1. Leishmania are single-celled parasites spread by sandflies that cause leishmaniasis. Sir William Leishman discovered Leishmania donovani in 1900 in India, where it was known as Dum Dum fever. 2. Leishmania exist in two forms - amastigotes found intracellularly in humans and promastigotes found in sandfly guts. Leishmania infect macrophages and spread infection between cells. 3. Leishmaniasis affects over 6 million people annually and comes in cutaneous, visceral, and mucosal forms that can cause skin sores, damage internal organs, or affect mouth/nose tissues. Diagnosis involves microscopic examination

1. 1
Leishmania and Leishmaniasis
Background (history)
 Sir William leishman; In 1900 sir William leishman discovered L.denovani in
spleen smears of a soldier who died of fever at Dum-Dum in India. The disease
was known locally as Dum-Dum fever or Kala azar.
 Charles Donovan; Charles Darwin also recognized these symptoms in other kala
azar patients and published his discovery a week after leishman. After examining
the parasite using Leishman ’s stain, these amastigotes were known as
Leishman-Donovan bodies
 Visceral leishmaniasis other names of dum-dum fever, death fever.
Introduction
 Leishmania is a genus of trypanosomes that are responsible for the disease
leishmaniasis.
 They are spread by sandflies of the genus Phlebotomus in the Old World, and of
the genus Lutzomyia in the New World.
 In many species of mammals; Leishmania of reptiles are mostly extracellular
parasite of gut.
 They occur as both amastigotes and promastigotes.
 The size is of about 1 to 5 µm but they usually about 3µm.
Microscopyof Leishmaniaspecie

2. 2
The parasite
 Phylum Sarcomastigophora
 Order Kinetoplastida
 Family Trypanosomatidae
 Genus Leishmania
Epidemiology
Leishmania currently affects 6 million people in 98 countries. About 0.9-1.6 million new
cases occur each year, and 21 species are known to cause disease in humans.
Structure
Leishmania species are unicellular eukaryotes having a well-defined nucleus and other
cell organelles including kinetoplast and flagella. Depending on the stage of their life
cycle, they exist in two structural variants, as:
1. The amastigotes form is found in the mononuclear phagocytes and circulatory
systems of humans. It is an intracellular and nonmotile form, being devoid of
external flagella. The short flagellum is embedded at 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. The promastigotes form is found in the alimentary tract of sandflies. It is an
extracellular and motile form. It is considerably larger and 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 it are the
kinetoplast
Hosts
Common Old World hosts are domestic and feral dogs, rodents, foxes, jackals, wolves,
raccoon-dogs, and hyraxes. Common New World hosts include sloths, anteaters,
opossums, and rodents.

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Life cycle
Leishmaniasis is transmitted by the bite of infected female phlebotomine sand flies. The
sand flies inject the infective stage (i.e., promastigotes) from their proboscis during
blood meals . Promastigotes that reach the puncture wound are phagocytized by
macrophages and other types of mononuclear phagocytic cells. Promastigotes
transform in these cells into the tissue stage of the parasite (i.e., amastigotes) , which
multiply by simple division and proceed to infect other mononuclear phagocytic cells
. Parasite, host, and other factors affect whether the infection becomes symptomatic
and whether cutaneous or visceral leishmaniasis results. Sand flies become infected by
ingesting infected cells during blood meals ( , ). In sand flies, amastigotes
transform into promastigotes, develop in the gut (in the hindgut for leishmanial
organisms in the Viannia subgenus; in the midgut for organisms in
the Leishmania subgenus), and migrate to the proboscis .

4. 4
Diseases
There are several different forms of leishmaniasis in people. Some people have a silent
infection, without any symptoms or signs.
 The most common form is cutaneous leishmaniasis, which causes skin sores. The
sores typically develop within a few weeks or months of the sand fly bite.. The
sores may start out as papules (bumps) or nodules (lumps) and may end up as
ulcers (like a volcano, with a raised edge and central crater); skin ulcers might be
covered by scab or crust. The sores usually are painless but can be painful.
 The other main form is visceral leishmaniasis, which affects several internal
organs (usually spleen, liver, and bone marrow) and can be life threatening. The
illness typically develops within months (sometimes as long as years) of the sand
fly bite. Affected people usually have fever, weight loss, enlargement (swelling) of
the spleen and liver and low blood counts—a low red blood cell count (anemia),
a low white blood cell count (leukopenia), and a low platelet count
(thrombocytopenia).
 Mucosal leishmaniasis is an example of one of the less common forms of
leishmaniasis. This form can be a sequela (consequence) of infection with some of
the species (types) of the parasite that cause cutaneous leishmaniasis in parts of
Latin America: certain types of the parasite might spread from the skin and cause
sores in the mucous membranes of the nose (most common location), mouth, or
throat.

5. 5
Marked splenomegaly(enlargement/swellingof the
spleen) inapatientinlowlandNepalwhohasvisceral leishmaniasis
Ulcerative skinlesion,witharaisedouterborder,on
a Guatemalanpatientwhohascutaneousleishmaniasis.

6. 6
Diagnosis
 Various laboratory methods can be used to diagnose leishmaniasis—to detect
the parasite as well as to identify the Leishmania species (type). Some of the
methods are available only in reference laboratories. In the United States, CDC
staff can assist with the testing for leishmaniasis.
 Tissue specimens—such as from skin sores (for cutaneous leishmaniasis) or from
bone marrow (for visceral leishmaniasis)—can be examined for the parasite under
a microscope, in special cultures, and by molecular tests. Blood tests that detect
antibody (an immune response) to the parasite can be helpful for cases of visceral
leishmaniasis; tests to look for the parasite (or its DNA) itself usually also are
done
Prevention & Control
 No vaccines or drugs to prevent infection are available. The best way for travelers
to prevent infection is to protect themselves from sand fly bites. To decrease the
risk of being bitten, follow these preventive measures:
 Avoid outdoor activities, especially from dusk to dawn, when sand flies generally
are the most active.
When outdoors(or in unprotected quarters)
 Minimize the amount of exposed (uncovered) skin. To the extent that is tolerable
in the climate, wear long-sleeved shirts, long pants, and socks; and tuck your shirt
into your pants. (See below about wearing insecticide-treated clothing.)
 Apply insect repellent to exposed skin and under the ends of sleeves and pant
legs. Follow the instructions on the label of the repellent. The most effective
repellents generally are those that contain the chemical DEET (N,N-
diethylmetatoluamide).
When indoors:
 Stay in well-screened or air-conditioned areas.
 Keep in mind that sand flies are much smaller than mosquitoes and therefore can
get through smaller holes.
 Spray living/sleeping areas with an insecticide to kill insects.

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 If you are not sleeping in a well-screened or air-conditioned area, use a bed net
and tuck it under your mattress. If possible, use a bed net that has been soaked in
or sprayed with a pyrethroid-containing insecticide. The same treatment can be
applied to screens, curtains, sheets, and clothing (clothing should be retreated
after five washings).