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Epidemiology and Ecology of Leishmaniasis

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Tonay Inceboz

Submitted: November 10th, 2018 Reviewed: April 15th, 2019 Published: October 22nd, 2019

DOI: 10.5772/intechopen.86359

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Leishmaniasis is the third most important vector-borne disease after malaria and lymphatic filariasis. It is common disease in all over the world. The vector for leishmaniasis is Phlebotomus and there have found around 20 different types of this vector. There are different clinical forms under the name of leishmaniasis such as kala-azar, dum-dum fever, white leprosy, espundia, pian bois, chiclero’s ulcer, uta. Environmental factors leading to climate changes and global warming are major risk factors for the spreading of the disease. Leishmania spp. to prevent the spread of the definitive host and intermediate hosts is difficult compared to Plasmodium spp. Therefore; leishmaniasis disease will retain its importance for many years.


  • leishmaniasis
  • neglected tropical diseases
  • vector-borne disease
  • epidemiology
  • ecology

1. Introduction

This fact is mainly due to the presence of many different species of leishmania, its vectors and hosts in different parts of the world. More than 20 pathologic species of leishmaniaand over 30 species of Phlebotomus—the vector- are known worldwide (Figure 1, Table 1).

Figure 1.

Taxonomy ofleishmaniafamily [1].

Old WorldL. donovaniL. major
L. infantumL. tropica
L. killickia
L. aethiopica
L. infantum
New WorldL. infantumL. infantumL. braziliensisL. braziliensis
L. mexicanaL. guyanensisL. panamensis
L. pifanoiaL. panamensis
L. venezuelensisL. shawi
L. garnhamiaL. naïffi
L. amazonensisL. lainsoni
L. lindenbergi
L. peruviana
L. colombiensisb
Principal tropismViscerotropicDermotropicDermotropicMucotropic

Table 1.

Leishmaniafound in humans [1].

Species status is under discussion.

Taxonomic position is under discussion.

On the other hand, deterioration of the eco-systems by human beings also contribute to the spread of the disease in the world.

Leishmaniasis has four clinical forms. These are cutaneous leishmaniasis (CL, local—LCL or diffuse—DCL), mucocutaneous leishmaniasis (MCL), visceral leishmaniasis (VL), post-kala-azar dermal leishmaniasis (PKDL), (Table 1).

In this section we aimed to reveal the epidemiologic analysis of different types of leishmaniasis in all over the world in every aspect.


2. Geographic distribution and incidence

Leishmaniasis, as being one of the world’s most neglected diseases, affects mainly the poor, developing countries; 350 million people are thought to be at risk of contracting leishmaniasis. It is estimated that approximately 12 million men are ill and 2 million new cases occur annually [1, 2].

With new epidemics occurring in endemic areas and the spread of leishmaniasis to previously free areas because of migration, tourism, and military activities. Leishmaniasis is a disease of the poor, occurring mostly in remote rural villages with poor housing and little or no access to modern health-care facilities. In endemic areas, diagnosis of any form of leishmaniasis puts a huge financial strain on an already meagre financial resource at both the individual and community levels [3].

Visceral leishmaniasis: approximately 90% of new cases occur in the world’s cases of India, Bangladesh, Nepal, Ethiopia, Sudan and Brazil are seen. The annual number of cases worldwide has been estimated to be visceral leishmaniasis, between 200,000 and 400,000. The two important causative agents of visceral leishmaniasis (VL), namely Leishmania(L) donovaniand L. infantum, cause significant health problems [1, 4].

Visceral leishmaniasis (VL), also known as “kala azar,” is caused by parasites of the L. donovanicomplex in some parts of the world. The L. donovanicomplex can be found throughout Asia, North Africa, Latin America and Southern Europe, affecting mostly vulnerable and uncared populations. As being the most severe form, VL is almost always fatal if left untreated. It is characterized by undulating fever, loss of weight, splenomegaly, hepatomegaly and/or lymphadenopathies and anemia L. infantum, the other causative agent of VL, is found in Southern Europe, North Africa and West and Central Asia [1, 5].

Post-kala-azar dermal leishmaniasis (PKDL) is another clinical composition of kala azar and it is seen in all areas endemic for L. donovani. It especially comments in East Africa and on the Indian subcontinent with a prevalence of 50 and 10%, respectively [1, 6].

Cutaneous leishmaniasis: approximately 90% of the world’s cases of Afghanistan, Pakistan, Sudan, Syria, Saudi Arabia, Algeria, Iran, Iraq, is seen in Brazil and Peru. The annual number of cases worldwide has been estimated to be visceral leishmaniasis, cutaneous leishmaniasis: between 700,000 and 1.2 million [1]. Old World species: L. major, L. infantum, and L. tropica, New World species, such as, L. amazonensis, L. chagasi, L. mexicana, L. viannia(V) naiffi, L.(V.) braziliensis, and L.(V.) guyanensis[6, 7]. Antroponotic cutaneous leishmaniasis (ACL) is caused by most Leishmaniaspecies, occur in most subtropical and tropical regions (for example, L. majorfrom Africa and Asia, and L. mexicanafrom Central and South America), and by many species in the subgenus Viannia, which are limited to Latin America (for example, L. (V) brasiliensis) [6].

