Protozoan Diseases: Leishmaniasis

Adrienne J Showler, Toronto General Hospital, Toronto, ON, Canada; and Bloomberg School of Public Health, Johns Hopkins
University, Baltimore, MD, USA
Andrea K Boggild, Toronto General Hospital, Toronto, ON, Canada; University of Toronto, Toronto, ON, Canada; and Public Health
Ontario, Toronto, ON, Canada
2017 Elsevier Inc. All rights reserved.
This article is an updated version of the previous edition article by Jean-Pierre Dedet, volume 4, pp. 367371, 2008, Elsevier Inc.

Introduction Leishmania vectors. Sand y vectors belong to the genera Phlebo-

tomus in the Old World (Africa, Europe, and Asia) and Lutzomyia
The leishmaniases are parasitic diseases caused by protozoa of in the New World (North, Central, and South America).
the genus Leishmania. An estimated 350 million people in
98 countries are at risk, with an annual incidence of
Reservoir
1.52 million cases (Alvar, 2012). Transmission occurs through
an insect vector, the phlebotomine sand y, within distinct local Diverse mammalian reservoir hosts maintain Leishmania in
ecological foci and through region-specic interactions with nature (Table 2). Rodents, hyraxes, marsupials, and edentates
animal or human reservoirs. The infection causes three major are common reservoirs of wild zoonotic CL. Dogs are true reser-
clinical syndromes: visceral, cutaneous, and mucocutaneous voirs of Leishmania infantum and Leishmania Viannia peruviana,
disease. Cutaneous and mucocutaneous disease can cause disg- two species that have peridomestic or even domestic transmis-
urement, and the more severe visceral disease results in 50 000 sion. Humans are the commonly recognized reservoir of Leish-
deaths annually (WHO, 2010). Multiple factors affect the clinical mania donovani VL and Leishmania tropica CL.
form and disease course including the infecting species,
geographic area of acquisition, and host immune status and
Life Cycle and Transmission
response to infection. The lack of effective national control
programs in endemic countries, reliance on inaccurate disease Leishmania parasites are alternately hosted by the insect (agel-
burden estimates, and inaccessibility of antileishmanial drugs lated promastigote stage) and by mammals (intracellular amas-
all contribute to its status as a neglected tropical disease. tigote stage). Sandies transmit leishmaniasis to humans by
inoculating metacyclic promastigotes into skin during a blood
meal. Macrophages in the human immune system ingest the
General Epidemiology of Leishmaniasis promastigotes, which then transform into the intracellular
amastigote form. Amastigotes replicate in human tissue and
Parasite
transfer back to sandies during subsequent blood meals. In
Leishmaniae are agellate protozoans of the genus Leishmania
(Kinetoplastida, Trypanosomatidae). These dimorphic para-
sites present as two principal morphological stages during their Table 1 Simplied classication of the genus Leishmania, derived
life cycle: the intracellular amastigote, in the cells of the from the phylogenetic analysis based on isoenzymesa and showing the
mammalian host mononuclear phagocyte system, and the ag- main anthropotropic species
ellated promastigote, in the intestinal tract of the insect vector.
Subgenus Leishmania
Over 30 morphologically indistinguishable species cause
Leishmania donovani complex L. donovani
human infection. Major clinical and research centers increas-
Leishmania infantum complex L. infantum (syn. Leishmania
ingly use DNA-based methods such as polymerase chain chagasi)
reaction (PCR), restriction fragment length polymorphism Leishmania tropica complex L. tropica
(RFLP) analysis, and nucleotide sequencing assays for species Leishmania killicki complex L. killicki
identication. However, isoenzyme electrophoresis remains Leishmania aethiopica complex L. aethiopica
the gold standard technique for identication and is the basis Leishmania major complex L. major
for the current classication (see Table 1). Leishmania mexicana complex L. mexicana
Leishmania amazonensis
Leishmania enrietti complex L. enrietti
Vector Subgenus Viannia
Leishmania Viannia braziliensis complex Leishmania braziliensis
Sandies are psychodid diptera of the subfamily Phlebotomi-
Leishmania peruviana
nae. Their developmental stages (eggs, four larval instars, and Leishmania Viannia guyanensis complex Leishmania guyanensis
pupae) occur in damp organically rich soil. The free-ying adult Leishmania panamensis
insects are about 24 mm in length, with a yellowish hairy body. Leishmania shawi
The adults rest in dark, sheltered places during the day and are Leishmania Viannia naiffi complex Leishmania naiffi
active at dusk and at night. Both sexes feed on plant juices. Leishmania Viannia lainsoni complex Leishmania lainsoni
Females also require a blood meal in order to lay eggs. The blood a
Adapted from Rioux, J.A., Lanotte, G., Serres, E., et al., 1990. Taxonomy of
meal transmits Leishmania parasites to mammalian hosts. About Leishmania: use of isoenzymes; suggestions for a new classication. Ann. Parasitol.
70 of 800 known sand y species are proven or suspected Hum. Comp. 65, 111125.

