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Hemoflagellates
are flagellated protozoa found in
peripheral
blood circulation
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Hemoflagellates complete their life cycle in two hosts:
vertebrate host
and
insect vector
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Hemoflagellates belong to:
Phylum:
Euglenozoa
Class:
Kinetoplastea
Order:
Trypanosomatida
Family:
Trypanosomatidae
Genera:
Leishmania
and Trypanosoma
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Morphology of hemoflagellates:
Oval
to
elongated body
,
nucleus
, and a
single flagellum
arising from
kinetoplast
Kinetoplast
consists of
blepharoplast
and
parabasal body
connected by a
delicate fibril
Axoneme
(or
axostyle
) extends from
blepharoplast
to the
cell wall
Exist in four morphological stages:
amastigote
,
promastigote
,
epimastigote
, and
trypomastigote
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Trypanosomes are
hemoflagellates
residing in
peripheral blood
and
tissues
of their host
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Human Trypanosomes:
Trypanosoma cruzi
: Causative agent of South American trypanosomiasis (Chagas’ disease)
Trypanosoma brucei
: Causes African trypanosomiasis with subspecies Trypanosma brucei rhodesiense and Trypanosma brucei gambiense
Trypanosoma rangeli
: Nonpathogenic species
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Animal Trypanosomes:
Trypanosoma brucei brucei
: Causes "nagana" in cattle
T. congolense
and T.vivax cause diseases similar to T. brucei brucei
Trypanosma evansi
: Causes "Surra" in horses and other animals
Trypanosma lewisi
: Causes a harmless infection in rodents
Trypanosma equiperdum
: Causes "Stallion’s disease" in horses
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Trypanosoma brucei complex consists of three subspecies:
T. brucei gambiense
,
T. brucei rhodesiense
, and
T. brucei brucei
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Trypanosoma brucei gambiense:
Endemic
in scattered foci in
West
and
Central
Africa
Principal vectors are
Glossina palpalis
and
Glossina tachynoides
Morphology includes
trypomastigote
form in vertebrate host and
epimastigotes
and
metacyclic
trypomastigotes in the tsetse fly vector
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Trypanosoma brucei gambiense
completes its life cycle in
two
hosts:
humans
and
tsetse flies
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Pathogenesis and Clinical Features of Trypanosoma brucei gambiense:
Causes
African trypanosomiasis
(
West African sleeping sickness
)
Chronic illness
with
initial parasitemia
,
lymph node localization
,
chancre
,
fever
,
anemia
,
weight loss
Invasion
of
CNS
marked by
headache
,
mental dullness
,
apathy
, and
sleepiness
Histopathology
shows
chronic meningoencephalitis
with
cellular infiltration
and
neuronal degeneration
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Trypanosoma brucei rhodesiense:
Found in
Eastern
and
Central
Africa
Principal vectors are
Glossina morsitans
,
G. palpalis
, and
G. swynnertoni
Causes
East African sleeping sickness
with
acute illness
and
lymphadenitis
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Diagnosis of Human African Trypanosomiasis:
Microscopic examination of lymph node
aspirates
,
CSF
, and
chancre fluid
Culture
,
animal inoculation
,
serodiagnosis
, and
molecular diagnosis
are also used
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Serodiagnosis
can detect specific antibodies or antigens in serum and CSF
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Molecular diagnosis involves
PCR
on clinical specimens
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Suramin
is the drug of choice for rhodesiense HAT
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Pentamidine
is the drug of choice for gambiense human African trypanosomiasis (
HAT
) before CNS involvement
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Melarsoprol
is the drug of choice for HAT with CNS involvement
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Prevention and control methods for African trypanosomiasis include
early diagnosis
and
treatment
, control of
tsetse fly population
, and minimizing contact with
tsetse flies
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Trypanosoma cruzi causes
Chagas' disease
, limited to
South
and
Central America
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Chagas' disease was first discovered by Brazilian scientist
Carlos Chagas
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Trypanosoma cruzi exists in two forms in humans:
amastigote
and
trypomastigote
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Amastigotes
are intracellular parasites found in various human tissues
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Trypomastigotes are
extracellular
and found in
peripheral
blood
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Diagnosis methods for Chagas' disease include
microscopic examination
,
culture
,
animal inoculation
,
histopathology
,
serodiagnosis
,
intradermal test
, and
molecular diagnosis
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Chagas' disease
can manifest as acute or chronic forms
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Trypanosoma cruzi
completes its life cycle in two hosts:
human
and
reduviid bug
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Nifurtimox
and
benznidazole
are used for treating Chagas' disease
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Prevention and control methods for Chagas' disease include
insecticide use
,
insect repellants
, and
improvement in housing
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Leishmaniasis
is caused by the protozoa of the genus
Leishmania
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Leishmaniasis can produce various clinical syndromes ranging from
self-healing cutaneous ulcers
to
fatal visceral disease
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Leishmaniasis
primarily affects the
reticuloendothelial system
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Leishmaniasis
is mainly a zoonotic disease affecting animals like dogs, foxes, jackals, and rodents
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Leishmaniasis
is transmitted by the bite of female sandfly vectors
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Leishmania has two subgenera:
L. Leishmania
and
L. Viannia
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Clinical syndromes of leishmaniasis include
visceral leishmaniasis
,
post-kala-azar dermal leishmaniasis
,
cutaneous leishmaniasis
,
diffuse cutaneous leishmaniasis
,
leishmaniasis recidivans
, and
mucocutaneous leishmaniasis
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Leishmania donovani
causes visceral leishmaniasis or kala azar, a major public health problem in many parts of the world
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In humans, the amastigotes of Leishmania donovani are found in the
reticuloendothelial system
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The parasite exists in 2 forms:
Amastigote
form found in humans and other mammals, known as
Leishman Donovan
(LD) body,
intracellular
Promastigote
form found in the sandfly and in culture
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History of Leishmania donovani:
Discovered in
1903
by Sir
William Boog Leishman
in
London
and Sir
Donovan
in
Chennai
Charles Nicolle
characterized the new world visceral leishmaniasis
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