Cutaneous leishmaniasis

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Cutaneous leishmaniasis
Other names: Oriental sore, Tropical sore, Chiclero ulcer, Chiclero's ulcer, Aleppo boil, Delhi Boil or Desert boil[1][2][3]
Cutaneous leishmaniasis in a man from French Guiana
SpecialtyInfectious disease
SymptomsSwallowing difficulty,skin ulcer,nosebleeds
CausesAbout thirty species of Leishmania
Diagnostic methodPCR test, clinical presentation
PreventionInsect repellant
TreatmentIt depends which species has caused the condition

Cutaneous leishmaniasis ( or Chiclero's ulcer[1])is the most common form of leishmaniasis affecting humans.[4] It is a skin infection caused by a single-celled parasite that is transmitted by the bite of a phlebotomine sand fly. There are many species of Leishmania that may cause cutaneous leishmaniasis.[5]

This disease is considered to be a zoonosis (an infectious disease that is naturally transmissible from animals to humans), with the exception of Leishmania tropica — which is often an anthroponotic disease (an infectious disease that is naturally transmissible from humans to vertebrate animals).[3]The most common causes by Old World species are L. major, L. tropica, and L. aethiopica;while the New World species, has L. mexicana and L. Viannia.[6] The treatment for cutaneous leishmaniasis depends on the species of Leishmania and the type of infection[7]

Signs and symptoms

The presentation for Cutaneous leishmaniasis is as follows:[8]


Leishmania is a genus of trypanosomes that are responsible for the disease leishmaniasis.[9][10][11] Leishmania species are unicellular eukaryotes having a well-defined nucleus and other cell organelles including kinetoplasts and flagella. Depending on the stage of their life cycle, they exist in two structural variants[12]

They are spread by sandflies of the genus Phlebotomus in the Old World, and of the genus Lutzomyia in the New World. At least 93 sandfly species are proven or probable vectors worldwide.[13]

Their primary hosts are vertebrates; Leishmania commonly infects dogs, sloths, rodents, and humans.[14]

Mechanism of infection

Lifecycle of Leishmania

Promastigotes of Leishmania are transmitted to human skin by the bite of a sandfly. Leishmania then invades human macrophages and replicates intracellularly. A raised, red lesion develops at the site of the bite. The lesion then ulcerates and may become secondarily infected with bacteria. In many species (for example, L. major) the lesion often spontaneously heals with atrophic scarring. In some species (for example, L. braziliensis) the lesion may spontaneously heal with scarring, but then reappear elsewhere (especially as destructive mucocutaneous lesions). Lesions of other Leishmania species may spontaneously heal and then reappear as satellite lesions around the site of the original lesion, or along the route of lymphatic drainage.[15][16][17][18]

Some species tend to cause cutaneous leishmaniasis, whereas some species tend to cause visceral leishmaniasis, though emerging research, due to high deployment rates of western countries to indigenous areas, is showing these species specific presentation lines are blurring.[19][15][16]


Diagnosis is based on the characteristic appearance of non-healing raised, scaling lesions that may ulcerate and become secondarily infected with organisms such as Staphylococcus aureus, in someone who has returned from an endemic area[20].[21][22]

Fine-needle aspiration of the lesion is confirmatory with identification of amastigote form of Leishmania.[23] The gold standard for diagnosis is a PCR test.[24]


The sand fly stings mainly at night, and it usually occurs about half a meter above the ground. To avoid the possibility of stinging, one should apply mosquito repellent, and cover the body.[25]