International Encyclopedia of Public Health, 2nd edition, Volume 6 http://dx.doi.org/10.1016/B978-0-12-803678-5.00359-3 97

 98
Protozoan Diseases: Leishmaniasis
Table 2 Main noso-epidemiological units of leishmaniases of the Old and New Worlds

Noso-epidemiological units a Parasite species Reservoir hosts Sand fly vector Clinical form Distribution and ecological patterns

Anthroponotic VL Leishmania donovani Humans Phlebotomus argentipes Kala-azar Rural disease

PKDL
Zoonotic VL Leishmania infantum Dogs Phlebotomus (Larroussius) spp. Infantile VL Rural disease
Zoonotic CL Leishmania major Gerbilline rodents Phlebotomus papatasi, Phlebotomus duboscqi Localized CL Rural disease of Old World arid and peri-arid
areas
Anthroponotic CL Leishmania tropica Humans Phlebotomus sergenti Localized CL Urban disease of Near and Middle East
Zoonotic CL Leishmania aethiopica Hyracods Phlebotomus longipes, Phlebotomus pedifer LCL; DCL Rural disease, Ethiopia
Zoonotic CL Leishmania killicki Unknown Unknown LCL
MCL, or espundia Leishmania Viannia Wild mammals Lutzomyia wellcomei; Lutzomyia intermedia; CL and MCL Sylvatic zoonosis of New World primary rain
braziliensis Lutzomyia gomezi; Lutzomyia ylephiletor; etc. forest
New World CL Leishmania Viannia Sloths, anteaters, Lutzomyia umbratilis; Lutzomyia whitmani Localized CL Sylvatic zoonosis of New World primary rain
guyanensis opossums forest
New World CL Leishmania Viannia Sloths, monkeys Lutzomyia trapidoi; Lutzomyia gomezi; Lutzomyia Localized CL Sylvatic zoonosis of New World primary rain
panamensis ylephiletor forest
Rodent enzootic Leishmania amazonensis Echimyd rodents Lutzomyia flaviscutellata LCL; DCL Sylvatic zoonosis of New World primary rain
leishmaniasis forest
New World CL, or chicleros Leishmania mexicana Rodents Lutzomyia olmeca LCL Sylvatic zoonosis of New World primary rain
ulcer forest
New World CL Leishmania Viannia naiffi Armadillos Lutzomyia ayrozai; Lutzomyia paraensis; Lutzomyia LCL Sylvatic zoonosis of New World primary rain
squamiventris forest
New World CL Leishmania Viannia lainsoni Agouti paca Lutzomyia ubiquitalis Sylvatic zoonosis of New World primary rain
forest
New World CL, or uta Leishmania Viannia Dogs Lutzomyia peruensis LCL Arid valleys of western slopes of Peruvian
peruviana Andes
a
Abbreviations: VL, visceral leishmaniasis; CL, cutaneous leishmaniasis; MCL, mucocutaneous leishmaniasis.

