October 2006 it received orphan drug status from the US Food and Drug administration. The drug is generally better tolerated than other drugs. Main side effects are gastrointestinal disturbance in the 1–2 days of treatment which does not affect the efficacy. Because it is available as an oral formulation, the expense and inconvenience of hospitalisation is avoided, which makes it an attractive alternative.

Paromomycin is said to be an inexpensive (US$10) and effective treatment for leishmaniasis.

The Institute for OneWorld Health has reintroduced the drug paromomycin for treatment of leishmaniasis, results with which led to its approval as an orphan drug. The Drugs for Neglected Diseases Initiative is also actively facilitating the search for novel therapeutics. A treatment with paromomycin will cost about $10. The drug had originally been identified in 1960s, but had been abandoned because it would not be profitable, as the disease mostly affects poor people.[21] The Indian government approved paromomycin for sale in August 2006.[22]

Drug-resistant leishmaniasis may respond to immunotherapy (inoculation with parasite antigens plus an adjuvant) which aims to stimulate the body's own immune system to kill the parasite.[23]

Several potential vaccines are being developed, under pressure from the World Health Organization, but as of 2006 none is available. The team at the Laboratory for Organic Chemistry at the Swiss Federal Institute of Technology (ETH) in Zürich are trying to design a carbohydrate-based vaccine [1]. The genome of the parasite Leishmania major has been sequenced,[24] possibly allowing for identification of proteins that are used by the pathogen but not by humans; these proteins are potential targets for drug treatments.

Peganum harmala

The compound vasicine (peganine), found in the plant Peganum harmala, has been tested in vitro against the promastigote stage of Leishmania donovani, the causative agent of visceral leishmaniasis. It was shown that this compound induces apoptosis in Leishmania promastigotes. "Peganine hydrochloride dihydrate, besides being safe, was found to induce apoptosis in both the stages of L. donovani via loss of mitochondrial transmembrane potential."[25]

Another alkaloid harmine found in Peganum harmala, ". . .because of its appreciable efficacy in destroying intracellular parasites as well as non-hepatotoxic and non-nephrotoxic nature, harmine, in the vesicular forms, may be considered for clinical application in humans."[26]

HIV Protease inhibitors have been found to be active against Leishmania species in two in vitro studies in Canada and India. The study reported that the intracellular growth of Leishmania parasites was controlled by nelfinavir and ritonavir in a human monocyte cell line and also in human primary monocyte-derived macrophages.[27]

Biology

A microbiologist working on L. major in a biocontainment hood

Leishmaniasis is caused by infection with the pathogen Leishmania. The genomes of three Leishmania species (L. major, L. infantum and L. braziliensis) have been sequenced and this has provided much information about the biology of the parasite. For example it is now understood that in Leishmania protein-coding genes are organized as large polycistronic units in a head-to-head or tail-to-tail manner; RNA polymerase II transcribes long polycistronic messages in the absence of defined RNA pol II promoters; and Leishmania has unique features with respect to the regulation of gene expression in response to changes in the environment. The new knowledge from these studies may help identify new targets for urgently needed drugs, and aid the development of vaccines.[1]

Vaccines

Currently there are no vaccines in routine use. However, the genomic sequence of Leishmania has provided a rich source of vaccine candidates. Genome-based approaches have been used to screen for novel vaccine candidates. One study screened 100 randomly selected genes as DNA vaccines against L. major infection in mice. Fourteen reproducibly protective novel vaccine candidates were identified. A separate study used a two-step procedure to identify T cell antigens. Six unique clones were identified: glutamine synthetase, a transitional endoplasmic reticulum ATPase, elongation factor 1gamma, kinesin K-39, repetitive protein A2, and a hypothetical conserved protein. The 20 antigens identified in these two studies are being further evaluated for vaccine development.[28]