Old World cutaneous leishmaniasis caused by L. tropica(seen particularly in the Mediterranean Basin, the Middle East, Pakistan and India) and L. infantum, (found sporadically in the Middle East, South Russia, and rural regions of Africa). New World cutaneous leishmaniasis, caused by L. brazilensisand L. mexicanais seen in Mexica and South America. Leishmaniasis exists on every continent except Australia, the Pacific Islands and Antarctica. The parasites that cause leishmaniasis are found in 98 countries around the world [7].

L. tropica, L. major, L. aethiopicaand L. infantumcauses Old World cutaneous leishmaniasis. Leishmania tropicais mainly seen in urban areas and causes ACL. Related vectors are Phlebotomus sergentiand Phlebotomus papatasii. Lesions are generally dry and remain without ulceration. During the course lesions change to papules [1, 8].

L. tropicais found in urban areas. It causes ACL via the vectors Phlebotomus sergentiand Phlebotomus papatasii. The lesions are dry and stay for a long period of time without ulceration. Thereafter, painless lesions as papules, tubercles or nodules subside without scarring in 9–12 months [8].

L. majorinfections generally cause wet lesions in habitants of rural areas. Incubation period is less than 4 months. Lesions are usually seen on the legs. They start as acute papillary infection in the bite area and advances into pustular ulcers in 1–3 weeks. The infection is categorized as “zoonotic cutaneous leishmaniasis (ZCL)” due to the transmission to rodents, dogs via Phlebotomus papatasi[9].

L. infantumoften causes small (0.5–1 cm), solitary ulcers on the face [10].

L. aetropicalesions are seen in the mouth and nose with local or wide spread dermal involvement. Lesions rarely become ulcerated. Healing may take 1–3 years or more [11].

L. braziliensis, L. mexicana, L. amazoensis, L. guyanensis, L. panamensisand L. peruvianacause New World cutaneous leishmaniasis [8, 12].

The disease caused by L. braziliensisis named “espundia.” The infection leads to metastatic lesions, damages and deformation of the cartilage and soft tissues by affecting buccal and nasal mucosa [13].

L. mexicanacauses usually solitary, painless lesions in the pinna. It leads to chronic lesions in the pinna called “chiclero’s ulcer” [14].

L. guyanensisinfection is consisted of flat ulcerative plaques with leakage in whole body. The lesion is called “pianbois” in Uruguay and Venezuella [15].

L. amazonensiscauses solitary or multiple lesions with rarely spontaneous remission. It is rare in humans [8].

L. peruvianainfection causes solitary or multiple painless dermal lesions they usually subsided spontaneously in 4–5 months. This infection is called uta [16].

Lesions of L. panamensisare ulcers without spontaneous improvement the reservoirs are dogs and monkeys [12].

L. venezuelensisgenerally causes solitary painless nodular lesion. [12, 17].

L. garnhamiusually causes solitary or multiple lesions and may spontaneously be healed in 6 months [12].

The Eastern Hemisphere (Old World): leishmaniasis is found in some parts of Asia, the Middle East, Africa (especially in the tropical region and North Africa), and Southern Europe.

The Western Hemisphere (New World), leishmaniasis is found in some parts of Mexico, Central America, and South America. It is not found in Chile or Uruguay.

Leishmaniasis is seen in most tropical and subtropical regions with climate, mainly in South and Central America, Africa, Asia, and Southern Europe. The leishmaniasis is considered as one of the neglected tropical diseases (NTD) (Figures 2 and 3) [18].

Figure 2.

World VL distribution in the last 10 years [19].

Figure 3.

World CL distribution in the last 10 years [19].


3. Epidemiology of leishmaniasis according to vector

  1. Phlebotomusspp. (sandfly). (Old World).

  2. Lutzomyiaspp. (New World).

Humidity and moisture, whether from rainfall or in the soil, have often been identified as important for the sandfly, with humidity influencing breeding and resting [6].

Sandflies belonging to either Phlebotomusspp. (Old World) or Lutzomyiaspp. (New World) are the primary vectors; domestic dogs, rodents, sloths, and opossums are amongst a long list of mammals that are either incriminated or suspected reservoir hosts [1, 21, 22]. Most of its foci in the Old World have a Mediterranean climate and sand fly vectors, usually Phlebotomus(Larroussius) species, Phlebotomusspecies (P. papatasi, P. sergenti, Phlebotomus alexandri, P. tobbi, Phlebotomus syriacus, Phlebotomus neglectus, Phlebotomus perfiliewi, Phlebotomus galilaeus, Phlebotomus transcaucasicus, and Phlebotomus halepensis) two Sergentomyiaspecies (Sergentomyia theodoriand Sergentomyia dentata), (Phlebotomus ariasiand Phlebotomus perniciosus, Phlebotomus longicuspis) can diapauses for human visceral leishmaniasis [21, 22, 23, 24].

In contrast to malaria, there is little evidence for the effect of vector control in leishmaniasis because terrestrial habitat of Phlebotomusis mostly unknown.


