Epidemiology of Leishmaniasis

Abstract

A zoonotic illness of importance to the public’s health is leishmaniasis. Leishmania donovani, Leishmania tropica, Leishmania major, Leishmania infantum, Leishmania chagasi, Leishmania mexican, and Leishmania braziliensis are the most recognised and widely distributed leishmania parasite species, and they are also the ones that cause the disease. On every continent and in more than 90 countries, the disease is present, however it appears to be absent from Australia. The disease is spread by Phlebotomus sandflies, and people, rodents, and other domestic animals act as reservoirs and unintentional hosts. Cutaneous leishmaniasis, diffuse cutaneous leishmaniasis, mucocutaneous leishmaniasis, and visceral leishmaniasis are the four ways the illness can present. The spread of the disease, as well as its appearance and reemergence, are caused by risk factors include regional warfare and wars, political instability, migration of people, substandard housing, climate, vegetation cover, p7oor socioeconomic standard of life, and lack of access to quality medical care. To eradicate the disease, particularly in poor nations where it is still a threat, there is a need for increased public education, government involvement, proper surveillance, and disease reporting.

1. Introduction

Leishmaniasis is a disease that is caused by the parasite Leishmania; comprising of at least 20 species that affect humans. The parasite is primarily transmitted by the sand flies that belongs to the Phlebotomus in the old world and Lutzomyia in the new world; however, other principal hosts are rodents such as Rhombomys opimus, Tatera indica, Meriones hurrianae, and Meriones libycus gerbils which are of the Zoonotic cutaneous leishmaniasis (ZCL) [1, 2, 3, 4, 5]. The disease is associated with and limited by the geographical distribution of its sand fly vectors. Fifteen geographical entities have been classified worldwide, of which 13 zoonotic in nature. In recent years, there have been significant increase in the number of regions becoming Leishmania-endemic, accompanied with an increased number of animal and human cases. These parasites have been reported to be maintained and circulated in mammals with each species having a specific reservoir host [6]. The clinical spectrum of the disease in humans can be asymptomatic infections in some individual and can result in high mortality, which depends on the form of the disease and can be categorised into three (4) namely; visceral leishmaniasis (VL), cutaneous leishmaniasis (CL), diffuse cutaneous leishmaniasis (DCL) and mucocutaneous leishmaniasis (MCL). In dogs, Leishmania infantum and Lieshmania chagasi are now regarded as synonyms and are the species known to be responsible for chronic visceral-cutaneous disease in this host (canine leishmaniosis). Asymptomatic infections occur in dogs and other canines thereby maintaining the presence of the parasite in endemic regions [6]. The ability of the host macrophages to effectively destroy the parasite is as a result of host- parasite interaction which is responsible for clinical appearance. Leishmaniasis is classified as a prominent neglected disease of the tropics due to the number of death per year (40,000) with a global distribution with Indian sub-continent having the highest number of cases followed by Bangladesh, Sudan, South Sudan, Ethiopia, and Brazil [7, 8].

1.1 Cutaneous leishmaniasis

The aetiological agent responsible for cutaneous leishmaniasis are as follows: Leishmania tropica, Leishmania major, and Leishmania aethiopica, also known as old- and new-world leishmania species, are found in southern Europe, the Middle East, Asia, and Africa, respectively. These species include Leishmania guyanensis, L. viannia braziliensis, L. viannia amazonesis, L. viannia panamensis, and the Leishmania mexicana complex (Latin America). Skin ulcers on the exposed body parts, such as the face, arms, and legs, as well as lesions that leave the patient permanently disfigured and prone to social judgement, are the hallmarks of cutaneous leishmaniasis. The incubation time is roughly 2 to 6 weeks [9]; cases of up to 3 years have been documented for Old World cutaneous leishmaniasis [10], whereas the incubation period for New World cutaneous leishmaniasis is typically 2 to 8 weeks [11]. Over 85% of newly discovered CL cases in 2018 that were reported to the WHO originated in Afghanistan, Algeria, Bolivia, Brazil, Colombia, Iran, Iraq, Pakistan, Syria, and Tunisia, while over 95% of newly discovered LV cases originated in Brazil, China, Ethiopia, India, Iraq, Kenya, Nepal, Somalia, and Sudan. Finally, four nations—Brazil, Bolivia, Ethiopia, and Peru—reported almost 90% of all new cases of mucocutaneous leishmaniasis (MCL) [12].