the sand y midgut, amastigotes develop into promastigotes to
complete the cycle.
Although most human transmission occurs via sand y
bites, other potential routes include intravenous drug use,
blood transfusions, organ transplantation, and congenital
infection.
Geographical Distribution
Leishmaniasis occurs in 98 countries, ranging over the inter-
tropical zones of America and Africa, and extending into
temperate regions of North America, South America, southern
Europe, and Asia. The limits of the disease are latitudes
45
north and 32
south.
Different forms of Leishmania concentrate geographically
based on the particular sand y and mammalian host ecology
and natural habitats. Several noso-epidemiological units are
identied where a particular Leishmania parasite species circu-
lates via specic sand y vectors and reservoir hosts to emerge
in a clinical form particular to an ecological region (see
Table 2).
Visceral Leishmaniasis
Visceral leishmaniasis (VL) is the most severe form of leish-
maniasis, with an annual incidence of 200 000400 000 cases
and an estimated case fatality rate of 1020% (Alvar, 2012).
Mortality varies dramatically depending on the setting, ranging
from 2% in endemic areas up to 90% during epidemics in low-
resource settings. However, estimates of both disease burden
and attributable mortality are highly imprecise due to lack of
epidemiologic data, particularly in Africa. Although VL is
endemic in 47 countries, 90% of global disease occurs in 6
countries: India, Bangladesh, Ethiopia, Sudan, South Sudan,
and Brazil (Alvar, 2012).
Two viscerotropic Leishmania species have distinct life cycles
and geographic distribution. The zoonotic species L. infantum
(known as Leishmania chagasi in the Americas) extends from
China to Brazil and is responsible for infantile VL. The anthro-
ponotic species L. donovani is restricted to India, Bangladesh,
Nepal, and East Africa. Rarely, a third species, L. tropica, can
cause visceral disease. Leishmania Viannia braziliensis is associ-
ated with visceral disease in the context of HIV infection,
most notably in Brazil.
Most Leishmania infections with viscerotropic species are
asymptomatic, with overt clinical disease manifesting in
specic age groups and in patients who are immunosuppressed
due to malnutrition, HIV, and chemotherapy. Endemic L. infan-
tum primarily affects children under age 5, although in Europe
immunosuppressed adults now represent about half of cases
(WHO, 2010). This shift in epidemiology reects both
increasing use of immunosuppressive drugs and outbreaks in
intravenous drug users with HIV coinfection. In L. donovani
endemic areas, VL manifests mainly in children and young
adults.
Endemic VL tends to be slow-onset and chronic, with
cardinal clinical features including fever; enlarged liver, spleen,
and lymph nodes; anorexia; failure to thrive; and cytopenias. In
India, the disease is also known as kala-azar, meaning black
Protozoan Diseases: Leishmaniasis 99
fever in Hindi, due to skin darkening that frequently accom-
panies infection. Some L. donovaniinfected patients develop
a chronic cutaneous form known as post-kala-azar dermal
leishmaniasis (PKDL) which acts as a reservoir for ongoing
transmission. Epidemic anthroponotic VL occurs in any age
group and is associated with more acute symptoms and high
mortality rates in populations without prior immunity.
Patients with VL in both endemic and epidemic settings are
vulnerable to other infections, including respiratory infections,
dysentery, and tuberculosis.
Cutaneous Leishmaniasis
Cutaneous leishmaniasis (CL) is the most common and
broadly distributed form of disease, with an annual incidence
of 700 000 to 1.2 million cases. Ten countries account for
7075% of global disease: Afghanistan, Algeria, Colombia,
Brazil, Iran, Syria, Ethiopia, North Sudan, Costa Rica, and
Peru (Alvar, 2012).
Old World CL occurs mainly in countries of the Near and
Middle East, with the highest incidence in Afghanistan, Iran,
Syria, Ethiopia, Algeria, and North Sudan (Alvar, 2012). Leish-
mania major and L. tropica are the predominant infecting
species. Leishmania major is zoonotic and has a wide distribu-
tion, including west, north, and east Africa; the Near and
Middle East; and Central Asia. Leishmania tropica is an anthro-
ponotic species found in various cities of the Near and Middle
East and extending into northern Africa. Other species have
more restricted distributions: Leishmania aethiopica in Ethiopia
and Kenya and L. infantum in southern Europe.
New World CL is endemic throughout Central and South
America with the exception of Chile and Uruguay. Leishmania
(Viannia) braziliensis has a wide distribution, extending from
southern Mexico to northern Argentina. Leishmania (Leish-
mania) amazonensis has a wide South American distribution,
but human cases of this rodent enzootic species are less
common. Other species have more restricted distributions:
Leishmania (Viannia) guyanensis (north of the Amazon basin),
Leishmania (Viannia) panamensis (Colombia and Central Amer-
ica), Leishmania (Leishmania) mexicana (Mexico and Central
America), and L. (V.) peruviana, which is restricted to Andean
valleys of Peru. With the exception of this last species, all Amer-
ican dermotropic species are responsible for sylvatic zoonoses
occurring within the rain forest.
Cutaneous leishmaniasis classically presents as a painless
lesion on an exposed area of skin, that evolves into an ulcer
over weeks to months. Many different lesion morphologies
are possible, and CL can mimic other skin disorders, including
cutaneous fungal and mycobacterial infections. In endemic
populations, CL is normally a self-healing disease with sponta-
neous cure occurring between 6 months and a few years,
depending on the causative Leishmania species. Cured lesions
cause permanent atrophic scars. However, CL can be disguring
when lesions are multiple, large, or located in sensitive areas
such as the face. Leishmania tropica may lead to recidivans leish-
maniasis, a destructive chronic form where new lesions emerge
at the margins of the atrophic scar.
In patients with a defective cell-mediated immune response,
some species (Table 2) result in diffuse cutaneous leishmani-
asis (DCL), a severe form characterized by nodular
100 Protozoan Diseases: Leishmaniasis

