Here you go the basic about lieshmana donovani.

1. Leishmania
&
Leishmaniasis
Supervisor,
Dr. Abhik Sen
Scientist-D & Head
Dept. of Molecular Biology
ICMR, RMRIMS, Patna-800007
Vicky Kumar Mahto
Ph.D. Research Scholar
Dept. of Molecular Biology
ICMR, RMRIMS, Patna-800007

2. Sir William Leishman
 1901, Sir William Leishman (London)
discovered L.donovani in spleen
smears of a soldier, who died of fever
at Dum-Dum, India.
 The disease was known locally as
Dum-Dum fever or kala-azar.
Charles Donovan
 Charles Donovan (Madras, India) also
recognized these symptoms in other
kala-azar patients and published his
discovery a few weeks after Leishman.
 After examining the parasite using
Leishman's stain, these amastigotes
were known as Leishman- Donovan
bodies.

3. Kingdom - Protista
Subkingdom - Protozoa
Phylum - Sarcomastigophora
Subphylum - Mastigophora
Class - Zoomastigophora
Order - Kinetoplastida
Suborder - Trypanosomatina
Family - Trypanosomatidae
Genus - Leishmania
Subgenus - Leishmania & Viania
Species - donovani, tropica, mexicana, braziliensis, etc.
SCIENTIFIC CLASSIFICATION

4. In Human infection is caused by more than 20 sps
of leishmania
Species Disease
L. donovani
L. infantum
L. chagasi
Visceral leishmaniasis (VL), Kala-azar, Black fever,
Dum-Dum fever, Sahib’s disease, Kala Dukh, White
leprosy
L. donovani Post kala-azar dermal leishmaniasis (PKDL), Dermal
leishmaniasis
L. mexicana
L. tropica
L. major
L. aethiopica
Cutaneous leishmaniasis (CL), Aleppo boil, Baghdad
boil, Delhi boil, Kandahar sore, Lahore sore, Oriental
sore
L. braziliensis Mucocutaneous leishmaniasis (MCL), Espundia,
Breda's disease, Bosch yaws, Bush yaws, Forest yaws,

5. Leishmania
Donovani
 It is an intracellular parasites belonging to genus Leishmania, a group of
haemoflagellate kinetoplastids that cause the disease leishmaniasis.
 In human blood it is responsible for visceral leishmaniasis (most severe
form of leishmaniasis).
 It infects the mononuclear phagocyte cells including spleen, liver, bone
marrow and lymphatic glands.
 Infection is transmitted by the bite of infected
female Sandfly (Tse-tse fly) of the genus
Phlebotomus in Old World (Africa, Asia &
Europe) Lutzomyia in New World (America
including North America, Central America &
South America.)
 Therefore, the parasite is prevalent throughout
tropical and temperate regions including Africa
(mostly in Sudan), China, India, Nepal, Southern
Europe, Russia and South America.

6. Morphology:- Parasite occures in two stages
Amastigote or Leishmanial
 In phagocytic cell of human, promastigote
transformed into amastigote and effect
Reticuloendothelial cells of Spleen, Liver,
Bone marrow, Intestinal mucosa,
Mesentric lymph node.
 This form is non-motile because flagellum
absent.
 Size ranges from 2-4 µm in diameter.
 Shape; Rounded or Oval.
 Nucleus relatively larger and situated
centrally.
 Divides by binary fission at 37oC.
Promastigote or Leptomonad
 In the midgut of sandfly amastigote
transform into promastigote and
migrate to the proboscis.
 This forms is motile because flagellum
present.
 Size; 15-20 µm in length and 1-2 µm in
width.
 Shape; Elongated, Slender or Spindle.
 Nucleus smaller and situated in the
middle of the cell or along the side of
cell-wall.
 Divides by binary fission at 27oC.
Axoneme

7. Leishmania metabolism
 Leishmania don’t have mouth or cytostome, so the nourishment is obtained
saprozoically through the general body surface from the host cells.
 The exchange of the gases and elimination of the waste products takes place by
the process of diffusion.
 Only asexual reproduction takes place in Leishmania through longitudinal
binary fission.
 Whole body is covered with pellicle that gives a definite shape to the body,
nucleus is covered by a double membrane with pores of size 1 µm in diameter.
Sand-fly habitat
 Genus- phlebotomus and lutzomyia sand flies commonly found In house-hold
rubbish, bark of old trees, cracks in walls.
 Usually feed at evening and night while the host asleep.
 30 out of 500 Sps. of phlebotomus can transmit diseases
Ex, P. argentipes (Indian sub- continent)
P. oriantalis (Africa, Mediterranean basin)
P. chinensis & alexandri (China)

8.  Leishmania is a digenetic parasite which requires two hosts to complete its life
cycle. The primary host is the principal host which is a vertebrate or human. In
the primary host the parasite feeds and multiplies itself asexually.
 On the other hand the secondary host is the intermediate host or vector which
is usually an invertebrate or a blood sucking insect. In the case of Leishmania it
is sand-fly (tse-tse fly) belongs to the genus phlebotomus.
 In human leishmania is transmitted by the bite of infected female
phlebotomus (P.argentipes) sandflies. The sandflies inject the infective stage
promastigotes during blood meals. Promastigotes that reach the puncture
wound are phagocytized by macrophages and they transform into amastigotes
and multiply in infected cells until it ruptures and affect different cells &
tissues.
 Sandflies become infected during blood meals on an infected host when they
ingest macrophages infected with amastigotes. In the sandfly's midgut, the
parasites differentiate into promastigotes, they multiply and migrate to the
proboscis.
Life cycle of leishmania

9. Life cycle of leishmania
(Human, Dog, Cat,
Fox, Sheep etc)
Infected

10. Reservoir & Infection
 Reservoir hosts- Wild and Domestic animals such as Fox, Wolves, Jackal, Rodents,
Cattle, Sheep, Horse, Cat and Dog. They are play important role in harbouring and
transmitting disease to humans.
 Incidental hosts- Human
 Source of infection- Asymptomatic carriers and PKDL patients.
 Leishmaniasis is more common in males as compared to females.
 Generally infection in Adventure travelers, Corps workers, Soldiers.