4. Host

4.1 Human

Leishmaniaspecies are transmitted to human via vectors, blood transfusion, organ transplantation or vertically via transplacental route. Other factors that cause the transmission of the disease are contact with contaminated materials or needle stick injuries in the labs [25, 26, 27].

Leishmania-infected humans especially in poor socioeconomic conditions play a pivotal role as a reservoir in transmission of the agent to vectors or to other hosts. In another words, one can say that human beings contribute the disease transmission by themselves [26, 27]. Poor living conditions in adobe, wooden houses, barns create a tendency towards an increase of vectors [27, 28, 29].

In all three clinical types of Leishmaniaspp., antimonials (sodium stibogluconate [SSG]), miltefosin (MIL), amfoterisin B (AmB) veparomomisin (PMM)) are being used [30]. Children and people with immune suppression, HIV infection or malignant diseases cause rapid spread of leishmaniasis. Apart from these, undiagnosed or untreated infected people create an important risk factor. Especially drug resistance and high expense of the medication cause insufficient treatment [27, 28, 29]. The first drug resistance was reported in VL treatment against SSG and against MIL, in India and Nepal, respectively [31, 32, 33]. Later, resistance against MIL was also reported in one patient with HIV and another two patients with Indian origin [34, 35].

Verma et al. showed that the effectiveness of PMM was decreased by 6 times for the promastigote forms of L. donavani[36]. Invasion of macrophages by PMM-R parasites led to increased nitric oxide (NO), whereas the levels of reactive oxygen species (ROS) remained unchanged. This finding shows resistance of Leishmaniaspp. against PMM [36]. Similarly, Deep et al., reported high recurrence rates in patients with VL and PKDL when treated with MIL [37].

In conclusion, due to immune problems of the patient, co-existence of other diseases, inappropriate use of the drugs during the medical treatment of leishmaniasis, “drug resistance” may occur via gene over-expression, deletion, single nucleotide polymorphisms generating stop codons or amplification of sets of genes [38, 39, 40]. This very important for epidemiological standpoint and thus proper use of drugs when needed should be stressed, and also new drug formulations and/or vaccine should be investigated.

Technological advances let the people travel all over the world. This may cause vectored spread or spread directly by infected people [41].

4.2 Dogs

Dogs are very important in terms of the epidemiology of leishmaniasis. All forms of leishmaniasis namely cutaneous, mucocutaneous and visceral types may be found in dogs. Since the infected dogs are important reservoir of the disease, their controls and treatments are mandatory for the disease control. Dogs as pets are being controlled by vets however stray or wild dogs, fox species like Lycalopex vetulus[42], Cerdocyonthous[43] may cause outbreaks. Dogs are natural hosts for L. infantum, L. chagasi, L. tropicaand L. peruvianaas well as being infected by them. Especially they are endemic in dogs in Mediterranean region, Asia and Latin America. Leishmania infantumis the causative agent of visceral leishmaniasis and it is prevalent especially in Mediterranean region. Vectors for this type are Phlebotomus ariasi, P. major, P. perniciosus, P. longicuspis, P. chiensis, P. mongolensis, P. papatasi[44, 45]. In the same region, the causative agent of zoonotic cutaneous leishmaniasis is L. tropicaand the vectors are P. perfilievi, P. papatasiand P. sergenti[1, 46]. In South America, the causative agent of canine cutaneous leishmaniasis is L. chagasiand the vectors are Lu. longipalpalis, Lu. evansi, Lu. gomezi[1].

4.3 Rodents

Comparing to dogs, eradication of the infectious agent of leishmaniasis from the rodents is more difficult and even sometimes impossible.

Different rodents such as Didelphis albiventris(opossum), Mus musculus(domestic mouse), Microtus socialis, Rattusrattus(black rat), Cercomys cunicularius(wild rat), Mesocricetus auratus(Syrian hamsters) in America, Africa and Asia lead to spread of leishmaniasis [47, 48, 49, 50, 51].

Phlebotomus papatasi, vector of L. tropica, transmitted cutaneous leishmaniasis to small rodents such as Psammomys obesus(Israel), Meriones crassus(Israel), Meriones libycus(Iran), Rhombomys opimus(Iran), Rhombomys opimus(Iran), Meriones sacramenti(Egypt) [9].

Rattus rattusand Rattus norvegicushave been found naturally infected with L. infantumin the Mediterranean and in Next Orient endemic areas (Table 2) [49, 52, 53].