disseminated skin lesions, subject to relapses and resistant to
treatment.
Mucocutaneous Leishmaniasis
New World species of the Viannia subgenus have the ability to
cause mucocutaneous disease, with primary or secondary
involvement of nasal, oral, and hypopharyngeal mucosae.
This form typically occurs 15 years after a primary cutaneous
infection and leads to disguring and mutilating facial lesions.
Risk of progression to mucocutaneous leishmaniasis (MCL)
depends on species and location of acquisition, as well as local-
ization of the original CL, with more than 90% of MCL due to
L. (V.) braziliensis and L. (V.) peruviana infection in high
Andean regions of Bolivia, Brazil, and Peru (Blum, 2012).
Currently there are no reliable estimates of global MCL inci-
dence due to lack of epidemiologic data (Alvar, 2012).
Diagnosis
Parasitologic diagnosis requires obtaining an appropriate tissue
specimen for testing with microscopy, culture, or molecular
techniques. To conrm suspected VL, biopsies or aspirates of
bone marrow and enlarged lymph nodes, liver, or spleen
provide appropriate samples. Tissue specimens for diagnosis
of CL can be obtained using a variety of techniques including
lesion scrapings, needle aspiration, punch biopsies, lter-
paper lesion impressions, and cytology brush scrapings.
PCR testing to detect kinetoplast or nuclear DNA is by far the
most sensitive diagnostic technique and also enables species-level
identication. Visualizing Leishmania amastigotes using direct
Giemsa-stained microscopy is the primary method used outside
of reference centers and in low-resource settings. Although Leish-
mania can be cultured using Nicolle-McNeal-Novy (NNN) or
Tobies medium, cultures are often not performed as they are
time-consuming, insensitive, and resource intensive.
Antibody-based serologic testing is a useful tool to facilitate
early diagnosis of visceral leishmaniasis in low-resource areas.
In particular, rK39-based rapid diagnostic testing is inexpen-
sive, easy to implement, and accurate in patients meeting the
VL clinical case denition. This test is now recommended as
the initial diagnostic modality in primary health-care centers
and district hospitals in highly endemic areas (WHO, 2010).
Serologic testing cannot be used to diagnose the tegumentary
forms of leishmaniasis (CL, MCL) or relapsed infection.
Treatment
Treatment options are summarized in Table 3. Both VL and
MCL require systemic treatment with amphotericin B, miltefo-
sine, or pentavalent antimonials. These drugs all require close
monitoring for side effects, including damage to major organs
such as the heart, kidneys, and liver. Drug administration is
logistically difcult, as amphotericin and antimonials require
either intravenous or intramuscular injections. Only miltefo-
sine can be given orally.
Limited cutaneous disease in immunocompetent patients
can often be cured using local methods including wound
care alone, intralesional pentavalent antimonials combined
with cryotherapy, thermotherapy, and paromomycin-

