**1. Introduction**

Leishmaniasis is a serious public health problem in many countries throughout the world. The illness is caused by numerous intracellular protozoan parasites of the genus *Leishmania*. The most frequent vectors of this neglected infectious illness are phlebotomine sandflies, *Phlebotomus* and *Lutzomyia*, which is most widespread in the tropics and subtropics of Africa, Asia, America, and southern Europe. This illness is the world's second most lethal parasitic killer (after malaria). It's multifaceted. It can be a deadly murderer in certain forms, or a merciless mutilator who disfigures its victims for life in others. There are now an estimated 12 million cases of leishmaniasis in 98 countries, with 1.5–2 million new cases emerging annually, 1–1.5 million instances of cutaneous leishmaniasis, and 5,00,000 cases of visceral leishmaniasis (VL). VL can create large-scale epidemics with a high case fatality rate. VL (kala-azar) is a latent danger to more than 147 million people residing in the disease-endemic South East Asia region of the Indian subcontinent, which is

caused by *Leishmania donovani*. Out of the five VL-affected nations in the area (India, Bangladesh, Nepal, Thailand, and Bhutan), India accounts for more than 80% of recorded cases, while Bhutan and Thailand have sporadic reports. Bihar is the most VL-endemic state in India, accounting for 90 percent of all VL cases in the country [1]. *L. infantum, L. chagasi,* or *Leishmania donovani* are the parasites that cause Visceral Leishmaniasis (VL) in North Africa and Southern Europe as well as Latin America and East Africa respectively [2]. The transmission of *L. donovani* is usually thought to be anthroponomic. Its prevalence is gradually growing around the world, creating a public health issue in the VL endemic zone. The classic WHO definition of Visceral Leishmaniasis is "a person with clinical symptoms (primarily persistent irregular fever, splenomegaly and weight loss) and serological and/or parasitological evidence." Leishmaniasis Post Kala Azar (PKDL) has been related to Visceral Leishmaniasis (VL). According to WHO, probable PKDL affects individuals from VL endemic areas who have numerous hypopigmented maculae, papules, plaques, or nodules but no corresponding loss of sensitivity. However, these are the circumstances in which *Leishmania* infection manifests as symptoms. Many people in endemic locations are infected with the parasite yet show no symptoms of the sickness, according to previous research. These are classified as asymptomatic stages of *Leishmania* infection. *L. donovani* infection can range from asymptomatic carrier to full-blown symptomatic illness with persistent fever, splenomegaly, pancytopenia, and hypergammaglobulinemia. Visceral leishmaniasis has an asymptomatic incubation period of variable duration [3]. A large majority of those who have been exposed to the parasite are asymptomatic, with just a tiny number of people exhibiting clinical manifestations [4, 5]. A disease is considered asymptomatic if it lacks the visible symptoms that are normally associated with it. Asymptomatic conditions may not be detected unless medical tests are performed. Importantly, doctors lack the tools necessary to tell apart asymptomatic patients from those who are suffering from something more subtle [6]. In a Mexican cutaneous leishmaniasis region in 1953, the term asymptomatic in *Leishmania* infection was first used [7]. Asymptomatic *Leishmania* infection was used initially in 1974 by Pampiglione but the description has remained ambiguous five decades later. At this time, there is no way of knowing who of the asymptomatically infected persons would acquire VL illness and when. Asymptomatic people are those who live in an endemic region and have an immune response to L*eishmania* (either antibodies or a particular cellular response), or who have parasites—or parasite DNA—in their blood, but are otherwise healthy [8]. Escalating asymptomatic leishmaniasis due to distinct *Leishmania* species like *L. donovani* and *L. infantum* is critical for determining trends in the disease's prevalence. This first interaction between parasite and host is known as infection. The parasite can be killed by inherent or acquired immunity in the host, or it might persist by using an effective mechanism that bypasses the host's defenses. If the parasite persists, it may lead to a fascinating dynamic interaction between the host and parasite, where the host becomes an asymptomatic carrier when everything is in balance. Due to co-evolution, it is quite frequent in several parasite illnesses for the number of patients to be less when compared to the vast number of persons with asymptomatic infection (in general, an infected person who is asymptomatic is not necessarily a patient). Because of this, asymptomatic instances of VL are common in regions with the disease [9, 10].