LeishmaniaspeciesDiseaseCountries (suspected)LandscapesReservoir hostsVector
Old World
L. donovaniAVL, DCL, CLNortheast India, Nepal, Bangladesh, (Bhutan), Sri Lanka, Republic of China, Sudan, Ethiopia, (Chad), (Yemen), KenyaRural, peri-domesticHuman anthroponosisP. (Eu.) argentipes, P. (La.) orientalis, P. (Sy.) martini
L. donovaniAVLPeople’s Republic of ChinaRural, peri-domesticUnknownP. (Pa.) alexandri, P. (Ad.)species
L. donovanib(L. archibaldi)AVL, ZVL, MLSudan, Ethiopia, (Chad), (Yemen)Rural, Acacia—BalanitesforestHuman anthroponosisP.(Larroussius) orientalis
L. donovanib(L. archibaldi)AVL, DCLSudan, Ethiopia, Kenya, (Uganda)Rural, savannatermite moundsHuman anthroponosisP. (Sy.) martini
L. infantumZVL, ZCLMed Europe, North Africa, Southwest Asia, People’s Republic of ChinaRural, peri-domesticDomestic dog, wild canids, domestic catP. (La.) ariasi, perniciosus
L. infantumc(L. chagasi)VL, CLLatin America: not Peru or GuianasRural, peri-domesticDomestic dog, wild canidsLu. (L.) longipalpis
L. majorZCLNorth Africa, Ethiopia, Kenya, Sudan, Meadle Asia IndiaPeri-domesticHuman anthroponosisP. papatasi, P. duboscqi
Le.(Le.) tropicaACLNorth Africa, Middle East, Iran, AfghanistanUrbanPeridomestic, including suburbs; humanP.(Paraphlebotomus) sergenti
Le.(Le.) tropicac (Le.(Le.) killicki)ZCLNorth Africa, MiddleEast, Sub-Saharan AfricaRuralRockyarid; hyraxes, RodentsP.(Adlerius) arabicus P.(La.) guggisbergi
Le.(Le.) aethiopica;ZCL,DCL, MLEthiopia, KenyaRural, Rocky highlandsHyraxesP.(La.) longipes P.(La.) pedifer
New World
Leishmania(Leishmania) infantumZVL, ZCLLatin America: not Peru, GuianasPeridomestic, including suburbsDomestic dogLutzomyia(Lutzomyia) longipalpiss.l.
Leishmania(Viannia) braziliensisZCL, MLEast of Andes: not Guyana, SurinamePeridomestic, silvaticRodents, marsupials, dogL.(Psychodopygus) wellcomei L.(Nyssomyia) neivai L.(Ny.) whitmani
Le.(V.) braziliensisZCL, MLWest of Andes, northern Venezuela: not El SalvadorPeridomestic, silvaticRodents, marsupials, dogL.(Pifanomyia) ovallesi
Le.(V.) peruvianaZCL, MLPeruPeridomestic, silvaticRodents, marsupials, dogL.(He.) peruensiss.l. L.(Pf.) verrucarums.l.
Le.(V.) guyanensisZCL, MLEast of Andes: not ParaguaySilvaticArboreal edentates, othersL.(Ny.) umbratilis
Le.(V.) panamensisZCL, MLWest of Andes, northern Venezuela: not Mexico, Belize, El SalvadorSilvaticArboreal edentates, othersL.(Ny.) trapidoi L.(Ny.) ylephiletor L.(Ny.) edentula L.(Tricholateralis) gomezi
Le.(V.) shawiZCLBrazilSilvaticArborealL.(Trichophoromyia) ubiquitalis L.(Pf.) nuneztovari
Le.(V.) lainsoniZCLBolivia, Peru, Brazil, French Guiana, SurinameSilvaticRodent Agouti pacaL.(Trichophoromyia) ubiquitalis L.(Pf.) nuneztovari
Le.(V.) colombiensisZCLPanama, Colombia, VenezuelaSilvaticCholoepushoffmanniL.(He.) hartmanni
Le.(V.) naiffiZCLBrazil, French Guiana, PanamaSilvaticDasypusnovemcinctusL.(Ps.) ayrozaiand other species L.(Ny.) trapidoic
Le.(Le.) amazonensisZCL, DCLEast of Andes: not Guyana, ParaguaySilvatic, non-climax forestTerrestrial rodents, MarsupialsL.(Ny.) flaviscutellata
Le.(Le.) mexicanaZCL, DCL, MLWest of Andes, southern United States: not PeruSilvatic, non-climax forestTerrestrial rodents, MarsupialsL.(Ny.) olmecaolmeca
Le.(Le.) venezuelensisZCL, DCLNorthern VenezuelaSilvaticUnknownL.(Ny.) olmecabicolor

Table 2.

Disease types and transmission cycles of leishmaniasis worldwide [6, 20, 21].

Abbreviations: TC, transmission cycle; A, anthroponotic; Z, zoonotic; V, visceral; C, cutaneous; M, mucosal; D, diffuse; L, leishmaniasis. P., Phlebotomus; Pa., Paraphlebotomus; Pf., Pifanomyia; Sy., Synphlebotomus La., Larroussius; Lu., Lutzomyia.


5. Transmission cycle

There are two different types of transmission;

  1. In many geographic areas, infected people are not needed to sustain the transmission cycle of the parasite in nature; transmission cycle continue via the infected animals (rodents or dogs, felines). Leishmaniainfection in reservoir animals are specifically named; if it is in dogs, it is named as canine leishmaniasis whereas in cats, it is called feline leishmaniasis dogs species of Leishmaniaspecies in the reservoir in animals, canine leishmaniasis, which is in feline called leishmaniasis. L. infantumis the most common and important cause of canine leishmaniasis worldwide. The zoonotic transmissionof L. infantum, from canine to humans, is not only in the Mediterranean region where it may have originated, but also it may be found in many of the drier regions of Latin America. Leishmaniaspecies reported from dogs include L. mexicana, L. donovani, and L. braziliensis. These Leishmaniaspecies are occasionally reported from the cats. Cats are at risk of infection especially in areas where these parasites are endemic [6, 54, 55].