Table 3 Treatment options for visceral, mucocutaneous, and cutaneous leishmaniasis

Drug Dose
a
Visceral leishmaniasis Liposomal amphotericin B Variable
Amphotericin B 1 mg kg1 IV daily  1520 days or 1 mg kg1 IV q2 days 
48 weeks
Sodium stibogluconate or Meglumine antimoniate 20 mg Sb kg1 per day IV or IM  28 days
Miltefosine 2.5 mg kg1 per day PO  28 days (maximum 150 mg day1)
Mucocutaneous Amphotericin B deoxycholate 0.51 mg kg1 daily IV  1520 days or 0.51 mg kg1
leishmaniasis q2 days  47 weeks
Liposomal amphotericin B 2040 mg kg1 total dose divided in 48 doses
Sodium stibogluconate or Meglumine antimoniate 20 mg Sb kg1 per day IV or IM  28 days
Miltefosine 2.5 mg kg1 per day PO  28 days (maximum 150 mg day1)
Cutaneous Cryotherapy intralesional antimony Intralesional antimony: 0.25 ml every 37 days  58
uncomplicatedb treatments, or until healed
15% paromomycin/12% MBCLc (Leshcutan) or 15% Apply to lesion BID  1020 days
paromomycin/0.5% gentamicin (WR 279 396)
Thermotherapy Single treatment 50
C for 3060 min
Cutaneous complicated Liposomal amphotericin B 3 mg kg1 IV daily  57 doses
Amphotericin B deoxycholate 0.51.0 mg kg1 IV every other day  2030 days
Sodium stibogluconate or Meglumine antimoniate 20 mg Sb kg1 per day IV/IM  20 days
Miltefosine 2.5 mg kg1 per day PO  28 days (maximum 150 mg day1)
Fluconazoled 400600 mg (68 mg kg1 per day) PO daily  46 weeks
Pentamidinee 23 mg kg1 IV/IM daily or every other day  47 doses
a
Treatment of choice.
b
Local treatments should generally be reserved for patients meeting the following criteria: small < 34 cm lesions, fewer than three to ve lesions, location in nonsensitive or
cosmetically disguring areas, not associated with lymphocutaneous spread, immunocompetent host, low risk for developing mucocutaneous disease.
c
MBCL methylbenzethonium chloride, the vehicle for Leshcutan ointment.
d
Efcacy not well established for New World CL.
e
Randomized controlled trials support use of pentamidine for Leishmania Viannia panamensis and Leishmania Viannia guyanensis infection. Variable cure rates observed for
Leishmania Viannia braziliensis.