### **2. Epidemiology**

It is essential to understand the global prevalence of asymptomatic leishmaniasis. In addition, it's critical to look at the variables that contribute to asymptomatic

#### *Visceral Leishmaniasis: Asymptomatic Facts DOI: http://dx.doi.org/10.5772/intechopen.101109*

infection. The variation arises because of changes in parasite virulence and host demographic characteristics, as well as from research designs and the tests employed to determine asymptomatic infection. Worldwide epidemiological statistics show that asymptomatic VL can come from both endemic and non-endemic areas. Those who are infected may unintentionally transfer the disease to others. They may go away on their own, or they may develop symptoms at a later time. As per some findings Asymptomatic infections are those who remain seropositive for many (up to 10–12) years without developing into active disease [11, 12], and are more prevalent in VL endemic regions [13]. In the New World, asymptomatic leishmaniasis was considerably more frequent than in the Old World. The higher prevalence might be explained by the greater diversity of leishmaniasis in the New World as a result of the vector's adoption of new hosts and climate change [14]. Asymptomatic leishmaniasis was less common in children than in the general population. This difference, however, was insignificant on a statistical basis. It was hypothesized that the rise in infection prevalence with age was owing to young children's reduced exposure to infectious sandfly bites [15]. Some indicators indicate that in VL endemic locations, the ratio of asymptomatic vs. active VL patients varies: 2.4:1 in Sudan, 4:1 in Kenya, 5.6:1 in Ethiopia, between 4:1 and 17:1 in the Indian subcontinent, and 50:1 in Spain [16]. Reports from the other endemic regions also confirm the existence of parasitic DNA in all VL causing species in asymptomatic individuals.

According to a meta-analysis of original articles reporting asymptomatic leishmaniasis, the prevalence of asymptomatic leishmaniasis was 11.3%, 95% confidence interval (CI) 8.6%–14.4%] in general population, 36.7% [95% CI 27.6%–46.8%] in inhabitants living in the same or neighboring household to the symptomatic patients, and 11.8% [95% CI 7.1–19%] in HIV infected patient. Meta-regression analysis also showed no significant change in the prevalence of asymptomatic leishmaniasis during the last 40 years [17]. From 1982 to 2015, the trend of total leishmaniasis' asymptomatic proportion did not change considerably, according to the meta-regression study [coefficient = 0.0350 (95% CI, −0.0213 to 0.0913), P = 0.2233] [17]. But, while the disease's geographical range is broad, it is not continuous. The study also suggest, for *L. donovani*, the pattern of asymptomatic infection has not altered over time [coefficient = 0.0015 (95 CI, −0.0531 to 0.0561), P = 0.9564]. In contrast, the frequency of asymptomatic *L. infantum* infection has grown with time, although this shift is statistically insignificant [coefficient = 0.0824 (95 percent CI, −0.0126 to 0.1774), P = 0.0892]. According to research on *L. infantum* in the New World, the prevalence has considerably grown over time [coefficient = 0.0908 (95% CI, 0.0321 to 0.1496), P = 0.002]. The frequency of asymptomatic leishmaniasis in children is also rising over time [coefficient = 0.0599 (95% CI, 0.0066 to 0.1133), P = 0.028]. Drought, hunger, and high population density all contribute to the spread of the illness. The infectionto-disease ratio varies from village to village and also changes over time within the same community [18]. Asymptomatic incident *L. donovani* infection is nine times more common than incident VL illness in VL high-endemic foci in India and Nepal [19]. Within the next 18 months, around 1 in 50 of new yet latent infections developed into VL. There is one important asymptomatic category comprises those individuals of endemic regions who turn seronegative in due course of time [19]. These people most likely acquire the required level of immune response following parasite exposure, which protects them from future illness development by efficiently removing living parasites. They are most likely not carrying live parasites and can be called real resistant instances. The spontaneous change of seropositive to seronegative status ranges from 33–86% [19–22]. However, a research conducted in Bangladesh found that this conversion rate drops to as low as 6.3% after a year

among those with high antibody titers [23]. These people give more tangible proof that a threshold immune response level is required to protect the host against parasites. Despite the fact that the majority of seropositive asymptomatic people go on to become seronegative, these individuals are known to contribute to the spread of disease outside of endemic areas [24, 25].