1.2 Mucocutaneous leishmaniasis

Leishmania viannia braziliensis, leishmania viannia amazonesis, leishmania viannia panamensis, and leishmania viannia guyanesis are the leishmania species that cause mucocutaneous leishmaniasis. The progression of this illness is controlled by parasite virulence and host cell mediated immunity. The condition starts with erythema and ulceration of the nose, which progresses to continuous degradation of the cartilage in the upper airway and facial structures, oronaso-pharyngeal mucosa, disfigurement, and obstruction of the airway [13].

1.3 Diffuse cutaneous leishmaniasis

Even in nations where leishmaniasis is endemic, diffuse cutaneous leishmaniasis is a rare manifestation of the illness. Leishmania mexicana and Leishmania aethiopica are the parasites that cause this type of leishmaniasis. A small, painless bump at the site of the innoculation causes spreading, non-ulcerating macules, nodules, and plaques that range in colour from erythematous to violet. The face, upper and lower limbs, and buttocks are the area most commonly affected [14, 15].

1.4 Visceral leishmaniasis

Leishmania donovani is the cause of visceral leishmaniasis. The most serious type of the disease, which affects internal organs like the spleen and liver and can be deadly if neglected, is Kala-azar cutaneous leishmaniasis, which ranges from hypopigmented macules to infiltrating papules [16]. The incubation period ranges from three to eight months [17]; symptoms include fever, weight loss, hepatosplenomegaly, lymphadenopathy, pancytopenia, and hypergammaglobulinaemia; skin pigmentation may also be present [18]; “kala azar,” also known as black disease, may be asymptomatic and self-resolving, but typically has a chronic course and can be fatal with or without treatment [19]; death typically results due to bacterial infections. In the Indian subcontinent, Bangladesh, India, and Nepal are the most severely affected and account for 28% of cases, while Brazil contributes 20%. The three eco-epidemiological hotspots where VL has been identified are East Africa, where countries like Ethiopia, Kenya, Somalia, South Sudan, Sudan, and Uganda contribute 45% of global cases (Figure 1 [20] and Table 1 [21, 22, 23]) [24].

Figure 1.

Shows the geographical distribution pattern of leishmaniasis [20].

	Leishmania species
Old world cutaneous leishmaniasis	Leishmania tropica, Leishmania major, Leishmania infantum, Leishmania aetheiopica
New world cutaneous leishmaniasis	Leishmania vianna subgenous (e.g., Leishmania vianna braziliensis, Leishmania vianna panamensis, Leishmania vianna guyanensis, Leishmania vianna peruviana, Leishmania amazonensis) and Leishmania Mexicana complex

Table 1.

Shows old world and new world cutaneous leishmaniasis [21, 22, 23].

2. Main text

2.1 Distribution pattern, vector and causative agents of Leishmaniasis

Leishmaniasis is endemic in several parts of Africa. In North Africa, nations including Morocco, Algeria, Tunisia, Libya, and Egypt have recorded numerous instances of the disease, with cutaneous and visceral leishmaniasis being the most prevalent types [25]. Important species that are spread by the phlebotomus sand fly include L. major, L. tropica, L. infantum, and Labrus donovani. L. major is the main cause of cutaneous leishmaniasis, with L. tropica and L. infantum playing a less significant role. Visceral leishmaniasis (VL) has been linked to L. donovani, L. infantum, and infrequently L. tropica. Zoonotic cutaneous leishmaniasis (ZCL) and Anthropogenic cutaneous leishmaniasis (ACL) are the two kinds of cutaneous leishmaniasis seen in this region [6, 26, 27, 28]; with ZCL being caused by L. major and transmitted by mainly by P. papatasi, P. duboscqi and P. salehi with P. papatasi considered among the most widespread invasive sandflies species in these regions and the also has a worldwide distribution; Psammomys obesus, Meriones libycus, Meriones shawi, Nesokia indica, and Rhombomys opimus rodents also transmit the disease, while ACL is caused by L. tropica is transmitted by P. sergenti and gundi and hyraxes and Leishmania killicki with dogs also serving as accidental host in some cases [6, 29, 30, 31, 32, 33]. Additionally, there are two types of visceral leishmaniasis: (ZVL). Anthropogenic visceral leishmaniasis (AVL), which is caused by L. infantum, is primarily zoonotic, with candida serving as the principal reservoir and humans serving as unintentional hosts [34, 35, 36]. The most common form of leishmaniasis in Morocco, Algeria, and Lybia is cutaneous leishmaniasis, which is caused by the L. tropica species [37, 38, 39, 40]. According to reports, L. tropica is a reservoir host in Ethiopia and Chad has noted an upsurge in visceral leishmaniasis in Central Africa [41, 42].

