a good review of leishmaniasis. Apologies' in advance for any mistake.

1. By:
Hira Nusrat

2.  Kingdom  Protozoa
 Sub- Kingdom  Protista
 Phylum  Sarcomastigophora
 Sub- Phylum  Mastigophora
 Class  Zoomastigphora
 Order  Kinetoplastida
 Sub-order  Tryponosomatina
 Genus  Leishmania
 Species  L. tropica complex
 L. donovani complex
 L. mexicana
 L.braziliensis
 L.infantum

4. L. donovani causes Viseral leishmaniasis or kala-azar. It also
causes the condition, Post-kala-azar dermal leishmaniasis
(PKDL).
History:
 Sir William Leishman in 1900 observed the parasite in spleen
smears of a soldier who died of "dumdum fever" or kala-azar
contracted at Dum Dum Calcutta.
 Leishman reported this finding from London1903. In the
same year, Donovan also reported the same parasite in spleen
smears of patients from Madras. The name Leishmania
donovani was, therefore given to this parasite.

5. GEOGRAPHICAL DISTRIBUTION :
90% are found in the Indian subcontinent and Sudan and Brazil
Morphology:
The parasite exists in two forms
 1. Amastigote form: In humans and other mammals.
 2. Promastigote form: In the sandfly.

6.  Amastigote: The amastigote form (LD body) is an ovoid or
rounded cell, about 2-4 μm in size. It is typically intracellular, being
found inside macrophages, monocytes, neutrophils or endothelial
cells. They are also known as LD bodies.
 Promastigote: It is a flagellar stage and is present in insect
vector, sandfly. The promastigotes, which are initially short, oval or
pear shaped forms, subsequently become long spindle-shaped cells,
15- 25 μm in length.

7.  Phlebotomus sand flies.
 These are blood sucking insects and contain more than 600
species.
 They belong to order dipetra.
 They have errected wings with hair.

8. .L. donovani completes its life cycle in two host; man and sand fly.
 Definitive host: Man.
 Vector: Female sand.fly (Phlebolomus species)
 Infective form: Promastigote form present in midgut of female sandfly.
 Mode of transmission:
 Humans acquire by bite of an infected female sandfly. The sandfly
regurgitates the promastigotes in the wound caused by its proboscis. These
are engulfed by the cells of reticuloendothelial system (macrophages,
monocytes and polymorphonuclear leukocytes) and change into amastigote
(LD bodies).

9.  The amastigote multiplies by binary fission producing
numerous daughter cells that distend the macrophage and
rupture it and enter into spleen, liver and bone marrow. The
liberated daughter cells are also phagocytosed by other
macrophages in the peripheral blood. When a vector sand-fly
feeds on an infected person the amastigotes present in
peripheral blood and tissue fluids enter the insect along with
its blood meal and reaches to the midgut.

10.  In the midgut (stomach) of the sandfly, the amastigote
elongates and develops into the promastigote form. The
promastigote multiples by longitudinal binary fission and
reaches enormous numbers and migrate from the midgut to the
pharynx and to the salivary galnd and the cycle repeats again.

12. Pathogenicity: L. donovani causes VL or kala-azar.
Kala-azar is a reticuloendotheliosis resulting from the invasion
of reticuloendothelial system by L. donovani. The parasitized
macrophages disseminate the infection to all parts of the body.
Spleen:
The spleen is the most affected organ. It is grossly enlarged and
the capsule is thickened and cellular destruction occurs in the
spleen.

13.  Liver
 The liver is enlarged and Kupffer cells and vascular
endothelial cells are heavily parasitized.
 Prothrombin production is commonly decreased.
Bone marrow:
 The bone marrow is heavily infiltrated with parasitized
macrophages, which may crowd the hematopoielic tissues.

14. Indian visceral leishmaniasis:
Caused by L. donovani producing the anthroponotic disease kala-azar.The
disease is not zoonotic human being the only reservoir host.
Vector is the sandfly, P. argentipes.
Mediterranean leishmaniansis:
Middle Eastern leishmaniasis caused by L. donovani infantum affecting
mostly young children. It is a zoonotic disease; the reservoir host is dog and
wild canines such as foxes, jackal and wolves.
Vectors are P. pernicious and P. papatasii.
American (New World) visceral leishmaniasis:
Caused by L. chagasi. It is present is most parts of Latin America and
resembles the disease caused by L. infatum.
Vector is P. longipalpis.

