Trypanosomiasis
Lecture with
Dr. Balsam Mahdi Nasir
MBBS/YEAR1/SEM2/2012
African trypanosomiasis
(sleeping sickness)
 Definition:
It is a vector-borne disease.
 Endemic to sub-Saharan Africa.
 It is caused by the single cell flagellate protozoan
Trypanosoma brucei.

 Geographic
distribution:
Trypanasoma brucei gambiense (West African sleeping
sickness or Gambian trypanasomiasis).
•
Trypanasoma brucei rhodesiense (East African sleeping
sickness or Rhodesian trypanosomiasis).
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Geographic distribution
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Mode of transmission
Via the bite of an infected tsetse fly.
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Morphology
In the vertebrate it exists as
a TRYPOMASTIGOTE.
Elongated rather flattened.
Spindle shaped organism.
Blunted posterior end.
Finely pointed anterior end.
Central large oval nucleus.
Kinetoplast is small and is
situated at the posterior end.
Undulating membrane.
Flagellum.
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Blood forms
1. Trypomastigote (long slender)→ dividing form.
2.Trypomastigotes (short broad stumpy form with
or without attenuated flagellum)→ non dividing
form → infective to tsetse fly.
3. Intermediate form.
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Tsetse fly
procyclic
trypomastigote
Epimastigote
Metacyclic
trypomastigote
Infective stage to human
Human
Trypomastigotes
Short
stumpy
form
Intermediate
form
Long
slender
form
Infective stage to tsetse fly
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Life cycle
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Life cycle
Definitive host
• Man, game and domestic animals.
 Intermediate host
• Tsetse fly (both male & female flies)
• Reservoir of infection
• Man (Trypanosoma brucei gambiense)→West
African trypanosomiasis.
• Animals (Trypanosoma brucei rhodesience)→ East
African trypanosomiasis.
 Infective stage to man
• Metacyclic trypomastigotes
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Pathogenesis and symptomatology
Gambian disease
of trypomastigotes.
Bite of infected •• Inoculation
Subcutaneous nodules→ 5-15 days → painless chancre→
resolve in 2-3 weeks.
tsetse fly
Incubation
period
Stage 1Blood
dissemination
Stage
1Lymphatics
Stage 2 CNS
invasion
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• Asymptomatic
• several weeks to months up to a year.
• Intermittent fever pattern, chills, headache, myalgia,
arthralgia..etc
•
Lymphadenopathy, especially in the posterior cervical nodes
(on the back of the neck) →Winterbottom’s sign.
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Occur at the end of 1st year or the beginning of the 2nd year
Daytime sleeping, mental dullness, apathy, tremors,
convulsions and coma followed by death from asthenia
during the 2nd or 3rd year
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Winterbottoms sign
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CDC DPDx Parasite Image Library
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RHODESIAN SLEEPING SICKNESS
clinical features
It is more acute
than the
Gambian form
Incubation
period 2-3
weeks
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Fever, weakness,
rapid loss of
weight and
myocarditis are
the usual
manifestation.
Fatal within a
year of onset
before
involvement of
the CNS.
Dr. Balsam
Mania and
delusion may
occur but the
typical sleeping
sickness picture
is seldom seen.
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A teenage girl in Uganda with sleeping sickness exhibiting the characteristic chancre on her leg at the site of tsetse fly inoculation (A), and a woman
in Uganda with a partially healedchancre just above her elbow (B). Although (C) may look painful, chancres are generallypainless with some
associated tenderness
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A woman caring for her comatose
husband who is dying of African
trypanosomiasis, Uganda, 1990
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Diagnosis
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Clinical
Patient from endemic area, irregular fever, palpable lymph nodes
(post. cervical).
Chronic disease with somnolence, personality changes and
neurological symptoms.
Laboratory
Direct microscopy of a wet smear of unstained blood or Geimsastained thick smear→ trypmastigote.
Chancre, lymph node, bone marrow and CSF aspirate→ wet
preparation.
Culture methods
The standard serologic assay to diagnose West African
trypanosomiasis is the card agglutination test for
trypanosomiasis (CATT).
Serological tests ELISA.
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Trypanosoma brucei
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TREATMENT
Haemo-lymphatic stage
Suramine sodium→ Rhodesian disease.