The countries of Sudan, South Sudan, Ethiopia, Kenya, Uganda, and Somalia make up one of the main geographic regions in East Africa most severely affected by VL, where the disease is primarily brought on by Leishmania donovani and, in certain cases, Leishmania infantum [43, 44, 45]. With the confirmation of Phlebotomus orientalis, Phlebotomus martini, Phlebotomus celiae, and Phlebotomus rodhaini as VL vectors [46, 47, 48, 49, 50], man and dogs serve as potential reservoir hosts. Subgenera such as Paraphlebotomus, Synphlebotomus, Larroussius, and Anaphlebotomus have also been reported [51, 52]. In East Africa, children under the age of 15 make up about 65% of VL cases, and having inadequate levels of protein, energy, iron, vitamin A, and zinc increases the risk of VL manifestation [53]. In East Africa, cutaneous and mucosal leishmaniasis have both been attributed to Leishmania donovani [54, 55, 56]. VL has been reported and is prevalent in Kenya, Uganda, and Somalia along their borders; L. donovani and L. infantum are the parasites responsible for the disease [57, 58, 59]. Every year, Sudan reports over two-thirds of the VL cases in East African nations; the majority of these cases are presumed to be caused by L. donovani [60, 61], and recent outbreaks in South Sudan have been linked to over 100,000 fatalities between 1983 and 2005 [62]. It is possible for VL to develop complications that lead to post-kala-azar cutaneous leishmaniasis, which is characterised by a macular or nodular rash that frequently starts at the mouth and is transmitted by P. argentipes and P. orientalis [63].

The disease has also been documented in Cameroon, Burkina Faso, Mauritania, Gambia, Guinea, and Nigeria in West Africa. Lieshmaniasis was originally identified in Niger, then in Nigeria, Senegal, and Mali. Mauritania, Gambia, Senegal, Nigeria, Cameroon, and Ghana are among the countries where CL is endemic and is caused by L. major [64, 65]. The only known case of MCL in the area is in Senegal, while the only instances of VL have been recorded in Togo and Burkina Faso with L. donovani as the causing agent [66]. Rodents including Mastomys erythroleucus, Tatera gambiana, Arvicanthis niloticus, and Mastomys erythroleucus, as well as dogs in Gambia, serve as the reservoir host for L. major. The parasites L. major and L. donovani, which transmit VL and CL in Ghana, Nigeria, and Senegal, respectively, are the most prevalent forms to be recorded together with P. duboscqi and P. rodhaini [66, 67, 68, 69].