  2. In some parts of the world, infected people are needed to sustain the cycle; this kind of transmission (human—Phlebotomus—human) is called anthroponotic transmission.

Full knowledge on these two transmission cycles is very important in effective prevention of leishmaniasis [54, 55].


6. Effect of deteriorated eco-system on spread of leishmaniasis

Unlike other parasites, it is extremely difficult to eradicate whole kinds of species of Leishmaniain nature. This is contrary to some other parasites. As example Plasmodium vivaxis specific to human, thus it can be eradicated by vector control. However, this is not the case for Leishmaniaspp. [54, 55].

There are many check points to establish the control of the disease. Firstly, all patients with leishmaniasis should be properly treated. Leishmaniatransmission is dependent on the togetherness of contaminated sandflies with the reservoir hosts, and humans. Additionally, climatic and environment factors are important, too.

As the development of chemical insecticides use such as dichlorodiphenyltrichloroethane (DDT) against mosquito was a key component of the eradication, similarly they were proposed to have an effect on the sandflies, vectors of visceral leishmaniasis [56, 57, 58]. Since DDT use is found to be harmful to the environment and people, its use is prohibited by the World Health Organization [59]. At the moment there isn’t any strategy to control Phlebotomineby using insecticides by governments [60, 61]. Preliminary experiments for developing a vaccine against Leishmaniaspp. was reported [62]. However, the vaccine did not appear to protect against visceral leishmaniasis [63]. fucose-mannose ligand from an extract of L. donovanihas been used in conjunction with a saponin adjuvant in attempts to vaccine [64]. Further studies are needed to develop an effective vaccine against leishmaniasis.


7. Summary

Leishmaniasis is still an important parasite disease in all over the world. The reasons are presence of many different species of Leishmania, and their ability to survive in many different organisms, such as vectors, dogs, rodents, humans. Leishmaniaspp. may cause different clinical scenarios by affecting different tissues and organs. As eukaryotic cells, Leishmaniaspp. can survive in the immune system of the most advanced organism, human. Presence of amastigote forms even in the hosts’ defensive cells shows the strength of the parasite.

Leishmaniasis is an important public health problem. Thus, relevant public health policies such as education of the people especially in endemic areas, multidisciplinary approach, diagnosis, treatment will be helpful in the elimination of the disease. Additionally, further epidemiological studies as well as vaccination studies will continue to strive for eradication.


