2. Trypanosomes
• General Feature
– actively motile flagellated
protozoa that live in blood
and lymph node
– Vector:- tsetse fly, bug
3. Morphology
Trypanosomes have a single central
nucleus and a single flagellum
originating at the kinetoplast and joined
to the body by an undulating membrane.
The outer surface of the organism is
densely coated with a layer of
glycoprotein, the variable surface
glycoprotein (VSG).
From the point of view of functional
and physiologic complexity, a
protozoan is more like an animal than
like a single cell.
4. Morphological Forms
TRYPOMASTIGOTE
• The kinetoplast (kt) is located on the
posterior end of the parasite. The
flagellum emerges from the posterior
end and folds back along the parasite's
body. This attachment of the flagellum
to the body forms an undulating
membrane (um) that spans the entire
length of the parasite and the free
flagellum emerges from the anterior
end. This is considered the anterior
end since the flagellum pulls the
organism and the end with the free
flagellum is the front in reference to
the direction of movement. The
undulating membrane functions like a
fin and increases the motility of the
organism.
5. Morphological Forms
EPIMASTIGOTE
• The kinetoplast (kt) is more
centrally located, usually just
anterior to nucleus (Nu). The
flagellum (fg) emerges from the
middle of the parasite and forms
a shorter undulating membrane
(um) than observed in
trypomastigotes. Epimastigotes
are noticeably less motile than
trypomastigotes.
6. Morphological Forms
PROMASTIGOTE
• The kinetoplast (kt) is
towards the anterior end and a
free flagellum (fg) with no
undulating membrane
emerges. The end that the free
flagellum emerges from in all
three motile forms is
designated as the anterior end
because they swim in that
direction. In other words, the
flagellum pulls the organism.
7. Morphological Forms
AMASTIGOTE
• The parasite is more spherical in
shape and has no free flagellum.
A basal body (bb) and the base
of the flagellum is still present.
The kinetoplast (kt) is usually
detectable as a darkly staining
body near the nucleus (Nu).
This form is a non-motile
intracellular stage.
8. Classified in to two groups based on the type of development in the
insect vector and mode of transmission
9. • Two distinct forms occur in humans
– African Trypanosomiasis
• Trypanosoma brucei gambiense
• Trypanosoma brucei rhodesiense
• Transmited by the Tsetse fly
– American Trypanosomiasis
• Trypanosoma cruzi
• Transmited by the tritomine bug
Genus Trypanosoma
11. A: Trypansoma brucei sp. in thick blood smears stained with Giemsa.
B: Trypanosoma brucei sp. in thin blood smears stained with Giemsa
A B
12. Trypanosoma brucei sp. in thin blood smears stained with Wright-Giemsa.
Trypanosoma brucei sp. in a thin blood smear stained with Giemsa
13. • It is caused by the flagellate protozoan, Trypanosoma brucei
• exists in 2 morphologically identical subspecies:
– Trypanosoma brucei gambiense
• Disease: West African or Gambian African trypanosomiasis
• Geographical Dist: Central & West Africa
– Trypanosoma brucei rhodesiense
• Disease: East African or Rhodesian African trypanosomiasis
• Geographical Dist : Central and East Africa
Human African Sleeping
Sickness
14. Major Differences Between African
Trypanosome Species
Attribute T. rhodesiense T. gambiense
tsetse vector G. morsitans group G. palpalis group
ecology dry bush, woodland rainforest, riverine, lakes
transmission cycle ungulate-fly-human human-fly-human
non-human reservoir wild animals domestic animals
epidemiology sporadic, safaris endemic, some epidemics
disease progression rapid, often fatal slow (~1 yr) acute ⇒ chronic
parasitemia high low
asymptomatic carriers rare common
15. Epidemiology
• Human trypanosomiasis has caused massive
epidemics in the past. At the turn of the
century, in Zaire and around Lake Victoria,
large epidemics caused at least three-quarters
of a million deaths. Although only
approximately 20000 cases are reported each
year to the World Health Organization, gross
under-reporting, reduced surveillance, and
recent epidemics in Zaire, Uganda, Tanzania,
Mozambique, and Sudan underline the
continuing importance of human
trypanosomiasis in public health.
Trypanosomiasis of domestic animals and
man remains an important deterrent to
development in endemic areas and shows
increased prevalence associated with war,
civil disturbance, and refugee groups as well
as deteriorating health services and disease-
specific control programmes.
16. Morphology
– spindle – shaped elongated body
(polymorphic -from long slender to short and blunt)
– Measuring 14-33 u X 1.5-3.5 u
– nucleus centrally located with karyosome
– kinetoplast found at the posterior end of the body
– undulating membrane originating from the blepharoplast
– Anterior flagellum runs along the edge of undulating
membrane
– volutin granules scattered in the cytoplasm
17. Habitat : blood, Lymph channel throughout the body, CSF,
Connective tissue, Intracellular space, brain
Vector : Tse-Tse fly – Glossina spp.
1. G. palpalis
2. G. tachinoides
3. G. morsitans
4. G. pallidipes
Mode of Transmission:
1. bite of infected tse-tse fly
2. congenital
3. sexual contact
4. human-fly-human transmission
T. b. gambiense
T. b. rhodesiense
18.
19.
20.
21.
22. Laboratory diagnosis
• A definitive diagnosis requires detection of trypanosomes in the
following samples;
– In blood,
– Lymph nodes,
– CSF,
– Skin chancre aspirates, or
– Bone marrow.