Syria has historically been endemic to CL due to L. tropica for centuries and, at one point, had the highest burden of this form of leishmaniasis in the region. Recent research indicates that political unrest, wars, and population migration have contributed to an increase in cases in the Middle East [70]. Due to the influx of migrants, these circumstances have caused outbreaks to be reported in 2012 in other countries including Lebanon, which have seen a rise in the number of cases recorded [71, 72]. L. tropica has also been claimed to be endemic in Israel and the Philistines, while the cycle of transmission is not completely understood. With a widespread geographic distribution throughout the region, Phlebotomus (Paraphlebotomus) sergenti has been identified as the primary vector of L. tropica [73, 74, 75]. Phlebotomus arabicus and Phlebotomus similis have also been documented. Leishmania major has reportedly been linked to CL in Southern Israel; this type of the illness is self-healing but makes the patient anxious. The reservoir host is the obese sand rat Psammomys obesus (Cricetidae: Gerbillinae), and P. obesus and the sand fly Phlebotomus papatasi (Diptera: Psychodidae) serve as the vectors [76]. Leishmania majori, the parasite that causes CL and VL, is the primary carrier of both the disease and its primary vector, P. papatasi. VL is primarily brought on by Leishmania infantum, though L. tropica can also be to blame in some cases. CL comes in two forms: ZCL and ACL, which are caused by L. major and L. tropica, respectively. Rodents are the main reservoir hosts, and some of the more endemic species include Rhombomys (R.) opimus, Meriones libycus, Tatera (T.) indica, and Meriones hurrianae. Phlebotomus papatasi transmits L. major, whereas Phlebotomus sergenti transmits L. tropica [70, 77, 78, 79]. ACL and ZCL are present, L. tropica and L. major are endemic in Saudi Arabia, and CL is declining with fewer instances being reported [80, 81, 82, 83]. The most common kind of leishmaniasis in Iraq is CL, which is caused by the parasites Leishmania tropica and Leishmania major [84, 85, 86]. ACL and ZCL are the two types of CL that are endemic in Pakistan [87]; L. tropica and L. major are the two known forms of the parasite that transmit CL [88, 89, 90]. The frequency of ACL is higher than ZCL in Afghanistan, where L. tropica is known to account for 96 to 98% of CL cases [91]. ACL is said to be endemic in Turkmenistan, with L. major as the causative agent [8].

Countries in Europe, including Greece, have reported occasional cases of CL caused by L. tropica; Phlebotomus sergenti has been identified as the disease’s primary vector and is thought to be responsible for its spread [92]. There have been reports of Phlebotomus tobbi and Phlebotomus perfiliewi as potential L. tropica vectors [93]. Although CL caused by L. tropica has not been documented in Europe, P. sergenti was found in Greek camps where 21 different sand fly species had significant levels of L. tropica infection. The emerging and re-emerging of leishmaniasis in Europe has been attributed to the introduction of exotic Leishmania species or strains via worldwide travelling of humans and domestic dogs; this is also responsible for the spread of visceral and cutaneous leishmaniasis caused by L. infantum and L. tropicai due to their endemicity from the Mediterranean region of Europe to neighbouring temperate areas where there are vectors without disease [90, 94]. A high risk of leishmaniasis spreading to Europe is posed by both zoonotic cutaneous and visceral leishmaniasis caused by L. infantum in the Mediterranean region and anthroponotic cutaneous leishmaniasis caused by L. tropica in Greece. Additionally, the presence of Phlebotomus sandflies without the disease is of public health concern [95]. A retrospective study of leishmaniasis across Europe revealed that cutaneous leishmaniasis was the prevalent form of the disease that occurred in 11 countries followed by visceral and mucosal disease with L. donovani, L. infantum (syn. L. chagasi in New World), L. major, L. amazonensis (syn. L. garnhami), L. Mexicana, L. aethiopica, L. tropica, L. braziliensis, L. peruviana, L. guyanensis, L. panamensis, L. lainsoni, L. naiffi, L. siamensis /Lechytia martiniquensis been the parasites identified and responsible for the disease [96].

In North America, parasite species in the genus Leishmania are responsible for different clinical pathologies of the disease which include VL that is deadly and caused by L. chagasi, as well as MCL, localised Leishmaniasis, diffuse Leishmaniasis; MCL has been reported to be caused by L. brasiliensis, L. panamensis and L. guyanensis; DCL are related to L. m. mexicana, L. amazonensis, L. pifanoi, L. guyanensis, and L. panamensis [97]. Female blood-feeding sand flies of the genus Lutzomyia (Diptera: Psychodidae: Phlebotomidae) are the transmission vector in Mexico, the United States, and Canada; humans are incidental hosts while mammals serve as reservoir hosts; L. mexicana is responsible for the majority of human cases that have been reported [98]. Leishmania infantum, which causes canine visceral leishmaniasis, has been reported in dogs and cats. While cutaneous Leishmania mexicana is endemic to the United States, visceral leishmaniasis is not considered endemic among humans but primarily affects dogs, which are thought to be the reservoir host for humans [99, 100].