Suramine sodium or Pentamidine isethionate→ Gambian
disease
CNS involvement
Melarsoprol → Rhodesian disease.
Melarsoprol or DEMO (eflornithine) → Gambian disease.
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PREVENTION AND CONTROL
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Elimination of the reservoir:
Early Diagnosis and Treatment to reduce the
reservoir of infection.
Breaking the channel of transmission:
Vector control.
Protection of susceptible:
Persons visiting endemic areas should wear
protective clothing and apply repellents.
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Chagas’ disease
American trypanosomiasis
 Definition
It is a vector-borne disease
 It is prevalent throughout South and Central America
 It is caused by the flagellate protozoan Trypanosoma

cruzi.
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Geographic distribution
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Mode of transmission
Contamination of wound site, conjunctiva, or mucosa
by infected feces of insect (reduviid bugs)
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Morphology
Trypomastigote
The same as
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Trypanosoma brucei.
Long thin form
2. Short stumpy form
3. In blood film they
appear C or U or S
shape.
1.
Blood
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Amastigote form
Oval bodies.
Nucleus.
Kinetoplast.
Habitat: Striated
muscle in heart,
skeletal, neurological
cells and cells of
reticuloendothelial
system.
Tissue
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Morphology
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Trypomastigote
Epimastigote
Metacyclic
trypomastigote
Reduviid bug
Human
Trypomastigote
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Amastigote
Trypomastigote
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Life cycle
Definitive host
• Man, wild and domestic animals.
 Intermediate host
• Triatomine bugs (reduviid bugs)
 Reservoir of infection
 Besides humans, the parasite infects a variety of
wild and domestic animals.
 Infective stage to man
• Metacyclic trypomastigotes
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Clinical features
Acute
• In less than 50% of
people bitten by a
triatomine bug,
characteristic first
visible signs can be a skin
lesion (chagoma ) or a
purplish swelling of the
lids of one eye (Romana
sign)
• After 1-2 weeks→ fever,
headache, malaise, muscle
pain, generalized
lymphadenopathy and
hepatosplenomegally.
• Cardiac abnormalities
followed by
meningoencephalitis.
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Chronic
•The parasites are hidden
mainly in the heart and
digestive tract muscle.
• Up to 30% of patients
suffer from cardiac
disorders.
• Up to 10% suffer from
digestive (megaesophagus
or megacolon), neurological
or mixed alterations.
•In later years the infection
can lead to sudden death or
heart failure caused by
progressive destruction of
the heart muscle.
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Romana sign
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Megacolon in patient
with Chagas disease
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Diagnosis
Clinical may be suspected when general, cardiac or
GIT symptoms are present in patients lived under low
SES in endemic regions.
 Laboratory
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Demonstration of the parasitic agent is the diagnostic
procedure in acute Chagas'' disease.
1.Microscopic examination
a)
of fresh anticoagulated blood for detecting motile
trypanosomes.
b)
of thin and thick blood smears stained with Giemsa
for identification of parasites.
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Trypanosoma cruzi
amastigotes in heart tissue
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Trypanosoma cruzi
trypomastigote in a thin
blood smear stained with
Giemsa
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Laboratory diagnosis
2. If the parasites are scanty in blood
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Culture of the blood or suspected tissue specimen.
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xenodiagnosis, where clean lab-reared reduviid
bugs are fed on the patient's blood, and their gut
contents examined for parasites 4 weeks later.
Demonstration of antibodies to T. cruzi are required to
diagnose chronic Chagas disease by serology –
complement-fixation, direct agglutination and indirect
haemagglutinatin and ELISA.
Treatment
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Nitrofurans and benzidazoles have been used in
acute disease.
Neither drug is expected to cure established
chronic disease.
It is unsatisfactory since the organisms are
within cells in established infections.
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Prevention and control
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Elimination of reservoirs:
Control and elimination of domestic and peridomestic animals.
Early diagnosis and treatment of infected cases.
Vector control:
Triatomine bugs are highly susceptible to chlorinated
hydrocarbon insecticides which form the major weapon for their
control.
Protection of susceptible:
Provision of better housing would prevent transmission because
most human infections are transmitted by bugs living in cracks
and crannies in the walls of ill kept tenement dwellings.
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