**1. Introduction**

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44 Leishmaniasis - Trends in Epidemiology, Diagnosis and Treatment

Health; 2009.

Leishmaniasis is considered by the World Health Organization (WHO) as one of the five endemic infectious and parasitic diseases of greatest importance and as a world-wide public health problem [1]. It is an infectious disease that evolves chronically and is caused by a protozoon of the genus *Leishmania*, which may appear as a clinical form which is visceral, cutaneous, mucocutaneous, mucousal and rarely diffuse [2]. The term Leishmaniasis refers to the infection of vertebrate hosts *Leishmania*, which, like the other trypanosomatids of the order Kinetoplastida, characteristically present an extranuclear DNA in its cytoplasm in a mito‐ chondrial organelle, the kinetoplast. This genus is characterized by having two ways of evolving during its biological cycle in host organisms: amastigote, which is an obligatory intracellular parasite in vertebrates, and promastigote, which develops in the digestive tube of invertebrate vectors or in axenic culture media [3].

In 1903, the agent of the disease was first described and separately by Leishman and Donovan. It is a protozoon identified in splenic tissue from two patients resident in India affected by a fatal disease [4]. It is primarily a zoonotic infection of wild animals, and more rarely pets, including marsupials, carnivores and even primates, with humans being accidental hosts.

All species of *Leishmania* are transmitted by the bite of female mosquitoes called phlebotominae of the genera *Lutzomyia* and *Phlebotomus*, this transmission being made by inoculation of promastigotes into the skin of the vertebrate host [5]. In larynegeal Leishmaniasis, contami‐ nation generally occurs starting with high lesions of the nasal cavities and oropharynx by contiguity. It is rare for parasites to be found inside the lesions [6].

The incubation period ranges from 2 weeks to several months [13]. Mucosal involvement is dependent on the combination of the virulence of the parasite and the immune cell response of the host. Within the population of infected individuals, 1-10% experience mucosal involve‐

ment [15]. Risk factors for the development of mucosal Leishmaniasis are: the presence of lesions above the pelvis, large skin ulcers and inadequate treatment of cutaneous Leishma‐ niasis [3].

For the diagnosis of mucosal Leishmaniasis, the clinical history and typical cutaneous scars have been considered as important clinical markers to corroborate the diagnosis of LM in patients with non-specific nasal/ oral granulomatous lesions [20].

In the Americas, pre-Colombus pottery, made by the Indians of Peru, has been found, dating from 400 to 900 AD. These show mutilations of lips and noses, characteristics of espundia, today known as muco-cutaneous leishmaniosis. Subsequently, through studies in paleome‐ dicine, mummies with skin lesions and mucosas characteristic of Leishmaniasis were found [9]. Historical findings suggest that American Cutaneous Leishmaniasis (ACL) already affected the peoples of America before contact with Europeans and Africans. It is assumed that it may have originated in the western Amazon region during archeological times by means of human migrations and later ascended to the high jungle and then to the hot inter-Andean lands across the frontiers of Bolivia and of Peru with Brazil [5].

In the Old World (Asia, Africa and Europe) written accounts of the disease date from the first century AD. About two thousand years later, in 1903, the agent of the disease is described for the first time and separately by LEISHMAN and DONOVAN. The disease was visceral Leishmaniasis and its agent, the species now known as *Leishmania donovani* [4].

The first reference to American Tegumentary Leishmaniasis (ATL) in Brazil is in the document of the Religious Political-Geographical Pastoral 1827, quoted in Tello's book entitled "Anti‐ guidad de la Syfilis en el Peru", where he recounts the journey of Friar Don Hipólito Sanches de Fayas y Quiros de Tabatinga (AM) to Peru, which crossed the regions of the Amazon basin [9]. In 1911, GASPAR VIANNA gave the parasite found by Lindenberg the name *Leishmania* brasiliensis, because he considered it morphologically different from *Leishmania* tropica. This characterized, from then on, the etiological agent of the disease being referred to as "Bauru ulcer", "angry angry" or "tapir-nose" [5].

In the 80s, the ATL was noted in 19 Federative Units (i.e. states), its geographical expansion being verified when, in 2003, autochthony was confirmed in all Brazilian states. It is seen to be widespread and, in some areas there is an intense concentration of cases, while in others, there are isolated cases [7]. The disease has been described in almost all American countries, from the extreme South of the United States to the North of Argentina, with the exception of Chile and Uruguay [22].