Leishmania (Viannia) braziliensis, L. (Viannia) amazonensis, L. (Viannia) guyanensis, and L. Infantum, associated with visceral leishmaniasis, were the four species of Leishmania cases reported in humans in South America. In addition, 28 species of Phlebotominae (23 species of Lutzomyia, 4 species of Brumptomyia, and 1 species of [101]. Both CL and MCL are induced by L. Braziliensis: Lutzomyia neivai, L. Whitmani, L. Cortelezzii complex (L. Cortelezzii, L. Sallesi), L. Migonei, and L. Pessoai, while V is brought on by L. Infantum was L. Longipalpis [102]. However, domestic and wild canids have been well established as the reservoir host of leishmania, with more than 20 species of the parasites being transmitted by the phlebotomine vectors (Diptera, Psychodidae); CL and VL are the two major forms of the disease where Leishmania (Viannia) braziliensis, Leishmania (Leishmania) amazonensis, L. mexicana, L. donovani causes VL in the old world, but L. infantum does so in the new world [103, 104, 105, 106, 107]. In Colombia several species of Leishmania parasites have been reported to infect humans with CL been the major form of the disease followed by MCL and VL; L. braziliensis, L. panamensis and L. guyanensis have been responsible for the outbreaks of CL; other parasites include L. lainsoni, L. amazonensis, L. infantum chagasi, L. Mexicana, L. colombiensis and L. equatoriensis, this country is ranked second only to Brazil in terms of cases of leishmaniasis [108, 109, 110]. In Bolivia, Leishmania (Viannia) lainsoni, Leishmania (Viannia) guyanensis, Leishmania (Viannia) panamensis and Leishmania (Leishmania) amazonensis have been described as a causal agent of Tegumentary leishmaniasis (TL) (CL, MCL, DCL) with transmission also reported to be zoonotic and caused by Nyssomyia neivai, Cortelezzii complex, Evandromyia sallesi, Migonemyia migonei and Micropygomyia quinquefer [111].

The parasite L. donovani, the vector Phlebotomus annandalei, Phlebotomus argentipes sensu stricto, and Phlebotomus glaucus, and the disease CL, MCL, and VL are all endemic throughout Asia [112]. VL, which is indigenous to Nepal and brought on by L. donovani, can occasionally lead to post-Kala-azar cutaneous leishmaniasis [113]. Similar to Kala-azar sickness, VL is chronic in Bangladesh and can lead to it. L. donovani is thought to be the main cause of the illness, while Phlebotomus papatasi is the disease’s vector in Asia [114, 115].

Leishmania donovani is the chronic disease that causes VL on the Indian subcontinent; however, L. tropica or L. infantum, particularly when co-infected with HIV, can also cause the illness; Phlebotomus argentipes is the vector for VL, with humans functioning as reservoir hosts. PKDL does not have an animal reservoir, and transmission is thought to be anthroponotic [116, 117]. VL is also known as kala-azar, which is the Hindi word for “black disease” (Table 2).

Clinical forms	Leishmania parasite	Geographical distribution
CL	L. major, L. tropica, L. infantum, and Labrus donovani; L. braziliensis: Lutzomyia neivai, Lu. Whitmani, L. Cortelezzii complex (L. Cortelezzii–L. Sallesi), L. Migonei, and L. Pessoai, L. (L.) peruviana, L. lainsoni, L. amazonensis, L. infantum chagasi, L. Mexicana, Leptodactylus colombiensis and L. equatoriensis	Morocco, Algeria, Tunisia, Libya, Egypt; Chad; Sudan, South Sudan, Ethiopia, Kenya, Uganda and Somalia; Niger, Nigeria, Senegal and Mali; Cameroon, Burkina Faso, Mauritania, Gambia and Guinea, Ghana; Syria, Lebanon, Israel, Philistines, Iran, Saudi Arabia, Iraq, Pakistan, Afghanistan, Turkmenistan; Greece; United State of America; Bolivia, Brazil, Colombia, Peru; Sri Lanka, China, Nepal Bangladish; India, and
MCL	L. viannia braziliensis, L. viannia amazonesis, L. viannia panamensis and L viannia guyanesis	Senegal; Colombia; Sri Lanka
DCL	L. Mexicana, L. aethiopica, L. amazonensis, L. pifanoi, L. guyanensis, and L. panamensis	Mexico, United States, and Canada
VL	L. donovani, L. infantum, L. tropica, L. chagasi	Ethiopia, Kenya, Somalia, South Sudan, Sudan, Chad, Togo, Burkina Faso, Cameroon and Uganda; Iran, Bangladesh, Sri Lanka and Nepal; India; Brazil, Argentina, Colombia; India

Table 2.