  1. 1. WHO Expert Committee. Control of the leishmaniasis: Report of a meeting of the WHO Expert Committee on the Control of Leishmaniases, Geneva, 2010; 22-26 March. WHO Technical Report Series; 949:1-186. Available from:
  2. 2. Ghaffar A. Microbiology and Immunology Online, Parasıtology—Chapter Two Blood and Tıssue Protozoa Part 1 Trypanosomiasıs and Leishmaniasis. 2013. Available from:
  3. 3. Okwor I, Uzonna J. Social and economic burden of human leishmaniasis. The American Journal of Tropical Medicine and Hygiene. 2016;94(3):489-493. DOI: 10.4269/ajtmh.15-0408
  4. 4. Zijlstra EE. Visceral leishmaniasis: A forgotten epidemic. Archives of Disease in Childhood. 2016;101(6):561-567
  5. 5. Gouzelou E, Haralambous C, Antoniou M, Christodoulou V, Martinković F, Živičnjak T, et al. Genetic diversity and structure inLeishmania infantumpopulations from southeastern Europe revealed by microsatellite analysis. Parasites & Vectors. 2013;6:342. DOI: 10.1186/1756-3305-6-342
  6. 6. Ready PD. Biology of phlebotomine sand flies as vectors of disease agents. Annual Review of Entomology. 2013;58:227-250. DOI: 10.1146/annurev-ento-120811-153557
  7. 7. de Vries HJ, Reedijk SH, Schallig HD. Cutaneous leishmaniasis: Recent developments in diagnosis and management. American Journal of Clinical Dermatology. 2015;16:99-109. DOI: 10.1007/s40257-015-0114-z
  8. 8. Krotoski MJ. Medical Parasitology. 8th ed. London: W.B. Saunders Company; 1999. pp. 147-154
  9. 9. Klaus SN, Frankenburg H, Ingber A. Epidemiology of cutaneous leishmaniosis. Clinical Dermatology. 1999;17:257-260. DOI: 10.1016/S0738-081X(99)00043-7
  10. 10. Bensaid M, Guerbouj S, Saghrouni F, Fathallah-Mili A, Guizani I. Occurrence ofLeishmania infantumcutaneous leishmaniasis in Central Tunisia. Transactions of the Royal Society of Tropical Medicine and Hygiene. 2006;100:521-526. DOI: 10.1016/j.trstmh.2005.08.012
  11. 11. Özbel Y, Töz ÖS. Leishmaniosis. In: Özcel MA, editor. Tıbbi Parazit Hastalıkları. 1.Baskı ed. İzmir: Meta Basım Matbacılık Hizmetleri; 2007. pp. 198-230
  12. 12. Achtman JC, Ellis DL, Saylors B, Boh EE. Cutaneous leishmaniasis caused byLeishmania(Viannia) panamensis in 2 travelers. JAAD Case Reports. 2016;2:95-97. DOI: 10.1016/j.jdcr.2015.11.018
  13. 13. Marsden PD. Mucosal leishmaniasis (“espundia” Escomel, 1911). Transactions of the Royal Society of Tropical Medicine and Hygiene. 1986;80:859-876. DOI: 10.1016/0035-9203(86)90243-9
  14. 14. Calvopiña M, Martinez L, Hashiguchi Y. Cutaneous leishmaniasis “chiclero’s ulcer” in subtropical Ecuador. The American Journal of Tropical Medicine and Hygiene. 2013;89:195-196. DOI: 10.4269/ajtmh.12-0690
  15. 15. Lainson R, Shaw JJ, Ready PD, Miles MA, Póvoa M. Leishmaniasis in Brazil: XVI. Isolation and identification ofLeishmaniaspecies from sandflies, wild mammals and man in north Para state, with particular reference toL. braziliensis guyanensiscausative agent of “pian-bois”. Transactions of the Royal Society of Tropical Medicine and Hygiene. 1981;75:530-536. DOI: 10.1016/0035-9203(81)90192-9
  16. 16. Llanos-Cuentas EA, Roncal N, Villaseca P, Paz L, Ogusuku E, Pérez JE, et al. Natural infections ofLeishmaniaperuviana in animals in the Peruvian Andes. Transactions of the Royal Society of Tropical Medicine and Hygiene. 1999;93:15-20. DOI: 10.1016/S0035-9203(99)90163-3
  17. 17. Ovallos FG, Silva YR, Fernandez N, Gutierrez R, Galati EA, Sandoval CM. The sandfly fauna, anthropophily and the seasonal activities of Pintomyia spinicrassa (Diptera:Psychodidae:Phlebotominae) in a focus of cutaneous leishmaniasis in northeastern Colombia. Memórias do Instituto Oswaldo Cruz. 2013;108:297-302. DOI: 10.1590/S0074-02762013000300007
  18. 18. WHO. Neglected Tropical Diseases, Hidden Successes, Emerging Opportunities. Geneva: World Health Organization; 2009. p. 59
  19. 19. Aversi-Ferreira RAGMF, Galvão JD, da Silva SF, Cavalcante GF, da Silva EV, Bhatia-Dey N, et al. Geographical and environmental variables of leishmaniasis transmission. In: Claborn DM, editor. Leishmaniasis—Trends in Epidemiology, Diagnosis and Treatment. InTech; 2014. DOI: 10.5772/57546
  20. 20. Pigott DM, Bhatt S, Golding N, Duda KA, Battle KE, Brady OJ, et al. Global distribution maps of the leishmaniases. eLife. 2014;3. DOI: 10.7554/eLife.02851
  21. 21. Ready PD. Epidemiology of visceral leishmaniasis. Clinical Epidemiology. 2014;6:147-154. DOI: 10.2147/CLEP.S44267
  22. 22. Amro A, Hamdi S, Lemrani M, Idrissi M, Hida M, Rhajaoui M, et al. MoroccanLeishmania infantum: Genetic diversity and population structure as revealed by multi-locus microsatellite typing. PLoS ONE. 2013;8:e77778. DOI: 10.1371/journal.pone.0077778
  23. 23. Kavur H, Eroglu F, Evyapan G, Demirkazik M, Alptekin D, Koltas IS. Entomological survey for sand fly fauna in imamoglu province (cutaneous leishmaniasis endemic region) of Adana, Turkey. Journal of Medical Entomology. 2015;52:813-818. DOI: 10.1093/jme/tjv064
