Leishmaniasis has been the cause of great suffering and death for hundreds of years. Representations of skin lesions and facial deformities have been found on pre-Inca pottery from Peru and Ecuador dating back to the first century AD. They are evidence that some forms of leishmaniasis prevailed as early as this period. The discovery of parasites in lesions of cutaneous or visceral leishmaniasis was reported in the late 1800s and early 1900s .

1756;Russel:The first description in English
1898;Borovsky noted the protozoal nature of the organism
1903;Leishman identified the parasite
1903;Donovan described identical organisms in a splenic puncture



Leishmaniasis is the result of infection with intracellular protozoan parasites belonging to the genus Leishmania. The organisms are found in two morphologic forms during their life cycle. In humans and other mammalian hosts, they exist within macrophages as round to oval nonflagellated amastigotes and in the arthropod vectors (sandflies) the parasites exist as elongated flagellated promastigotes

About 30 species of sandflies can become infected when taking a blood meal from a reservoir host. In the old world genus Phlebotomus and in the new world genus Lutzomia are responsible for transmitting the disease. Sandflies are small mosquito-like insects 1.5 to 4 mm in length and their small size allows them to pass through ordinary mesh screens and mosquito netting.

Hosts are infected humans, wild animals, such as rodents, and domestic animals, such as dogs. Most leishmaniases are zoonotic (transmitted to humans from animals), and humans become infected only when accidentally exposed to the natural transmission cycle. However, in the anthroponotic forms (those transmitted from human to human through the sandfly vector), humans are the sole reservoir host.


Leishmaniasis presents itself in humans in four different forms with a broad range of clinical manifestations. All forms can have devastating consequences. Similar to Hansen disease, leishmaniasis is a disease in which the clinical diversity reflects a complex interplay between the virulence of the infecting species and the host's immune response. At one extreme, localized cutaneous disease demonstrates a vigorous immune response, with most cases resolving without intervention. This form of disease exhibits a helper T-cell subtype 1 (TH1) immune response, with interleukin 2, interferon g, and interleukin 12 as the prominent cytokines that induce disease resolution. At the other extreme, with visceral or diffuse cutaneous disease, patients exhibit relative anergy to the Leishmania organism and have a prominent helper T-cell subtype 2(TH2) cytokine profile.

Visceral leishmaniasis (VL), also known as kala azar, is the most severe form of the disease, which, if untreated, has a mortality rate of almost 100%. It is characterized by irregular bouts of fever, substantial weight loss, swelling of the spleen and liver, and anaemia.

Mucocutaneous leishmaniasis (MCL), or espundia, produces lesions which can lead to extensive and disfiguring destruction of mucous membranes of the nose, mouth and throat cavities.

Cutaneous leishmaniasis (CL) can produce large numbers of skin ulcers—as many as 200 in some cases—on the exposed parts of the body, such as the face, arms and legs, causing serious disability and leaving the patient permanently scarred. Diffuse cutaneous leishmaniasis (DCL) never heals spontaneously and tends to relapse after treatment. The cutaneous forms of leishmaniasis are the most common and represent 50-75% of all new cases.


Geographic Distribution

Increased Prevalence

Leishmania/HIV Co-infection

Leishmania/HIV co-infection is emerging as an extremely serious, new disease and it is increasingly frequent. Leishmania/HIV co-infections are considered a real threat, especially in south-western Europe where between 25% and 70% of adult VL cases are related to HIV

and where 1.5%to 9% of AIDS cases suffer form newly acquired or reactivated VL.

Intravenous drug users have been identified as the main population at risk.

 It is anticipated that the number of Leishmania/HIV co-infections will continue to rise in the coming years and there are indications that cases are no longer restricted to endemic areas. The overlapping geographical distribution of VL and AIDS is increasing due to two main factors: the spread of the AIDS pandemic in suburban and rural areas of the world, and the simultaneous spread of VL from rural to suburban areas.There are important clinical, diagnostic, chemotherapeutic, epidemiological and economic implications of this trend.

This duo of diseases produces cumulative deficiency of the immune response since Leishmania parasites and HIV destroy the same cells, exponentially increasing disease severity and consequences. VL is considered a major contributor to a fatal outcome in co-infected patients. Lately, however, use of tritherapy, where it is available, has improved the prognosis for Leishmania/HIV cases.

Specific Problems

The main alternative drugs include pentamidine, amphotericin B and amphotericin B encapsulated in liposomes. This encapsulation reduces the occurrence of side-effects, but relapses still occur and the drug remains extremely expensive.

