Leishmania donovani

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Leishmania donovani
"Leishmania donovani" in bone marrow cell
Leishmania donovani in bone marrow cell
Scientific classification Edit this classification
Domain: Eukaryota
Phylum: Euglenozoa
Class: Kinetoplastea
Order: Trypanosomatida
Genus: Leishmania
Species:
L. donovani
Binomial name
Leishmania donovani
(Laveran et Mesnil, 1903) Ross, 1903
Synonyms
  • Leishmania archibaldi (invalid subgroup)[1]

Leishmania donovani is a species of

temperate regions including Africa (mostly in Sudan), China, India, Nepal, southern Europe, Russia and South America.[2][3][4] The species complex is responsible for thousands of deaths every year and has spread to 88 countries, with 350 million people at constant risk of infection and 0.5 million new cases in a year.[5]

L. donovani was independently discovered by two British medical officers

genome sequence of L. donovani obtained from southeastern Nepal was published in 2011.[8]

L. donovani

sensu stricto is in a species complex with the closely related L. infantum, which causes the same disease. The former is commonly found in East Africa and the Indian subcontinent, while the latter is found in Europe, North Africa, and Latin America. The split is done in 2007, and references to L. donovani often still refer to the entire complex (sensu lato).[1] As of 2022, the parasite causes 50,000 to 90,000 infections worldwide.[9]

Discovery

One of the earliest known epidemics of L. donovani infection (kala-azar as it was called in

British Medical Journal, which appeared on 11 May.[11]

Another British medical officer

Madras. After reading Leishman paper, Donovan confirmed on 17 June that the parasites (by then known as "Leishman bodies") were definitely the causative agents of kala-azar.[12][13] He wrote a commentary of his discovery in relation to that of Leishman in the same journal using the same title as that of Leishman's, that appeared on 11 July 1903.[14]

Soon a controversy arose as to whom such a monumental discovery should be credited. Donovan sent some of his slides to

scientific name Piroplasma donovanii. It was Ross who resolved the conflict of priority in the discovery and correctly identified the species as member of the novel genus Leishmania. He gave the popular name "Leishman-Donovan bodies", and subsequently the valid binomial Leishmania donovani, thereby equally crediting the two rivals.[10][15][16]

Structure

Leishmania donovani is a unicellular eukaryote having a well-defined nucleus and other cell organelles including a kinetoplast and a flagellum. This species has n=36 chromosomes.[17] Depending on its host it exists in two structural variants, as follows:[16][18][19][20]

  1. Amastigote form found in the mononuclear phagocyte and circulatory systems of humans. It is an intracellular and non-motile form, being devoid of external flagellum. The short flagellum is embedded in the anterior end without projecting out. It is oval in shape, and measures 3–6 μm in length and 1–3 μm in breadth. The kinetoplast and basal body lie towards the anterior end.
  2. Promastigote is formed in the
    alimentary tract
    of the sandfly. It is an extracellular and motile form. It is considerably larger and more highly elongated, measuring 15–30 μm in length and 5 μm in width. It is spindle-shaped, tapering at both ends. A long flagellum (about the body length) is projected externally at the anterior end. The nucleus lies at the centre, and in front of which are kinetoplast and basal body.

Infection and life cycle

Life cycle of Leishmania donovani

Leishmania donovani is a digenetic parasite passing its life cycle in two different hosts.

Definitive host

In humans the metacyclic promastigotes are injected by sandfly through the skin during its blood meal. When sandfly bites using its proboscis it ejects the parasites that are stored inside the hollow tube. Some promastigotes may enter the blood stream directly where some are destroyed by macrophagic cytolysis. But many are also taken up through phagocytosis by mononuclear phagocytes in liver, spleen and bone marrow.[21] Inside the cells they undergo spontaneous transformation into oval-shaped amastigotes.[22][23]

binary fission. Multiplication continues until the host cell can no longer hold and ruptures. In a fully congested cell there can be as many as 50 to 200 amastigotes, which are released into tissue cavities. Each individual amastigote is then capable of invading fresh cells. As a result, the entire tissue is progressively infected and destroyed. A number of free amastigotes then enters the blood stream where many are phagocytosed by macrophages. These free and phagocytosed amastigotes in peripheral blood are then sucked up by blood-feeding sandfly.[25][26][27]