History

Descriptions of conspicuous lesions similar to cutaneous leishmaniasis (CL) has been discovered on tablets from King Ashurbanipal from the 7th century BC, some of which may have been derived from even earlier texts from 1500 to 2500 BC. Muslim physicians including Avicenna in the 10th century AD gave detailed descriptions of what was called Balkh sore.[29] In 1756, Alexander Russell, after examining a Turkish patient, gave one of the most detailed clinical descriptions of the disease. Physicians in the Indian subcontinent would describe it as Kala-azar (pronounced kālā āzār, the Urdu, Hindi and Hindustani phrase for black fever, kālā meaning black and āzār meaning fever or disease). As for the new world, evidence of the cutaneous form of the disease was found in Ecuador and Peru in pre-Inca potteries depicting skin lesions and deformed faces dating back to the first century AD. 15th and 16th century texts from the Inca period and from Spanish colonials mention "valley sickness", "Andean sickness" or "white leprosy" which are likely to be CL.[30]

Who first discovered the organism is somewhat disputed. It is possible that Surgeon major Cunningham of the British Indian army saw it first in 1885 without being able to relate it to the disease.[31][32] Peter Borovsky, a Russian military surgeon working in Tashkent, conducted research into the etiology of oriental sore, locally known as Sart sore, and in 1898 published the first accurate description of the causative agent, correctly described the parasite's relation to host tissues and correctly referred it to Protozoa. However, because his results were published in Russian in a journal with low circulation, his priority was not internationally acknowledged during his lifetime.[33] In 1901, Leishman identified certain organisms in smears taken from the spleen of a patient who had died from "dum-dum fever" (Dhum dhum is an area close to Calcutta) and in 1903 Captain Charles Donovan (1863–1951) described them as being new organisms.[30] Eventually Ronald Ross established the link with the disease and named the organism Leishmania donovani. The disease was a major problem for Allied troops fighting in Sicily during the Second World War, and it was then that research by Leonard Goodwin showed that Pentostam was an effective treatment.[34]

Leishmaniasis as part of the CVBDs

CVBD stands for Canine Vector-borne diseases, which are diseases transmitted through Ectoparasites.