containing cream. Systemic treatment is indicated for
complicated cutaneous disease, including lesions that are
large (>34 cm), multiple (>35), located in sensitive areas
such as the face, neck, or genitalia, or refractory to local or
topical treatment. For CL due to L. Viannia complex infec-
tions, clinicians must also consider risk of future MCL in
choosing between local treatment and more toxic systemic
therapy (Blum, 2012), although data to support that paren-
teral versus oral treatment reduces downstream risk of MCL
are lacking.
Treatment in resource-limited settings is challenging due to
the complexity and potential toxicity of treatment regimens,
lack of access to antileishmanial drugs, and need for long-
term follow-up in the case of MCL and VL. Therapeutic failure,
relapse, and increasing drug resistance complicate treatment in
HIV-coinfected patients.
Risk Factors
Environmental Risk Factors
Human intrusion into a leishmaniasis natural focus represents
the major risk factor of infection by exposure to sand y vectors.
For example, in the case of sylvatic zoonotic New World CL,
leisure or work activities in tropical rain forests expose individ-
uals or groups to infection (see Table 2). Population move-
ments, such as rural to suburban migration, returnees, and
refugees due to civil unrest, are factors for the spread of leish-
maniasis or for dramatic epidemic outbreaks by exposing thou-
sands of nonimmune individuals to infection (Desjeux, 2001).
Human infrastructure and changes in land use may alter local
microclimates as well as humanenvironmental interactions
resulting in increased transmission. This is particularly evident
in peri-urban areas in South America, where major increases in
infection have occurred in deforested areas aficted by poverty
and overcrowding at the margins of expanding cities.
Small shifts in temperature, humidity, and precipitation
have a potentially signicant impact on Leishmania distribu-
tion, both due to altered distribution of reservoir hosts and
susceptibility of leishmania promastigotes to minor environ-
mental changes. Temperature uctuations due to the El Nio
phenomenon resulted in increased numbers of reported Leish-
mania cases. Global warming is expected to cause expansion of
Leishmania-endemic areas, with extension of autochthonous
transmission well into southern Europe and the southern
United States bordering Mexico.
Immunosuppression as an Individual Risk Factor
Immunosuppression is the major individual risk factor facili-
tating the development of severe disease following infection.
The spread of HIV to rural areas where VL is endemic, and
the spread of VL to suburban areas, has resulted in a progres-
sively increasing overlap between the two diseases, initially in
the Mediterranean basin, and, more recently, in other historical
foci of VL, such as East Africa, India, and Brazil.
Control Strategies
Intervention strategies for prevention or control are hampered
by the diversity of the structure of leishmaniasis foci, with
Protozoan Diseases: Leishmaniasis 101
many different reservoir hosts of zoonotic forms and a multi-
plicity of sand y vectors, each with a different pattern of
behavior. A WHO Expert Committee described 11 distinct
eco-epidemiological entities and dened control and ectopara-
siticide strategies for each (WHO, 2010).
Prevention
The aim of prevention is to avoid host infection (human or
canine) and subsequent disease. It includes means to prevent
intrusion of people into natural zoonotic foci and protection
against infective sand y bites. Prevention can be at an indi-
vidual or collective level. It includes the use of repellents,
pyrethroid-impregnated bed nets, self-protection insecticides,
indoor residual spraying, and forest clearance around human
settlements. Insecticide collars and ectoparasiticides are avail-
able for dog protection.
Control
Control programs attempt to interrupt the life cycle of the
parasite and to limit or ideally eradicate the disease. The struc-
ture and dynamics of natural foci of leishmaniasis are so
diverse that a standard control program cannot be dened
and control measures must be adapted to local situations.
The strategy depends on the ecology and behavior of the two
main targets, the reservoir hosts and the vectors.
Control measures will be very different depending on
