This document summarizes information about Leishmaniasis, which is caused by obligate intracellular protozoa of the genus Leishmania and transmitted by sand flies. It discusses the morphology and life cycle of Leishmania donovani, the species responsible for visceral leishmaniasis. The document covers the classification, pathogenesis, clinical manifestations, laboratory diagnosis, treatment, and prevention of leishmaniasis. It identifies dogs and rodents as common reservoir hosts and describes the promastigote and amastigote stages that occur in the sand fly and human hosts, respectively.

1. By :
S.Gowtham,
III – B.Sc Microbiology.
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2. Content
• Leishmaniasis
• Morphology
• Classification
• Life cycle
• Pathogenesis
• Laboratory Diagnosis
• Treatment
• Prevention
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3. •1900 – Sir William Leishman discovered
Leishmania in spleen smears of a soldier who died
of fever at Dum Dum, India.
•Charles Donovan also recognized these symptoms
in other Kala Azar patients and published his
discovery a few weeks after Leishman.
•Leishmaniasis is categorized into three types:
•Cutaneous Leishmaniasis
•Mucocutaneous Leishmaniasis
•Visceral Leishmaniasis
•Leishmaniasis is the second killer disease after
malaria.
•Leishmaniasis is a vector-born disease that is
transmitted by a female sand flies and caused by
obligate intracellular protozoa of the genus
Leishmania.
•It is a zoonotic disease.
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4. Morphology
•Leishmania donavani is a species of
intracellular parasites belonging to the genus
Leishmania that cause the disease
Leishmaniasis.
•It is a human blood parasite responsible for
visceral Leishmaniasis or Kala-azar, the most
severe form of Leishmaniasis.
•Infection is transmitted by species of sand fly
belonging to the genus Phlebotomus and
Lutzomyia.
•Geographical distribution - Endemic in
India, China, Russia, Africa, Southern Europe
and South America.
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5. Morphology
Hosts
• Definitive host – man
• Intermediate host – Female sand fly
• Reservoir of infection – Dog (China & Brazil), Man (India), Rodents
(Africa) and Jackals (Russia).
Habitat - In reticulo-endothelial system of vertebrate hosts.
Stages
• Promastigote
• Amastigote
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6. Promastigote
• Flagellar stage
• Present in sandfly.
• Spindle shaped.
• 15-20 micrometer in length.
• 1-2 micrometer in width.
• Large nucleus centrally
situated.
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7. Amastigote
• Aflegellar stage.
• Present in host.
• Round or oval.
• 2-4 micrometer.
• Small nucleus situated
middle of the cell or
along the sides of cell
wall.
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8. Classification
Leishmania tropica
Leishmania major
Leishmania aethiopica
Leishmania mexicana
Leishmania braziliensis
Leishmania donovani
Leishmania infantum
Leishmania chagasi
Kingdom : Protisda
Subkingdom : Sarcomastigophora
Phylum : Protozoa
Subphylum : Mastigophora
Class : Zoomastigophora
Order : Kinetoplastida
Genus : Leishmania
Species : donovani
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9. Lifecycle
Sand fly
stages
Sand fly injects
infected
macrophages
when it takes a
blood meal.
Promastigotes
divide and
migrate to the
anterior midgut
and foregut.
Amastigotes
transform into
Promastigotes in
midgut.
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10. Lifecycle
Human
Stages
Sand fly injects
promastigotes
into the skin
during a blood
meal.
Promastigotes
are phagocytized
by neutrophils
that are rapidly
recruited to the
bite site.
Infected
neutrophils
release the
parasites, which
are then
consumed by
macrophages.
Promastigotes
transform into
amastigotes
inside
macrophages.
Amastigotes
multiply in
cells of
various
tissues.
Sand fly ingests
infected
macrophages
when it takes a
blood meal.
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11. Pathogenesis
Infections range from asymptomatic to
progressive fully developed Kala-azar.
Incubation period is usually 2-4
months.
Symptoms begins with low-grade fever
and malaise, followed by progressive
wasting, anemia and protrusion of the
abdomen from enlarged liver and spleen.
In acute cases with chills, fevers up to
104 degrees Fahrenheit and vomiting;
death may occur within 6-12 months.
Immediate cause of death is usually an
invasion of a secondary pathogen that the
body is unable to combat.
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12. ClinicalManifestations
1. Fever.
2. Spleen enlargement.
3. Lymphadenopathy.
4. Darkening of the skin.
5. Complications – Pneumonia, TB,
Dysentery, Hemorrhage.
6. Prognosis
i. Early treatment – cure rate
>90%.
ii. Not treated – Death occurs in
2 years.
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13. Laboratorydiagnosis
Diagnosis
Direct
evidences
Thick film
method
Blood
culture
Biopsy
Indirect
evidences
Blood
count
Serum test
Other
methods
Animal
inoculation
Leishmanin or
Montenegro
test
Adler’s test
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14. Laboratory diagnosis
Direct evidences
 Thick film blood method
Peripheral blood by thick film
method.
 Blood culture in NNN medium
Promastigote form.
 Biopsy material
Lymph node puncture.
Sternal or iliac crest puncture.
Spleen puncture.
Serological tests
 Direct agglutination test
 ELISA
 IFAT
Thick blood film
L. donovani in NNN medium
Biopsy
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15. Treatment
1. Sodium stibo gluconate solution
o Inhibits glycolase enzymes and fatty
acids oxidation.
2. Amphotericin B
o Binds with ergosterol leading to the
altered permeability to cations,
water, glucose and affect membrane-
bound enzymes.
3. Pentamidine
o Inhibits DHFR and interferes with
aerobic glycolysis in protozoa, also
inhibits protein synthesis.
4. Miltefosine
o Effects cell signaling pathways and
synthesis of the cell membrane.
5. Interferon
o Macrophage activation.
6. Paramomycin & Miltefosine
Specific therapy
supplemented with
Treatment of
secondary
microbial infections
High calories – high
protein diet
Blood transfusion
in severe anemia
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16. Prevention
 Reduction of sand fly
population - by insecticides
mainly DDT, dieldrin,
malathion.
 Reduction of reservoir - by
killing all the infected dogs in
the cases of zoonotic Kala-azar.
 Education in the community –
about the cases and modes of
transmission of Leishmaniasis.
 Prevention of exposure to sand
fly using infect repellent, bed
nets and window mess as
needed.
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17. Any queries…?
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