Epidemiological Changes

Clinical Patterns 

Old world cutaneous leishmaniasis begins as a small erythematous papule, which may appear immediately after the bite of the sandfly but usually appears 2 to 4 weeks later. One or more lesions occur on unclothed part of the body. Lesions may be associated with sporotrichotic spread and usually heal spontaneously. The sequence of nodule, crusting, ulceration and healing with scar formation is common to all the self-healing sores.

Clinical variants of CL:

Diffuse cutaneous leishmaniasis (DCL): Analogous to lepromatous leprosy, individuals with DCL fail to mount a cell-mediated immune response to the Leishmania parasite. Consequently, patients develop multiple widespread cutaneous papules and nodules and are anergic to leishmanin skin testing.

Recidivans cutaneous leishmaniasis (RCL): A relatively uncommon clinical         variant of leishmaniasis, RCL presents as a recurrence of lesions at the site of apparently healed disease years after the original infection.Typically, RCL lesions occur on the face, and RCL presents as an enlarging papule, plaque, or coalescence of papules that heals with central scarring. Relentless expansion at the periphery may cause significant facial destruction similar to the lupus vulgaris variant of cutaneous tuberculosis.

Post kala azar dermal leishmaniasis (PKDL): Endemic to India and the Sudan, this form of leishmaniasis develops months to years after the patient’s recovery from visceral leishmaniasis. Cutaneous lesions demonstrate great variability, ranging from hypopigmented macules to erythematous papules and from nodules to plaques. As in leprosy, the wide clinical spectrum of PKDL reflects the immune response of the individual to the Leishmania organism. Lesions may be numerous and persist for decades. Isolated parasites from the lesions are identical to those causing the original visceral disease.


Differential diagnosis of LCL is extensive and includes impetigo, pyoderma gangrenosum, deep fungal infection, mycobacterial infection, sarcoidosis, and squamous cell carcinoma. In the endemic areas the clinical diagnosis is not difficult but the definite diagnosis rests on finding parasites in the skin. Usually, making a smear of material from the sore and staining it with Wright’s, Giemsa or Leishman’s stain on a microscope slide best achieve this. In addition, Polymerase chain reaction (PCR) is one of the newest techniques used to identify leishmaniasis and shows significant promise as a method applicable for both detection and speciation. Most research laboratories have reported higher sensitivity and specificity with PCR than with other currently available diagnostic methods.


The treatment of leishmaniasis depends on the clinical form of the disease. For 50 years, the mainstay of antileishmanial therapy has been pentavalent  antimony (sodium stibogluconate or meglumine antimonate).

Other measures include freezing, local heat, oral ketoconazole, rifampicin and topical paromomycin. Surgical excision usually is not recommended because of the risk of relapse and cosmetic disfigurement.

To date, no vaccines are available commercially.

The World Health Organization Response

WHO has set the following objectives:

1. To provide early diagnosis and prompt treatment;

2. To control the sandfly population through residual insecticide spraying of houses

and through the use of insecticide-impregnated bed nets;

3. To provide health education and produce training materials;

4. To detect and contain epidemics in the early stages;

5. To provide early diagnosis and effective management for Leishmania/HIV coinfections.


Because of the anticipated substantial increase in Leishmania/HIV co-infections, they are among the priorities for WHO's Department of Communicable Disease Surveillance and Response (CSR).

The evolution of Leishmania/HIV co-infection is being closely monitored by extending the geographic coverage of the surveillance network and by improving case reporting. WHO encourages active medical surveillance, especially in south-western Europe, of intravenous drug users, the main population at risk. Finally, because case notification of leishmaniasis is compulsory in only 40 of the 88 endemic countries, WHO strongly suggests the remaining 48 endemic countries follow suit.


Leishmaniasis is a disease caused by protozoa, and it affects as many as 12 million people worldwide, with 1.5-2 million new cases each year. Transmitted by the bite of a sandfly, the clinical spectrum of leishmaniasis ranges from a self-resolving cutaneous ulcer, to a mutilating mucocutaneous disease, to a fatal systemic illness. The global incidence of this infectious disease has been increasing during recent years because of increased international travel, human alteration of vector habitats, and concomitant factors that result in increased susceptibility such as HIV infection and malnutrition. Many Leishmania species transmit the disease, and the clinical spectrum, although once believed to be predictable, continues to evolve. Diagnosis may be difficult because of the small size of the protozoa sequestered within macrophages of the skin, bone marrow, and reticuloendothelial system. Therapy has long been a challenge for the more severe forms of the disease and is made more difficult by the emergence of drug resistance. No effective vaccine is available for leishmaniasis.



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