**1. Introduction**

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350 Leishmaniasis - Trends in Epidemiology, Diagnosis and Treatment

#### **1.1. Leishmaniasis**

Leishmaniasis is a vector-born disease caused by protozoan parasites in the genus *Leishma‐ nia*. Leishmaniasis is a potentially lethal, neglected disease that mostly affects economically disadvantaged individuals in many developing countries. Human infection occurs through the bite of infected female phlebotomine sand flies followed by injection of promastigote forms into the skin, which penetrate the macrophages and/or other types of mononuclear phagocytic cells. The promastigotes then transform into amastigotes (tissue stage of the parasite) in these cells and replicate, resulting in the bursting of the host cell and infection of other mononuclear phagocytic cells. Sand flies become infected by ingesting amastigote-infected cells during blood meals. These evolutionary forms transform into promastigotes in the gut of the insect and migrate to the proboscis, infecting other people through the bite (Scheme 1).

Depending on the *Leishmania* species involved and the host immune response, infection can lead to tegumentary or visceral manifestations of the disease. The tegumentary form of leishmaniasis (TL) includes cutaneous (CL), mucocutaneous (MCL), and diffuse (DL) clinical manifestations. All tegumentary forms have a major impact on patient life, because the skin lesions can lead to disfigurement and social stigmatization [2, 3]. Visceral leishmaniasis (VL), or Kala-azar, affects organs and internal tissues such as spleen, liver, bone marrow, and lymph

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**Scheme 1.** Leishmaniasis life cycle. 1- sand flies inject promastigotes during blood meals ;2-promastigote infects mac‐ rophages and other types of mononuclear phagocytic cells;3-promastigotes transform into amastigotes; 4-amasti‐ gotes multiply. 5- sand flies become infected by ingesting macrophages infected with amastigotes during blood meals; 6- parasitized cells ; 7- in sand flies, amastigotes transform into promastigotes, in the gut; 8- promastigotes di‐ vide and migrate to proboscis based on CDC, 2013 [1].

nodes. With the progression of VL, splenomegaly and hepatomegaly lead to a distended abdomen and pain. Eventually, VL may lead to death caused by secondary infections, severe anemia, or organ failure [4]. Both TL and VL are endemic diseases in several countries. In fact, the number of cases of leishmaniasis may be underestimated because only 40 of the 88 countries where the disease frequently occurs report cases on a regular basis [5, 6].

The World Health Organization (WHO) estimates that 1.6 million new leishmaniasis cases occur annually, of which 500,000 correspond to VL (90% of them occurring in Bangladesh, Brazil, Ethiopia, India, Nepal, and Sudan) and 1.1 million to CL (90% of them occurring in Afghanistan, Algeria, Brazil, Iran, Peru, Saudi Arabia, Sudan, and Syria) [7]. Leishmaniasis currently affects an estimated 12 million people and approximately 350 million people live at risk of infection [1], whereas an estimated half a million people die annually of VL. In addition, immunosuppressive conditions such as AIDS contribute to the emergence of severe clinical forms of the disease. To date, the greatest prevalence of *Leishmania*-HIV co-infection has been reported in the Mediterranean basin [8, 9]. In some east African regions, up to 40% of patients with VL are co-infected with HIV, which further complicates treatment [10].