15. Clinical features of kala-azar:
 High-grade fever.
 Splenomegaly .
 Hepatomegaly.
 Anemia
 Leukopenia.
 Dysentry.
 Skin becomes dry, rough and darkly pigmented hence the name
(kala-azar).
 The hair becomes thin and brittle.

16. DIAGNOSIS:
 Microscopy is done by use of gemsa stain..
 Examination of skin scraping.
 Bone marrow puncture by using puncture needle.
Serological test:
 Elisa.
 PCR.
TREATMENT:
 Liposomal amphotericin B
 Miltefosine.

17.  Leishmania tropica complex
 lt includes three species:
 1. Leishmania tropica
 2. Leishmania major
 3. Leishmania aethiopica.
 All these species cause old world cutaneous leishmansisis.
The disease is also known as oriental sore, Delhi boil, Bagdad
boil, or Aleppo button.

18.  L. tropica and L. major are found in Middle-East, India,
Afghanistan, Eastern Mediterranean countries and North Africa.
 L. aethiopica occurs in Ethiopia and Kenya.
Habitat: L. tropica causing CL (old world CL) are essentially
the parasite of skin. The amastigote forms occur in the
reticuloendothelial cells of the skin, whereas promastigote forms
are seen in sand fly vector.
 Life cycle: The life cycle of L. tropica is similar to that of
L. donovani.
Vectors: The vectors of L. tropica complex are Phlebotomus
sandflies. The following species of sand flies act as vector:
 • P. sergenti- L. tropica
 • P. papatasi- L. major
 • P. longipes- L. aethiopica

19.  Clinical features
 causing painless dry ulcerating lesions, leading to
disfiguring scars.
Laboratory diagnosis:
 Microscopy:
 • Smear is made from the material obtained from the indurated
edge of nodule or sore

21. L. braziliensis complex and L. mexicana complex
 History and distribution: Lindenberg and Paranhos (1909)
first described amastigotes in the ulcers of skin in a man in
Brazil. Vianna (1911) named the species as L. braziliensis. L.
braziliensis complex and L. mexicana complex cause new
world leishmaniasis in Central and South America.
 Habitat: These occur as intracellular parasite. The amastigote
form is seen inside the macrophages of skin and mucous
membrane of the nose and buccal cavity. The promastigote
form occurs in vector species.

22.  Vector: Lutzomyia.
 Life cycle: The life cycle of Leishmania species causing the
new world cutaneous and mucocutaneous leishmaniasis is
similar to that of L. donovani except the amastigotes are found
in the reticuloendothelial cells and lymphoid tissues of skin,
but not in the internal organs.The infection is transmitted to
man from animals by bite of sand fly vectors of genus
Lutzomyia.

23.  Clinical features:
 L. braziliensis causes the most severe and destructive form of
cutaneous lesion. It involves the nose, mouth and larynx.
Subsequent mucocutaneous involvement leads to nodules
inside the nose, perforation of the nasal septum, and
enlargement of the nose and lips (espundia).
 Laboratory diagnosis:
 Microscopy: Amastigotes are demonstrated in smears taken
from lesions of skin and mucous membrane.
 Serology: Elisa
 Biopsy: Slit skin biopsy for amastigote detection.

24. ESPUNDIA DISEASE

25. Treatment
A pentavalent antimonial compound is moderately effective
for mild mucocutaneous leishmaniasis.
Amphotericine-B is the best alternative drug currently
available.
In case of respiratory complications, glucocorticoids can be
used.

26. Preventive Measures
 Preventing sand fly bites is the most immediate form of protection.
 Control of sand fly population by insecticides and sanitation measures.
 Personal protection by use of protective clothing and use of insect repellent.
 Elimination of mammalian reservoir.
Vaccine
There are no vaccines or drugs that prevent leishmaniasis but a recently
developed polyvalent vaccine has been reported to be successful in reducing
the incidence of cutaneous leishmaniasis in Brazil.