Studies conducted in recent years show that the plant Bougainvillea glabra may protect against the sand fly. The plant was found to be toxic to sand flies and that the life span of flies that ate from this plant was significantly shortened and sometimes led to their premature death before they could spread the disease.[26][27]Hebrew University study found that some plants attract sand flies. These plants often attract sand flies up to 14 times more than Bougainvillea glabra, but unlike Bougainvillea glabra, are not toxic to the sand flies. Based on this information, the dispersion of sand flies can be controlled by limiting the growth of these plants near populated areas. Alternatively, these plants may serve to capture and control sand flies by using their odor compounds or the plants themselves alongside simple glue traps, or by spraying them with deadly pesticides for sand flies which are safe for humans and mammals (e.g., boric acid or spinosad) thereby stopping the spread of the disease. Of the dozens of plants examined, the three plants that attracted especially sand flies are the Ochradenus baccatus, Prosopis farcta, and Tamarix nilotica.[28]


New World cutaneous leishmaniasis


Pentavalent antimonial drugs (sodium stibogluconate (SSG) and meglumine antimonate have been used since the 1940s, but they are expensive, toxic, and painful.[29] Treatments that work for one species of Leishmania may not work for another; therefore, it is recommended that the exact species be identified prior to initiating treatment. Unfortunately, leishmaniasis is an orphan disease in developed nations, and almost all the current treatment options are toxic with significant side effects.[29][30][31]

The best-studied treatments for ACML caused by two Leishmania species are listed below. However, one should note that most of the studies examining treatments of ACML were poorly designed. Therefore, no definitive treatment guidelines or recommendations are currently available, as large-scale and well-conducted studies are necessary to evaluate the long-term effects of current treatments.[29]

  • Leishmania braziliensis and Leishmania panamensis: There is good evidence that oral allopurinol plus intramuscular MA is superior to either medication alone. In addition, a 20-day course of intravenous MA was better than a 7-day course as well as a 3- or 7-day course of intravenous MA with paromomycin + 12% methylbenzethonium chloride.[29]
  • For L. braziliensis, oral pentoxifylline plus intravenous SSG seems to be more efficacious than intravenous SSG alone, and intravenous MA was superior to intramuscular paromomycin sulfate and IV pentamidine. Likewise, intramuscular MA was shown to be better than the Bacillus Calmette-Guerin vaccine.[29]
  • For L. panamensis, oral ketoconazole, oral miltefosine, and topical paromomycin + 12% methylbenzethonium chloride were shown to be superior to placebo.[29]

There is no strong evidence for the efficacy of surgery, oral itraconazole and fluconazole, oral antibiotics (rifampicin, metronidazole, cotrimoxazole), intravenous or topical amphotericin B, oral dapsone, photodynamic therapy, promoting healing therapies, laser, or cryotherapy treatments.[29]

Old World cutaneous leishmaniasis

Paromomycin structure

Similar to ACML, the treatment recommendations for Old World cutaneous leishmaniasis (OWCL) are uncertain due to the variability of and inconsistencies within the research.[32]

Most studies done to assess treatments of OWCL included two species of parasites, Leishmania major and Leishmania tropica. The most well-studied treatments for OWCL are oral itraconazole and topical paromomycin.[32]

People treated with oral itraconazole for an average of 2.5 months had a higher cure rate compared to placebo, but they also had a higher rate of side effects, including gastrointestinal complaints, abnormal liver function, headaches, and dizziness.[32]

People treated with topical paromomycin showed no difference in cure rate compared to placebo, but patients treated with paromomycin had a higher rate of adverse skin reactions.[32]

The treatments for other Leishmania species responsible for OWCL, such as L. infantum, L. aethiopica, and L. donovani, have not been thoroughly studied. In addition, the effects of leishmaniasis treatment in children, women of childbearing age, patients with comorbidities, and immunocompromised patients have not been well established.[32]


Cutaneous leishmaniasis in North Africa; Leishmania infantum=green, Leishmania major=blue, Leishmania tropica=red[33]

Cutaneous leishmaniasis is endemic in all tropical and subtropical areas of the world.The distribution of this disease is very tightly linked to geography, and villages even several miles apart can have very different rates of cutaneous leishmaniasis.[34][33]

