**2. Epidemiology**

Visceral leishmaniasis (VL), also known as kala-azar, is a disease caused by an obligate intracellular protozoon belonging to the family Trypanosomatidae, genus *Leishmania*. It is transmitted through the bite of infected female sand flies and is widely distributed throughout the world (**Figure 2**). Currently, the World Health Organization considers VL as a neglected disease. An estimated 500,000 new cases of human VL occur per year [2]. Its epidemiology is extremely complex and depends on social and environmental variables, the species of *Leishmania* and the vector involved, and the behavior of reservoirs and hosts (**Table 1**).

**Figure 2.** World distribution of human visceral leishmaniasis, 2013 [3].


Adapted with permission from Refs. [4–6].

**Table 1.** Visceral leishmaniasis: species, region of occurrence, vectors, reservoirs, and mammal hosts.

#### **2.1. Biological cycle**

According to Pan American Health Organization (PAHO) and World Health Organization (WHO), there are more than 12 million people infected with leishmaniasis, and 350 million are at risk in the world. Cutaneous leishmaniases are concentrated in ten countries, four of which are in the Americas: Brazil, Colombia, Peru, and Nicaragua. Ninety percent of visceral leishmaniasis cases occur in Brazil, Ethiopia, India, Bangladesh, Sudan, and South Sudan. In the Americas, an average 60,000 cases of cutaneous and mucosal leishmaniasis and 4000 cases of visceral leishmaniasis are diagnosed annually, with a fatality rate of 7% (**Figure 1**) [1].

20 Canine Medicine - Recent Topics and Advanced Research

**Figure 1.** High-burden countries for both visceral and cutaneous leishmaniasis [2].

with emphasis in Brazil.

**2. Epidemiology**

The aim of this chapter is to describe the main aspects of canine visceral leishmaniasis (CVL)

Visceral leishmaniasis (VL), also known as kala-azar, is a disease caused by an obligate intracellular protozoon belonging to the family Trypanosomatidae, genus *Leishmania*. It is transmitted through the bite of infected female sand flies and is widely distributed throughout the world (**Figure 2**). Currently, the World Health Organization considers VL as a neglected disease. An estimated 500,000 new cases of human VL occur per year [2]. Its epidemiology is extremely complex and depends on social and environmental variables, the species of *Leishmania* and the vector involved, and the behavior of reservoirs and hosts (**Table 1**).

The life cycle of *L. infantum* is heteroxenic, that is, the parasite develops in two types of hosts: in the intermediate host, or the vector, the promastigote form develops in the insect gut; once in the definitive host, the amastigote develops as an obligate intracellular parasite in macrophages. During blood meals, vectors ingest macrophages containing *Leishmania* amastigotes, which will then multiply by binary division and differentiate into promastigotes. Promastigotes bind to the epithelium of the sand fly's esophagus or pharynx by the flagellum and then differentiate into metacyclic promastigotes, which is the infectious stage, unable to divide or bind to the midgut, remaining free in the digestive tract lumen [5, 7, 8].

Transmission occurs when the infected vector does a new blood meal and inoculates the infective form of *Leishmania* in the host. The sand fly regurgitates around 1000 metacyclics into the wound caused on the skin of a mammal [9]. When inoculated into the host organism, the parasite is phagocytized by the cells of mononuclear phagocytic system and loses the flagella. Next, it multiplies intensively by binary division, to the point of rupturing the host cell and releasing amastigotes, which then will be phagocytized by other cells and spread via blood and lymph to other tissues and organs [5, 7, 8].