  24. 24. Kasap OE, Belen A, Kaynas S, Simsek FM, Biler L, Ata N, et al. Activity patterns of sand fly (Diptera:Psychodidae) species and comparative performance of different traps in an endemic cutaneous leishmaniasis focus in cukurova plain, Southern Anatolia, Turkey. Acta Veterinaria. 2008;78:327-335. DOI: 10.2754/avb200978020327
  25. 25. Silva Jde A, Araújo Ide M, Pavanetti LC, Okamoto LS, Dias M. Visceral leishmaniasis and pregnancy in renal transplanted patient: Case report. Jornal Brasileiro de Nefrologia. 2015;37:268-270. DOI: 10.5935/0101-2800.20150041
  26. 26. de Silva AA, Silva Filho ÁPE, Sesso Rde C, Esmeraldo Rde M, de Oliveira CM, Fernandes PF, et al. Epidemiologic, clinical, diagnostic and therapeutic aspects of visceral leishmaniasis in renal transplant recipients: Experience from thirty cases. BMC Infectious Diseases. 2015;25(15):96. DOI: 10.1186/s12879-015-0852-9
  27. 27. Fishman JA. Infections in immunocompromised hosts and organ transplant recipients: Essentials. Liver Transplantation. 2011;17(Suppl 3):S34-S37. DOI: 10.1002/lt.22378
  28. 28. Alvar J, Aparicio P, Aseffa A, Den Boer M, Canavate C, et al. The relationship between leishmaniasis and AIDS: The second 10 years. Clinical Microbiology Reviews. 2008;21:334-359. DOI: 10.1128/CMR.00061-07
  29. 29. van Griensven J, Ritmeijer K, Lynen L, Diro E. Visceral leishmaniasis as an AIDS defining condition: Towards consistency across WHO guidelines. PLoS Neglected Tropical Diseases. 2014;17(8):e2916. DOI: 10.1371/journal.pntd.0002916
  30. 30. Croft SL, Coombs GH. Leishmaniasis—Current chemotherapy and recent advances in the search for novel drugs. Trends in Parasitology. 2003;19:502-508
  31. 31. Mittal MK, Rai S, Ashutosh, Ravinder, Gupta S, Sundar S, et al. Characterization of natural antimony resistance inLeishmania donovaniisolates. The American Journal of Tropical Medicine and Hygiene. 2007;76(4):681-688
  32. 32. Rijal S, Ostyn B, Uranw S, Rai K, Bhattarai NR, Dorlo TP, et al. Increasing failure of miltefosine in the treatment of Kala-azar in Nepal and the potential role of parasite drug resistance, reinfection, or noncompliance. Clinical Infectious Diseases. 2013;56(11):1530-1538. DOI: 10.1093/cid/cit102
  33. 33. Mondelaers A, Sanchez-Cañete MP, Hendrickx S, Eberhardt E, Garcia-Hernandez R, Lachaud L, et al. Genomic and molecular characterization of miltefosine resistance inLeishmania infantumstrains with either natural or acquired resistance through experimental selection of intracellular amastigotes. PLoS ONE. 2016;11(4):e0154101. DOI: 10.1371/journal.pone.0154101
  34. 34. Srivastava S, Mishra J, Gupta AK, Singh A, Shankar P, Singh S. Laboratory confirmed miltefosine resistant cases of visceral leishmaniasis from India. Parasites & Vectors. 2017;10(1):49. DOI: 10.1186/s13071-017-1969-z
  35. 35. Cojean S, Houze ÂS, Haouchine D, Huteau F, Lariven S, Hubert V, et al.Leishmaniaresistance to miltefosine associated with genetic marker. Emerging Infectious Diseases. 2012;18(4):704-706. DOI: 10.3201/eid1804.110841
  36. 36. Verma A, Bhandari V, Deep DK, Sundar S, Dujardin JC, Singh R, et al. Transcriptome profiling identifies genes/pathways associated with experimental resistance to paromomycin inLeishmania donovani. International Journal for Parasitology: Drugs and Drug Resistance. 2017;7(3):370-377. DOI: 10.1016/j.ijpddr.2017.10.004
  37. 37. Deep DK, Singh R, Bhandari V, Verma A, Sharma V, Wajid S, et al. Increased miltefosine tolerance in clinical isolates ofLeishmania donovaniis associated with reduced drug accumulation, increased infectivity and resistance to oxidative stress. PLoS Neglected Tropical Diseases. 2017;11(6):e0005641. DOI: 10.1371/journal.pntd.0005641
  38. 38. Ponte-Sucre A, Gamarro F, Dujardin J-C, Barrett MP, LoÂpez-VeÂlez R, Garcõ Âa-HernaÂndez R, et al. Drug resistance and treatment failure in leishmaniasis: A 21st century challenge. PLoS Neglected Tropical Diseases. 2017;11(12):e0006052. DOI: 10.1371/journal.pntd.0006052
  39. 39. Hefnawy A, Berg M, Dujardin JC, De Muylder G. Exploiting knowledge onLeishmaniadrug resistance to support the quest for new drugs. Trends in Parasitology. 2017;33(3):162-174. DOI: 10.1016/
  40. 40. Rastrojo A, García-Hernández R, Vargas P, Camacho E, Corvo L, Imamura H, et al. Genomic and transcriptomic alterations inLeishmania donovanilines experimentally resistant to antileishmanial drugs. International Journal for Parasitology: Drugs and Drug Resistance. 2018;8(2):246-264. DOI: 10.1016/j.ijpddr.2018.04.002
  41. 41. Kotton CN. Travel and transplantation: Travel-related diseases in transplant recipients. Current Opinion in Organ Transplantation. 2012;17:594-600. DOI: 10.1097/MOT.0b013e328359266b
