**3.3. Diagnosis and treatment**

The diagnosis of VL is still a challenge, especially in needy regions. Even though serological and molecular tests have improved the laboratory diagnosis of VL considerably, none of the available methods present 100% sensitivity and specificity [31]. The gold standard diagnosis method is still the identification of the parasite, with visualization of amastigotes from bone marrow or visceral aspirates, which holds 100% specificity. However, the sensitivity of the parasitological test varies depending on the sample, and aspirations are invasive and can cause life‐threatening hemorrhages. Serological methods, on the other hand, are highly sensi‐ tive but with varying specificity [32], showing cross‐reactivity with trypanosomiasis, malaria, tuberculosis, brucellosis and typhoid fever [31]. In addition, antileishmanial antibodies can be found in asymptomatic individuals and are still present after treatment and recovery, making the evaluation of therapeutic response difficult [33, 34]. Molecular techniques are remarkably sensitive and specific and can differentiate asymptomatic from clinically active infection even in HIV coinfected patients, but are costly [35, 36].

The first choice of treatment for VL is the antimonial N‐methyl glucamine followed by amphotericin B (AmpB) and derivatives [37] (**Table 1**). The AmpB isolated in 1955 as a natural antibiotic was first reported as having antileishmanial activity in the early 1960s. Currently, its liposomal formulation is used to treat VL with a 95% cure rate for a single‐course therapy [38, 39]. Although there are no absolute contraindications against the use of AmpB, nephrotoxicity [40] and hematotoxicity [41] should be considered [42].


\* The duration of treatment should be based on clinical outcome, considering the speed of response and the presence of comorbidities. Source: Ministério da Saúde [46].

**Table 1.** Medvications for treatment of VL according to molecular formula, presentation, dose and route of administration recommended in Brazil.

The liposomal form of AmpB is ideal in the treatment of leishmaniasis, since enables the drug to concentrate specifically at the site of infection, reducing the concentration in others organs [43, 44]. More recently, other drugs such as miltefosine, paromomycin and pentamidine have been used in the treatment of VL in some countries of Africa and Asia, but the efficacy and required dosage of several of these medicines have not been demonstrated in all endemic areas and may differ between these areas [20].

Some criteria need to be observed for the choice of treatment, such as assessment and stabili‐ zation of clinical conditions and comorbidities present at the diagnosis of VL and electrocar‐ diogram. The use of methylglucamine antimoniate has been especially critical in cases where resistance against pentavalent antimonials is widely spread [45].

Unfortunately, the majority of the population affected by VL is of low income, having no access to diagnosis and treatment options, thereby increasing the mortality rate due to the infection. In endemic areas, VL diagnosis is in most cases based only on clinical characteristics and epidemiologic aspects. Despite the urgent needs, research and development on leish‐ maniasis have been regrettably neglected.