See also

References

  1. ^ a b Myler P; Fasel N (editors). (2008). Leishmania: After The Genome. Caister Academic Press. ISBN 978-1-904455-28-8. http://www.horizonpress.com/leish. 
  2. ^ James, William D.; Berger, Timothy G.; et al. (2006). Andrews' Diseases of the Skin: clinical Dermatology. Saunders Elsevier. ISBN 0-7216-2921-0. 
  3. ^ Leishmaniasis. Seattle Biomedical Research Institute.
  4. ^ Hope for tropical disease vaccine. BBC News. April 23, 2006.
  5. ^ "Houston Chronicle: Texas Doctors Find Skin Disease Moving North". http://www.chron.com/disp/story.mpl/headline/metro/5137795.html. Retrieved on 2007-09-15. 
  6. ^ leishmaniasis un brote serio[dead link]
  7. ^ Nota interior[dead link]
  8. ^ Welcome to www.serviciojesuitaarefugiados-vzla.org[dead link]
  9. ^ Al Jazeera English - CENTRAL/S. ASIA - Kabul: A city in intensive care
  10. ^ e-Ariana - Todays Afghan News
  11. ^ e-Ariana - Todays Afghan News
  12. ^ 650 U.S. Troops Deployed in Iraq Infected with Leishmaniasis
  13. ^ Business: Company's mesh will help troops beat 'Baghdad boils'
  14. ^ http://www.pdhealth.mil/downloads/Leishmaniasis_exsu_16Mar042.pdf
  15. ^ Dacie, John V.; Bain, Barbara J.; Imelda Bates (2006). Dacie and Lewis practical haematology. Philadelphia: Churchill Livingstone/Elsevier. ISBN 0-443-06660-4. 
  16. ^ a b Soto, J., Toledo, J. T. (2007). "Oral miltefosine to treat new world cutaneous leishmaniasis". Lancet Infect Dis 7 (1): 7. doi:10.1016/S1473-3099(06)70665-X. PMID 17182338. http://linkinghub.elsevier.com/retrieve/pii/S1473-3099(06)70665-X. 
  17. ^ Arevalo J, Ramirez L, Adaui V, et al. (June 2007). "Influence of Leishmania (Viannia) species on the response to antimonial treatment in patients with American tegumentary leishmaniasis". J. Infect. Dis. 195 (12): 1846–51. doi:10.1086/518041. PMID 17492601. http://www.journals.uchicago.edu/doi/abs/10.1086/518041?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dncbi.nlm.nih.gov. 
  18. ^ Sundar S, Chakravarty J, Rai VK, et al. (September 2007). "Amphotericin B treatment for Indian visceral leishmaniasis: response to 15 daily versus alternate-day infusions". Clin. Infect. Dis. 45 (5): 556–61. doi:10.1086/520665. PMID 17682988. http://www.journals.uchicago.edu/doi/abs/10.1086/520665?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dncbi.nlm.nih.gov. 
  19. ^ Mueller M, Ritmeijer K, Balasegaram M, Koummuki Y, Santana MR, Davidson R (January 2007). "Unresponsiveness to AmBisome in some Sudanese patients with kala-azar". Trans. R. Soc. Trop. Med. Hyg. 101 (1): 19–24. doi:10.1016/j.trstmh.2006.02.005. PMID 16730363. http://linkinghub.elsevier.com/retrieve/pii/S0035-9203(06)00101-5. 
  20. ^ Jha TK, Sundar S, Thakur CP et al. (1999). "Miltefosine, an oral agent, for the treatment of Indian visceral leishmaniasis". New Engl J Med 341: 1795–800. doi:10.1056/NEJM199912093412403. PMID 10588964. 
  21. ^ A Small Charity Takes the Reins in Fighting a Neglected Disease, New York Times, July 31, 2006.
  22. ^ NEW CURE FOR DEADLY VISCERAL LEISHMANIASIS (KALA-AZAR) APPROVED BY GOVERNMENT OF INDIA, Institute for OneWorld Health Press Release, Sept 8, 2006.
  23. ^ Badaro R, Lobo I, Munos A, et al. (October 2006). "Immunotherapy for drug-refractory mucosal leishmaniasis". J. Infect. Dis. 194 (8): 1151–9. doi:10.1086/507708. PMID 16991091. http://www.journals.uchicago.edu/doi/abs/10.1086/507708?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dncbi.nlm.nih.gov. 
  24. ^ Ivens AC, et al. (2005). "The genome of the kinetoplastid parasite, Leishmania major". Science 309 (5733): 436–42. doi:10.1126/science.1112680. PMID 16020728. 
  25. ^ Misra P. et al. (2008). "Antileishmanial activity mediated by apoptosis and structure-based target study of peganine hydrochloride dihydrate: an approach for rational drug design.". Journal of Antimicrobial Chemotherapy 62 (5): 998–1002. doi:10.1093/jac/dkn319. PMID 18694906. 
  26. ^ Lala S. et al. (2004). "Harmine: evaluation of its antileishmanial properties in various vesicular delivery systems.". Journal of Drug Targeting 12 (3): 165–75. doi:10.1080/10611860410001712696. PMID 15203896. 
  27. ^ Trudel N. et al. (2008). "Intracellular survival of Leishmania species that cause visceral leishmaniasis is significantly reduced by HIV-1 protease inhibitors". Journal of Infectious Diseases 198 (9): 1292–1299. doi:10.1086/592280. 
  28. ^ Myler P; Fasel N (editors). (2008). Leishmania: After The Genome. Caister Academic Press. ISBN 978-1-904455-28-8. http://www.horizonpress.com/leish. 
  29. ^ Cox, Francis E G (1996). The Wellcome Trust illustrated history of tropical diseases. London: The Wellcome Trust. pp. 206–217. ISBN 1869835867, 9781869835866. OCLC 35161690. http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=126866#id2621583. 
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External links

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Infectious diseases - Parasitic disease: protozoan infection: unicellular bikont (A06-A07, B50-B64)
Chromalveolate
Excavata
Leishmaniasis
Archaeplastida

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