The table below shows the clinical form of leishmaniasis and their geographical distribution [21, 22, 23].

3. Leishmaniasis and HIV co-infection

There have been reports of leishmania-HIV co-infection in 45 countries in 2021, with Brazil, Ethiopia, and Bihar in India having the highest number of cases [118]. According to a report by the WHO in 2022, people who have leishmaniasis and HIV are at an increased risk of developing full clinical disease, high relapse rates, and mortality rates. Leishmaniasis and HIV co-infection have also been shown to occur in CL and VL [119, 120]. A change in immune response brought on by immunosuppression caused by a low CD4 T-lymphocyte count and the development of immunological activation with cell senescence are two examples of the clinical manifestation of VL [121].

4. Risk factors in the distribution of Leishmaniasis

Conflict, climate (temperature, rainfall, relative humidity, precipitation), physical (geographical barriers), and biotic (distribution and abundance of vertebrate hosts) factors, socioeconomic circumstances, environmental (land degradation, agricultural activities, deforestation due to urbanisation), domestic animals and living standards, immune response of hosts, and conflict have all been linked to the distribution of leishmaniasis [6]. Although no consistent pattern has been identified, civil wars, social unrest, migration, forced population displacement, rainfall, humidity, temperature, soil types and moisture contents, and land cover type are significantly associated with the distribution pattern of these sandflies and contribute to emerging and re-emerging outbreaks [18].

5. Climatic conditions

Leishmaniasis is a disease that is sensitive to climate because variations in temperature, precipitation, and humidity have a significant impact on the life cycles of the parasite’s vectors and reservoir hosts. Climate changes can also affect the distribution, survival, and population of the vectors and reservoir hosts [122]. Sandflies have been reported to be abundant between the months of June and September with P. argentipes being active between this period in India with temperature ranging between 27 and 31°C [123, 124]. Fluctuations in temperature can negatively affect the developmental life cycle of leishmania promastigote in sandflies, which can result in the transmission of the parasite into areas not previously endemic for the disease.

5.1 Vegetation cover

Leishmaniasis outbreaks have been shown to decrease with the improvement of vegetation types that limit rodent growth [125]; it has also been established that areas with thick or dense vegetation cover have a higher risk of leishmaniasis infection and transmission [126]. Forest fragmentation and deforestation have been linked to an increased risk for leishmaniasis.

5.2 Age and gender

Leishmaniasis has been found to affect adults more frequently than children; this could be because younger people are less exposed to the parasites and vectors that cause the disease, especially in rural areas where adults are more engaged in farming and other socioeconomic activities than children are. It has also been found that men are generally more susceptible to infection, though this could vary [127, 128].

5.3 Housing and socio-economic conditions

Poor housing and the lack of good sanitary conditions in terms of waste management, sewage disposal, and drainages in the majority of rural and semi-urban centre provide breeding and resting sites for sandflies, bringing this vector closer to human habitation. These sandflies feed on blood meal. Other good breeding sites for these vectors include cracks and crevices in walls, roofs that are poorly made, and thatched homes [129]. The disease spreads as a result of people moving from rural to urban areas for economic reasons [130, 131, 132].

5.4 Domestic animal breeding

It has been discovered that there may be a significant risk of infection in houses where animals are housed, bred, or live in close proximity to people. This is because some of these animals may act as reservoir hosts for the disease; leishmaniasis, particularly the VL, affects dogs and felines [133].