whether the disease is anthroponotic or zoonotic. In the New
World, almost all the leishmaniases are sylvatic, and cost-
effective control is not usually feasible. Even removal of the
forest itself may not be effective, as various Leishmania species
have proved to be remarkably adaptable to environmental
degradation.
Case detection and treatment are recommended when the
reservoir host is human or dog, while destruction may be the
chosen intervention if the reservoir host is a wild animal. The
toxicity and complexity of the current antileishmanial drug
regimens limit their use for systematic treatment of cases. The
high level of asymptomatic infection both in human and
canine hosts affects the efciency and the feasibility of system-
atic case detection and treatment programs.
Vector control is limited to insecticide spraying and elimina-
tion of sand y breeding sites (rodent burrows for Phlebotomus
papatasi and Phlebotomus duboscqi). Malaria control programs
based on indoor residual insecticide spraying have temporarily
decreased leishmaniasis incidence in several countries,
including India, Italy, Greece, parts of the Middle East, and
Peru. Unfortunately, a resurgence of leishmaniasis occurred
once spraying ceased.
In practice, control programs include several integrated
measures targeted not only at the reservoir host and vector,
but also at associated environmental changes. Health education
campaigns can considerably improve the efciency of control
programs. Multiple countries have implemented national leish-
maniasis programs to control endemic disease and combat
epidemics (India, China, and Brazil for VL; Central Asian repub-
lics of the former USSR and Tunisia for CL).
Although a 2010 WHO expert report concluded that exist-
ing diagnostic tools and treatments are sufcient to achieve
102 Protozoan Diseases: Leishmaniasis
adequate Leishmania control, this will only be accomplished
with dramatically increased funding and political commitment
on a global level.
Conclusion
The leishmaniases are an important public health problem in
tropical and subtropical countries, principally in rural and
peri-urban populations living in poverty. Transmission occurs
within the context of complex local ecology, characterized by
distinct interactions between insect vectors, mammalian reser-
voirs, and the environment. Despite progress in understanding
of most facets of their epidemiology, control of leishmaniasis
remains unsatisfactory.
See also: Land Use/Land Change and Health; Re-emerging
Diseases: Overview; Skin Diseases (Noncancerous).
References
Alvar, J., Velez, I.D., Bern, C., et al., 2012. The WHO Leishmaniasis Control Team:
leishmaniasis worldwide and global estimates of its incidence. PLoS One 7,
e35671.
Blum, J., Lockwood, D.N.J., Visser, L., et al., 2012. Local or systemic treatment for
New World cutaneous leishmaniasis? Re-evaluating the evidence for the risk of
mucosal leishmaniasis. Int. Health 4, 153163.
Desjeux, P., 2001. The increase in risk factors for leishmaniasis worldwide. Trans. R.
Soc. Trop. Med. Hyg. 95, 239243.
Rioux, J.A., Lanotte, G., Serres, E., et al., 1990. Taxonomy of leishmania: use of
isoenzymes. Suggestions for a new classication. Ann. Parasitol. Hum. Comp. 65,
111125.
World Health Organization, 2010. Control of the Leishmaniases. Technical Report
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Further Reading
Blum, J., Buffet, P., Visser, L., Harms, G., Bailey, M.S., Caumes, E., et al., 2014.
LeishMan recommendations for treatment of cutaneous and mucosal leishmaniasis
in travelers, 2014. J. Trav. Med. 21, 116129.
Hodiamont, C.J., Kager, P.A., Bart, A., de Vries, H.J.C., van Thiel, P.P.A.M., et al.,
2014. Species-directed therapy for leishmaniasis in returning travellers:
a comprehensive guide. PLoS Negl. Trop. Dis. 8, e2832. http://dx.doi.org/
10.1371/journal.pntd.0002832.
Monge-Maillo, B., Lpez-Vlez, R., 2013. Therapeutic options for old world cutaneous
leishmaniasis and new world cutaneous and mucocutaneous leishmaniasis. Drugs
73, 18891920.
Relevant Websites
http://www.cdc.gov/Ncidod/dpd/parasites/leishmania CDC, Division of Parasitic
Diseases, Leishmania Infection (last accessed on 20.05.16.).
http://www.who.int/leishmaniasis World Health Organization, Leishmaniasis: Back-
ground Information (last accessed on 20.05.16.).