  42. 42. Lund PV. Fortsatte Bemaerkninger over BrasiliensuddÖ de Dyrskagning. Kongelige Danske Videnskabernes Selskabs Naturvidenskabeligeog Mathematiske Afhandlinger. 1842;9:1-136
  43. 43. Lainson R, Elizabeth FR.Lutzomyialongipalpis and the eco-epidemiology of American visceral leishmaniasis, with particular reference to Brazil: A review. Memórias do Instituto Oswaldo Cruz. 2005;100:811-827. DOI: 10.1590/S0074-02762005000800001
  44. 44. Capelli G. Asymptomatic and symptomatic dogs in endemic areas, their role in the epidemiology of canine leishmaniosis. In: The 2nd Canine Vector-Borne Disease (CVBD) Symposium; Mazara del Vallo, Sicily, Italy; 2007. pp. 58-63. Available from:[Accessed: 14 june 2016]
  45. 45. Baneth G, Koutinas AF, Solano-Gallego L, Bourdeau P, Ferrer L. Canine leishmaniosis—New concepts and insights on an expanding zoonosis: Part one. Trends in Parasitology. 2008;24:324-330. DOI: 10.1016/
  46. 46. Banuls AL, Hide M, Prugnolle F.Leishmaniaand the leishmaniases: A parasite genetic update and advances in taxonomy, epidemiology and pathogenicity in humans. Advances in Parasitology. 2007;64:1-109-455-458. DOI: 10.1016/S0065-308X(06)64001-3
  47. 47. Sherlock IA. Ecological interactions of visceral leishmaniasis in the state of Bahia, Brazil. Memórias do Instituto Oswaldo Cruz. 1996;91:671-683. DOI: 10.1590/S0074-02761996000600003
  48. 48. Lainson R. The American leishmaniases: Some observations on their ecology and epidemiology. Transactions of the Royal Society of Tropical Medicine and Hygiene. 1983;77:569-596. DOI: 10.1016/0035-9203(83)90185-2
  49. 49. El-Adhami B. Isolation ofLeishmaniafrom a black rat in the Baghdad area, Iraq. The American Journal of Tropical Medicine and Hygiene. 1976;25:759-761
  50. 50. Inceboz T, Lambrecht FY, Eren MŞ, Girginkardeşler N, Bekiş R, Yilmaz O, et al. Evaluation of 131I-pentamidine for scintigraphy of experimentallyLeishmania tropica-infected hamsters. Journal of Drug Targeting. 2014;22:416-420. DOI: 10.3109/1061186X.2013.878943
  51. 51. Pourmohammadi B, Motazedian MH, Kalantari M. Rodent infection withLeishmaniain a new focus of human cutaneous leishmaniasis, in northern Iran. Annals of Tropical Medicine and Parasitology. 2008;102:127-133. DOI: 10.1179/136485908X252223
  52. 52. Pozzio E, Gradoni L, Bettini S, Gramiccia M. Leishmaniasis in Tuscani (Italy) V. Further isolation ofleishmaniafrom Rattusrattusin the province of Grosseto. Annals of Tropical Medicine and Parasitology. 1981;75:393-395
  53. 53. Papadogiannakis E, Spanakos G, Kontos V, Menounos PG, Tegos N, Vakalis N. Molecular detection ofLeishmania infantumin wild rodents (Rattus norvegicus) in Greece. Zoonoses and Public Health. 2010;57:e23-e25. DOI: 10.1111/j.1863-2378.2009.01264.x
  54. 54. Ashford RW. The leishmaniases as model zoonoses. Annals of Tropical Medicine and Parasitology. 1997;91:693-701. DOI: 10.1080/00034989760428
  55. 55. Lukes J, Mauricio IL, Schönian G, Dujardin JC, Soteriadou K, Dedet JP, et al. Evolutionary and geographical history of theLeishmania donovanicomplex with are vision of current taxonomy. Proceedings of the National Academy of Sciences of the United States of America. 2007;104:9375-9380. DOI: 10.1073/pnas.0703678104
  56. 56. Deane LM. Leishmaniose visceral no Brasil. Serviço Nacional de Educação Sanitária. 1956:1-162. Available from:
  57. 57. Deane LM. Epidemiologia e profilaxia do calazaramericano. Revista Brasileira de Malariologia. 1958;10:431-450. Available from:
  58. 58. Alencar JE. Profilaxia do calazar no Ceará Brasil. Revista do Instituto de Medicina Tropical de São Paulo. 1961;3:175-180. Available from:
  59. 59. World Health Organization (WHO). Control of Leishmaniasis. Tech Rep Series. 793, Geneva; 1990. 158 pp
  60. 60. Alencar JE. Kala-azar in Brazil. Scientific Reports of the Istituto Superiore di Sanità. 1962;2:116-123
  61. 61. Apostila UFPE. Available from:;16:99-109
  62. 62. Mayrink W, Genero O, Silva JCF, Costa RT, Tafuri WL, Toledo VPCP, et al. Phase I and II open clinical trials of a vaccine againstLeishmaniachagasi infection in dogs. Memórias do Instituto Oswaldo Cruz. 1996;91:695-697. DOI: 10.1590/S0074-02761996000600006
  63. 63. Genaro O, Pinto JA, Costa CA, França-Silva JC, Costa RT, Silva JC, et al. Phase III randomized double blind clinical trial on the efficacy of a vaccine against canine visceral leishmaniasis in urban area of Montes Claros, MG, Brazil. Memórias do Instituto Oswaldo Cruz. 1996;91(Suppl):166. Available from:
  64. 64. Silva VO, Borja-Cabrera GP, Correia Pontes NN, Souza EP, Luz KG, Palatinik M, et al. A Phase III trial of efficacy of the FML-vaccine against canine calazar in an endemic area of Brasil (São Gonçalo do Amarante, RN). Vaccine. 2000;19:1082-1092. DOI: 10.1016/S0264-410X(00)00339-X

Written By

Tonay Inceboz

Submitted: November 10th, 2018 Reviewed: April 15th, 2019 Published: October 22nd, 2019