Intermediate host

L. donovani undergo further development only in the

buccal cavity. This process is known as anterior station development, which is unique in Leishmania. A heavy infection of pharynx can be observed within 6 to 9 days after initial blood meal. The promastigotes become infective only by this time, and the event is called the metacyclic stage.[16][29] The metacyclic promastigotes then enter the hollow proboscis where they accumulate and completely block the food passage. Immediately upon biting a human, the parasites are released, which invariably results in infection.[26]

The stages of development in sandfly can be described as follows:[18]

  1. Soon after entering the gut, the amastigotes get coated with peritrophic matrix, which is composed of chitin and protein complex. This protects the parasites from the digestive enzymes of the host.
  2. The amastigotes travel as far as the abdominal midgut and first transform into a weakly motile "procyclic promastigotes" on the gut wall within 1–3 days.
  3. The young promastigotes secrete a neuropeptide that stop peristalsis of the gut. The surface lipophosphoglycan (LPG) of the promastigote serves as an attachment to the gut epithelium. These factors prevent the expulsion of promastigotes during excretion of the insect.[30]
  4. During 4–7 days the peritrophic matrix is degraded by the
    activity of chitinases
    . This release the more actively motile "nectomonad promastigotes" which migrate anteriorly until they reach the opening of the thoracic gut.
  5. Another transformation takes place by which they turn into "leptomonad promastigotes". These are fully motile and capable of binary fission. Multiplication and migration towards thoracic midgut cause congestion of the pharynx and buccal cavity. Here they secrete promastigote secretory gel (PSG), which is composed of soluble acid phosphatase and phosphoglycoprotein.[31][32]
  6. After 6–9 days the promastigotes become metacyclic. Some are also transformed into non-replicating promastigotes, which also become metacyclic. The sandfly is able to regurgitate and eject the parasites from its proboscis with the help of PSG when it bites.

Reservoir host

Dogs are known to be susceptible to L. donovani infection.

rodents are also reported to harbour L. donovani.[36]

Epidemiology

It is estimated that visceral leishmaniasis (VL) affects more than 100 million people worldwide,

Sudanese population.[41] Moreover, due to emergence of drug resistance the prevalence is not subsiding, and in fact has spread to central Europe. For example, during the late 1990s hundreds of cases were reported in Switzerland.[42]

Pathogenicity

L. donovani is the causative agent of visceral leishmaniasis, traditionally known as kala-azar ("black fever", particularly in India), because of its characteristic symptoms. The disease is highly lethal if not treated properly. The incubation period generally ranges from 3 to 6 months, and in some cases may be over a year. In Indian leishmaniasis, incubation can be as short as 10 days. The target cells are those of mononuclear phagocyte system. The two main tissues of infection are spleen and liver.[43]

Clinical symptoms include

septicaemia and even HIV infection.[26][44][45]

Cellular invasion and immunological response

Amastigotes of L. donovani enter macrophages via a

T-cell responses.[49]

Treatment

The conventional treatment method is an

pentostam.[citation needed] Unfortunately, these chemotherapeutics are so poisonous that about 15% of the patients die from the treatments.[citation needed] To compound the situation, drug resistance has evolved in the parasites against the traditional antimonials. According to rough estimates, about 40% of patients in India are already resistant to this therapy.[42]

Another antimicrobial drug

hypoxia, and its chronic effect is nephrotoxicity.[51]

In 1999, an anticancer drug

diarrhoea in 20–28% patients, which were rather mild. The drug has been officially approved in India. The recommended dosage is 100 mg per day over a period of four weeks.[53][54]

Evolution

L. donovani is now considered to be a species complex as indicated by different pathological symptoms occurring in different geographical areas where the species of the vector sandfly are also different. However, none of the parasites are morphologically distinguishable, except by molecular analysis, making them cryptic species. Molecular data show that genotype is strongly correlated with geographical origin.[55] DNA sequencing of different geographical strains indicates that the protozoan complex can be classified into two valid taxa, L. donovani and L. infantum. The genus Leishmania most likely originated in South America, from where it migrated to Asia. L. donovani and L. infantum diverged ~1 Mya, with further divergence of infraspecific genetic groups between 0.4 and 0.8 Mya.[1]

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External links
Retrieved from "https://en.wikipedia.org/w/index.php?title=Leishmania_donovani&oldid=1219659070"