**4.1 Cutaneous leishmaniasis**

CL causing *Leishmania* parasites are divided into New world and Old world species. The New World species affect mainly Central and South America and include *L. amazonensis*, *L. braziliensis*, *L. mexicana,* and *L. guyaensis*, among others. The Old World species examples include *L. tropica, L. major,* and *L. aethiopica* that are common in the Indian subcontinent, the Middle East, the Mediterranean basin, and East

Africa. CL is usually a limited cutaneous disease. The lesions develop as papules at the sand fly bite site and progress over weeks to months to develop larger nodules that eventually ulcerate (**Figure 3**). Lesions are often itchy and may have a hyperkeratotic wart-like appearance. These lesions often self-heal in 2–18 months, leaving a permanent, often disfiguring, scar, leading to major cosmetic concern and social stigma.

increased number of lymphocytes making it difficult to histologically distinguish

*Diffuse cutaneous leishmaniasis* presents with multiple widespread nontender, non-ulcerating lesions, resembling lepromatous leprosy, and a negative leishmanin skin test (LST). The skin is heavily infiltrated by organisms and the patients lack a cellular immune response. These are caused *by L. amazonensis, L. aethiopica, and L.*

*Disseminated cutaneous leishmaniasis* presents with 10 or more mixed-type lesions in multiple body parts and is mostly seen in Latin America with frequent involvement of the mucosa. Histologically, the organisms are scant in the skin lesions, and

Most cases of diffuse cutaneous leishmaniasis and *L. recidivans* are chronic and resistant to treatment, may be exceedingly disfiguring, and can be associated with

*L. infantum/L. chagasi* predominantly causes VL; however, it may lead to atypical cutaneous disease. Reported cases are autochthonous, seen in immunocompe-

L. donovani is also mainly responsible for VL; however, some atypical autoch-

ML presents as destructive lesions involving oronasal mucosa with involvement of the nasal septum, lips, and palate. Ninety percent of ML cases show a previous CL scar. The disease is often chronic and progressive with destructive, disfiguring midfacial lesions leading to extensive mutilation. Secondary infection and respiratory tract invasion may lead to patient's demise. It is frequently seen in immunocompromised individuals and being a potentially life-threatening disease requires immediate/early diagnosis and treatment [21, 22]. Less than 5% of patients infected by *L. braziliensis* and a small percent of those infected by *L. panamensis* and *L. guyanensis* can develop mucosal involvement months to years after cutaneous dis-

*L. donovani* is the main species causing VL and humans are the main reservoir for it. *L. infantum* also causes visceral disease; however, it is zoonotic. VL is characterized by a "pentad" of persistent irregular fever, hepatosplenomegaly, weight loss, pancytopenia, and hypergammaglobulinemia. The fever characteristically shows a double rise in 24 hours with spikes of fever and afebrile intervals in between. It is the most devastating and fatal forms of leishmaniasis. The spectrum ranges from asymptomatic infection to fulminant life-threatening disease. The disease may present with an acute or insidious onset, however the typical presentation is that of wasted, thin, cachectic appearance with prominent abdominal distention due to hepatosplenomegaly. Jaundice is considered to be a bad prognostic sign. The incubation period is 2 weeks–8 months. High parasite burden is often associated with malnutrition and wasting in particular in children [23, 24]. VL is often associated with hyperpigmentation of the skin most likely secondary to production of adrenocorticotropic hormones. In such cases it is referred to as kala-azar/black fever [25]. VL, if untreated, is fatal within 2 years; mortality is mostly due to secondary bacterial infection, immunosuppression, hemorrhage due to hematopoietic

patients show positive antibodies against *Leishmania* and positive LST test.

tent hosts, and diagnosed in different regions [19].

thonous CL cases by *L. donovani* are reported [19].

**4.2 Mucocutaneous leishmaniasis**

from tuberculosis.

*DOI: http://dx.doi.org/10.5772/intechopen.90680*

*Leishmaniasis*

low mortality rates.

ease resolution [13].

**4.3 Visceral leishmaniasis**

infiltration, and severe anemia [13].

**303**

*mexicana.*

Approximately 10% of CL cases may progress to severe disease such as diffuse CL, ML, disseminated CL, and/or *L. recidivans* [1, 20].