11. Leishmaniasis world wide
 Leishmaniasis is a globally important but neglected disease.
 It is the second-largest parasitic killer in the world (after malaria) and
endemic in 4 continents and over 88 countries, in which 72 are developing
countries:
 WHO estimates that 350 million people are at constant risk of infection and
2 million new cases every year and around
70 thousand deaths every year
90% VL: Bangladesh, Brazil,
China, Ethiopia, India, Kenya,
Nepal, Somalia, Sudan, East and
North Africa
90% CL: Afghanistan, Algeria,
Brazil, Colombia, Iran, Iraq,
Syrian, Sudan, Somali and Saudi
Arabia
90% MCL: Bolivia, Brazil,
Ethiopia and Peru.

12. Leishmaniasis in India
 World’s largest foci of Visceral Leishmaniasis, accounting for 50% of the total
burden.
 Endemic in 4 states & 52 districts in Eastern India.
Bihar- 32 districts
Jharkhand- 4 districts
West Bengal- 11 districts
Uttar Pradesh- 5 districts
 An estimated 165.4 million
population is at risk
 About 1 lakh cases occur
annually

13.  Most severe form
 Caused by L. donovani, L. infantum, L. chagasi
 It is transmitted by P. argentipes
 Incubation period is usually 2-4 months.
 Fatal after 2-3 years if not treated.
 Splenomegaly; spleen enlargement
 Hepatomegaly; liver enlargement
 Lymphadenopathy; lymph nodes abnormal in size
 Dark skin, Low grade fever, Weight loss, Bone marrow
hyperplasia, Hypergammaglobulinnemia, Epistaxis,
Proteinuria, Hematuria, Cachexia.
 Anemia (low RBC), Leukopenia (low WBC) &
Thrombocytopenia (low platelets) are common
 Congenital infection, Blood transfusion, Organ
transplantation, Shared needles, Accidental
inoculation of promastigotes in lab workers.
Visceral leishmaniasis

14.  Rare but varies Geographically.
 It is sequel of visceral leishmaniasis.
 Caused by L. donovani (It is the only parasite causing this disease in India).
 Normally develop during therapy, few months or years later after recovery
from kala azar. Recently it is believed that PKDL may appear without passing
through visceral stage.
 Self limiting (resolving in six months).
 In PKDL condition parasite invades skin cells, resides and develops there and
manifests as Dermal leisions, Hypopigmented macules, Papuples, Nodules.
 It appears on face, upper arms, trunks and other parts of the body people
with PKDL are considered to be a potential source of Leishmania infection.
Post kala-azar dermal leishmaniasis

15.  Most common form
 Old world CL- caused by L.tropica, L.aethiopica, L.major
 New world CL- caused by L.mexicana, L.braziliensis, L.guyanensis
It is transmitted by P.sergenti, P.papatasi
 It causes one or more sores, papules or nodules on the skin.
 Sores develop within a few weeks of the sandfly bite, but they appear up to
months later. Sores change in size and appearance over time. It look
somewhat like a volcano.
 Sores are usually painless but can become painful if secondarily infected.
 Skin sores can heal on their own, but this can take months or even years and
leave significant scars or disfiguring if they occur on the face.
Cutaneous Leishmaniasis

16.  Less common form
 Caused by L.braziliensis and occasionally by
L.panamensis, L.tropica, V. brazilliensis.
 Affected skin & mucous membrane. Such
as Mouth, Nose and Throat
(Pharynx and Larynx) cavities.
 Symptoms- Epistaxis, Edema, Erythema of
nasal mucosa, Perforation nasal septum,
Enlargement of Lip & Nose, Larynx-voice
change.
 It may occur months to years after original
skin lesion.
 Generally it is not treated.
Mucocutaneous leishmaniasis

17. THANK YOU

18. In Details
 Hyperplasia; enlargement of tissue caused by an increase in the reproduction rate of its
cells, often as an initial stage in the development of cancer.
 Hypergammaglobulinemia; increased levels of a certain immunoglobulin in the blood
serum.
 Epistaxis; defined as acute hemorrhage from the nostril, nasal cavity, or nasopharynx.
 Proteinuria; presence of abnormal quantities of protein in the urine, which may indicate
damage to the kidneys.
 Hematuria; presence of red blood cells in the urine.
 Cachexia; weakness and wasting of the body due to severe chronic illness.
 Hypopigmented macules; also known as “ash-leaf spots,” can be present at birth and
are most common on the trunk and lower extremities.
 Throat cavities; (Pharynx and Larynx)
 Edema or water retention; occurs when fluid builds up in the tissues. Caused swelling.
 Erythema; redness of the skin or mucous membranes, caused by hyperemia (increased
blood flow) in superficial capillaries. It occurs with any skin injury, infection, or
inflammation.
 Perforation; ruptured or hole in the wall or part of the organ.