23. • Lymph node aspirate
– Is commonly used as a rapid test for trypanosomes at a high dry
magnification (X 400).
– It requires immediate search for parasites because they are mobile for
only 15-20 minutes.
• Blood smear
– A wet smear of unstained blood for mobile trypanosomes, again for 15-
20 minutes
– Giemsa-stained thick smear (more sensitive)
– wright and leishman stains are inadequate.
– Better assays
– Hematocrit centrifugation technique for buffy coat examination,
– Miniature anion-exchange centrifugation technique, which filters out
the red cells but not the trypanosomes.
• Chancre aspirate
– Can be used as a wet preparation, especially in the east african form of
the disease, but a blood smear is more sensitive.
24. • CSF assay
– Lumbar puncture should always be performed in patients
with parasitemia or lymphadenopathy.
– The double centrifugation technique is the most sensitive
method to detect the trypanosomes.
– Other CSF findings include elevated WBC count, elevated
IgM, and elevated total protein levels.
25. • Other Tests:
Serologic antibody detection- Field diagnosis
– The standard serologic assay to diagnose West African
trypanosomiasis is the card agglutination test for
trypanosomiasis (CATT).
– The CATT
• can be conducted in the field without electricity
• results are available in only 10 minutes.
• It is highly sensitive (96%) but less specific because of cross-
reactivity with animal trypanosomes.
– Commercial antibody tests for Eastern African
trypanosomiasis are not available.
• Other tests developed but not frequently used clinically
include:
• antibody detection in the CSF and enzyme-linked
immunoassay (ELISA), polymerase chain reaction (PCR).
26. Treatment
• Medicine for the treatment of African trypanosomiasis
is available. Treatment should be started as soon as
possible and is based on the infected person's symptoms
and laboratory tests results.
• Patients need to be hospitalized for treatment and
require periodic follow-up exams for 2 years.
• The current standard treatment for first stage disease is:
Intravenous pentamidine (for T.b. gambiense); or
suramin (for T.b. rhodesiense).
• The current standard treatment for second stage disease
is: Intravenous melarsoprol.
• In areas with melarsoprol resistance or in patients who
have relapsed after melarsoprol monotherapy, the
treatment should be: melarsopsol and nifurtimox, or
eflornithine.
30. Classification
• Eukaryota (organisms with nucleated
cells),Kingdom Protista, Phylum Protozoa.
• Trypanosoma cruzi.
• T. cruzi reproduce asexually by binary
fission.
• Like all other trypanosomes, T. cruzi live one
stage of their lives in the blood and/or tissues
of vertebrate hosts and during other stages
they live in the digestive tracts of
invertebrate vectors (temporary hosts).
• Trypanosoma cruzi belongs to the
subkingdom Protozoa. They are flagellar
organisms that have one nucleus and an
organelle, the kinetoplast, that gives rise
to one mitochondrion and mitochondrial
DNA.
32. Life cycle of Trypanosoma cruzi.
• An infected triatomine insect
vector (or “kissing” bug) takes a
blood meal and releases
trypomastigotes in its feces near
the site of the bite wound.
• Inside the host, the
trypomastigotes invade cells,
where they differentiate into
intracellular amastigotes .
• The amastigotes multiply by
binary fission and differentiate
into trypomastigotes, and then are
released into the circulation as
bloodstream trypomastigotes
33. Epidemiology
• Chagas disease is transmitted
by cone-nosed triatomine
bugs of several genera
(Triatoma, Rhodnius,
Panstrongylus).
• Trypanosoma cruzi can
also be transmitted through
blood transfusions, organ
transplantation,
transplacentally, breast
milk and in laboratory
accidents.
34. Clinical Symptoms.
The incubation period is 7-14 days.
The human disease occurs in 3 stages:
• the acute stage shortly after the infection;
• the indeterminate stage;
• the chronic stage that may develop over 10
years.
35. Acute phase of Chagas disease
• A local skin nodule called a chagoma
can appear at the site of inoculation.
• When the inoculation site is the
conjunctival mucous membranes, the
patient may develop unilateral
periorbital edema, conjunctivitis, and
preauricular lymphadenitis. (Romaña's
sign).
• The acute phase is usually
asymptomatic, but may present
symptoms of fever, anorexia,
lymphadenopathy, mild
hepatosplenomegaly, and myocarditis.
36. Chronic stage of Chagas disease
The disease affects the nervous
system, digestive system and heart:
• dementia,
• damage to the heart muscle
(cardiomyopathy), altered heart rate
or rhythm,
• sometimes dilation of the digestive
tract (megacolon and
megaesophagus),
• Weight loss.
• Swallowing difficulties may be the
first symptom of digestive
disturbances and may lead to
malnutrition.
• Left untreated, Chagas disease can
be fatal, in most cases due to the
cardiomyopathy component.
38. Treatment
• No effective treatment.
• Available drugs only kill extracellular
parasites.
• Benznidazole and Nifurtinox: current drugs
of choice. Required daily for up to 2
months or more.
• Hospitalization may be needed because of
adverse effects
39. Prevention
• There is no vaccine or drug to prevent
Chagas disease. When traveling to areas
where Chagas disease occurs, follow these
precautions:
• Avoid sleeping in poorly constructed
thatch, mud, or adobe houses. If that is not
possible, use a bednet.
• Use insecticides to kill insects and
reduce the risk of transmission.
• Be aware of the risk of contracting
Chagas disease through blood transfusions. In
many countries, the blood supply is not well
screened.