Most species of Leishmania are capable of infecting humans and causing cutaneous leishmaniasis. In the New World, these organisms include L. amazonensis, L. braziliensis, L. guyanensis, L. lainsoni, L. lindenbergi,[35] L. mexicana, L. naiffi, L. panamensis, L. peruviana, L. shawi, and L. venezuelensis. Old World species that cause cutaneous leishmaniasis include L. aethiopica, L. infantum, L. major, and L. tropica. With the exception of L. tropica — which is commonly associated with human settlements and therefore considered to be an anthroponotic species — all of these organisms are zoonotic.[3] As demographic changes occur in developing nations, some species that have traditionally been considered to be zoonotic (e.g., L. panamensis) are becoming primarily human pathogens.[36]

Dogs and rodents serve as the primary animal reservoir hosts in the sylvatic cycle, but people with chronic PKDL can also serve as important reservoir hosts for cutaneous leishmaniasis.[37] The most common vectors for cutaneous leishmaniasis in the Old World are sandflies of the genus Phlebotomus, while Lutzomyia and those within the family Psychodidae are the most common vectors in the New World. There are more than 600 species of phlebotomine sandflies, and only 30 of these are known vectors.[38] Cutaneous leishmaniasis has been seen in American and Canadian troops coming back from Afghanistan.[39]

Outbreak in 2016

The Middle East, in 2016, seems to be experiencing an increase in the cutaneous leishmaniasis disease due to migrants fleeing the Islamic State of Iraq and the Levant. Reports of the increase in the disease have surfaced in Turkey, Lebanon, and elsewhere.[40][41]

The huge increase in the spread of the disease is attributed to the refugee crises in the Middle East and North Africa over the past five years, particularly due to the displacement of millions of Syrian refugees.[42] The outbreak among Syrian refugees was documented by the World Health Organization (WHO) in 2012 and recognized as ongoing.[43]

A recent study with large series of cases from Mid-western region of Nepal have demonstrated that cutaneous leishmaniasis is an under recognized medical condition posing health challenges mandating new guidelines for its elimination/ eradication.[23]


A 2015 review article claimed that the development and use of a vaccine would be the best way to eliminate leishmaniasis from South Asia.[44] Attempts to create a vaccine with live, inactivated or attenuated Leishmania have failed.[45] Attempts to create a peptide, DNA, or protein vaccine have shown efficacy in animal vaccine models but not effective in humans.[45] There are a series of challenges with explanations in molecular biology which explain the difficulty of vaccine development.[45]

Vaccine development is difficult because the parasites live in humans, sandflies, and other animals, so a vaccine in humans alone would not eliminate the protozoan in insects and animals.[46] There is a challenge in interpreting the data in animal models to apply to humans.[47] Another challenge is effectively transferring knowledge from laboratory settings to field practice.[47] There is also a basic lack of scientific understanding of how an antiparasitic vaccine should generate and maintain immunological memory during parasitic infection.[47]The development of a vaccine using CRISPR-Cas9 technology was published in 2020[48] which showed that inoculation with a live attenuated Leishmania major strain induces durable protection, analogous to leishmanization. Another gene deletion mutant was created in a Leishmania mexicana strain in 2022, showing complete inhibition of the typical cutaneous lesions in mouse models thanks to a diminished induction of the Th2 cytokines.[49]

Other animals

A dog in Nicaragua with cutaneous leishmaniasis affecting the ear

Besides humans, cutaneous leishmaniasis often affects other animals, notably in dogs as canine leishmaniasis.[3]

Canine leishmaniasis was first identified in Europe in 1903, and in 1940, 40% of all dogs in Rome were determined to be positive for leishmaniasis.[50]

Traditionally thought of as a disease only found near the Mediterranean basin, 2008 research claims new findings are evidence that canine leishmaniasis is currently expanding in continental climate areas of northwestern Italy, far from the recognized disease-endemic areas along the Mediterranean coasts.[51]

Cases of leishmaniasis began appearing in North America in 2000,[52] and, as of 2008, Leishmania-positive foxhounds have been reported in 22 U.S. states and two Canadian provinces.[53]


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