5.5 Host immune responses and parasite factor

In order for the infection to take hold, promastigotes must infiltrate macrophages and avoid inducing host defences. Additionally, the progression of intracellular infection by amastigotes depends on the preservation of macrophages in an inert, deactivated state. Through cell-mediated immunity and delayed-type hypersensitivity, an immunocompetent host defence system is equipped with and reacts to non-specific innate and antigen-specific acquired mechanisms; these inflammatory responses play a critical role in disease expression and may result in asymptomatic infection and self-healing or may result in clinical manifestation of disease. People with weakened immune systems, such as HIV patients, are more susceptible to infection since their immune systems are unable to defend them against the parasites. The parasite, however, can alter intracellular kinases, phosphatases, signalling pathways, the responsiveness of macrophages to the parasite and secretion of cytokines, as well as dendritic cell and macrophage mechanisms. This allows the parasites in the case of an infection to alter, temper, or hinder with intracellular kinases, phosphatases, signalling pathways, the responsiveness of macrophages to the parasite and secretion of the parasite can also disrupt dendritic cells, which are important for antigen presentation, T-cell co-stimulation, and the effective establishment of acquired Th1 responses [134].

6. Life cycle of leishmania parasite

Leishmania parasites go through two main stages in their life cycle: the extracellular stage in invertebrate hosts and the intracellular stage in vertebrate hosts. The parasite has two primary morphologies: amastigote and promastigote, with the former occurring in vertebrate hosts and the latter in invertebrate hosts. The promastigotes are injected into the host circulation by female sandflies during a blood meal on a vertebrate host; after this inoculation, the promastigotes are phagocytosed by the host macrophages; the macrophage ruptures and releases a large number of amastigotes into circulation. Monocytes and macrophages in the spleen, liver, lymph nodes, bone marrow, and other tissues of reticulo-endothelial cells are invaded by the released amastigotes. The female sandflies then consume free amastigotes from the blood as well as intracellular amastigotes from the monocytes. The promastigotes in the sand fly’s midgut move over a period of 6 to 9 days to its pharynx and buccal cavity, where the sand fly can spread the parasites to a new host after a blood meal [135].

7. The vector for leishmaniasis

Only 21 of the 700 species of sandflies (family Phlebotominae) are known to be disease vectors. The majority of these species belong to the genera Phlebotomus, Sergentomyia, and Lutzomyia; the Lutzomyia group includes species from the old and new worlds. Old-world species are those that can be found in South and Central Asia, the Indian subcontinent, the Middle East, North and East Africa, and Southern Europe; new-world species are those that can be found in Brazil and other Latin American nations, Mexico, and the United States. These fly species are absent from Australia but are indigenous to over 90 other nations and are found on every continent [136]. The following list includes the phlebotomous sandfly species that cause leishmaniasis in the old world. The transmission of L. major, L. tropica, L. infantum, and L. aethiopica is carried out by P. longicuspis, P. papatasi, P. ariasi, P. pedifer, P. duboscqi, P. rhodaini, P. segenti, and P. sergenti. The new world sandfly genus Lutzomyia includes species including L. hartmanni, L. gomezi, L. longipalpis, L. Ayacuchensis, L. Sanguinaria, L. Trapidoire responsible for the transmission of L. infantum, L. vianna equatorensis, L. colombiensis, and L. vianna braziliensis, among others. The Psychodopygus, which includes species like P. panamensis, P. carrerai, and P. amazonensis, is another type of sandfly of significant medical and veterinary significance [42, 134, 135, 136, 137, 138, 139, 140, 141, 142, 143, 144].

8. Conclusions

L. donovani, L. tropica, and L. major are the species that cause infection in Africa, L. tropica, L. major, and Leishmania infantum are the species that cause infection in the Middle East, L. tropica, L. infantum, and Europe, L. mexicana and L. chagasi are the species that cause infection in North America, and Leishmania (Viannia) braziliensis is the species that causes infection in South America. The disease is spread by numerous different species of Phlebotomus sandflies. Risk factors for the disease include climatic factors, vegetation cover, age and gender, housing and socioeconomic circumstances, animal breeding, and host immunity. Additionally, migration of people from other continents has been to blame for the emergence and re-emergence of the disease in Europe where there is civil and regional strife, political instability, and increased disease transmission and dissemination between continents. Obstacles to the quest to eradicate the disease include limited access to health care, a lack of national policy, and the maintenance of such policy, if it exists, particularly in developing nations.

Acknowledgments

Non to be disclosed.

Conflict of interest

The authors declare no conflict of interest.