TRYPANOSOMA

SRI SUNDARI
Trypanosomes
⦿ We will discuss two groups.
⚫ African group (transmitted by tsetse flies
belonging to the genus Glossina)
⚫ New World (transmitted by bugs)
 African Sleeping Sickness
⦿ The Trypanosoma
brucei group.
⚫ T. brucei brucei
⚫ T. brucei gambiense
⚫ T. brucei rhodesiense
T. b. brucei
⦿ Occurs in the circulatory system of most
native antelopes, ruminants, and other wildlife
in Africa.

⦿ Non-pathogenic to these animals (does not kill

them!).

⦿ However it is fatal to introduced

livestock like cattle, causing a
wasting disease called Nagana.
T. b. gambiense: Chronic or
Gambian Sleeping Sickness
⦿ Occurs in people.
⦿ Fatal if not treated.
⦿ Chronic infections (low-level infection that last
a long time).

⦿ Does not occur in either native

animals or livestock.
T. b. gambiense: Chronic or
Gambian Sleeping Sickness
⦿ Occurs in people.
⦿ Fatal if not treated.
⦿ Chronic infections (low-level infection that last
a long time).
⦿ Does not occur in either native animals or
livestock.

⦿ It is transmitted from person to

person by the Tsetse fly.
T. b. rhodesiense: Acute or
Rhodesian Sleeping Sickness
⦿ Causes acute infections in people.
⦿ Usually fatal within a year.
⦿ Occurs in native animals but it is not fatal in
these animals.

⦿ Transmission by Tsetse fly.

T. b. rhodesiense: Acute or
Rhodesian Sleeping Sickness
⦿ A more recent colonizer of people and
therefore does not do well in people and kills
them.

⦿ It has not been around long enough

to have adapted to its host (humans).
The Vector Glossina
The Vector Glossina
Biology of
Glossina spp.
The Vector Glossina
⦿ “Host” seeking behavior:
⚫ Visual sense used to search for animal or
human to feed on.
⚫ Spend most of their time resting on
vegetation waiting in ambush for their
prey to come into range.
The Vector Glossina

⦿ The genus is divided into 23 species (three species

groups).
⦿ Most of these can transmit Trypanosomes.

⦿ However two species are important in the

transmission to people, Glossina palpalis
(T. b. gambiense) and Glossina morsitans
(T. b. rhodesiense).
Life Cycle
⦿ Only 2 stages in life cycle –
Epimastigote and Trypomastigote.
 Trypanosoma brucei life cycle

1. Uninfected tsetse fly

(Glossina) bites an infected
vertebrate host and ingests
trypomastigote circulating in
the bloodstream.

2. Trypomastigotes
multiply by
longitudinal binary
fission in fly gut.
 Trypanosoma brucei life cycle
3. Trypomastigotes migrate
to the salivary glands and
transform into epimastigotes
and multiply for several
generation.
 Trypanosoma brucei life cycle
3. Trypomastigotes migrate to the
salivary glands and transform into
epimastigotes and multiply for several
generation.

4. Epimastigotes transform
back into Metacyclic
Trypomastigotes (short
stumpy forms) in the salivary
glands. These form the
infective stage.
 Trypanosoma brucei life cycle
3. Trypomastigotes migrate to the
salivary glands and transform into
epimastigotes and multiply for several
generation.

4. Epimastigotes transform back into

Metacyclic Trypomastigotes (short
stumpy forms) in the salivary glands.
These form the infective stage.

5. Tsetse fly bites a human or

ruminant host and inoculates
metacyclic trypomastigotes
into bloodstream.
 Trypanosoma brucei life cycle
3. Trypomastigotes migrate to the salivary glands
and transform into epimastigotes and multiply for
several generation.

4. Epimastigotes transform back into

Metacyclic Trypomastigotes (short
stumpy forms) in the salivary glands.
These form the infective stage.

5. Tsetse fly bites a human or ruminant

host and inoculates metacyclic
trypomastigotes into bloodstream.

6. Trypomastigotes live and

multiply in the blood and
lymph. In some cases,
trypomastigotes migrate to
the central nervous system.
Trypanosoma brucei life cycle
⦿ For our purposes we will consider
only two life cycle stages
trypomastigotes in vertebrate host
and epimastigote in Glossina which
will be transmitted anterior station or
salivarian transmission to the
vertebrate host.
African Trypanosomiasis Course
of Infection
⦿ There are four phases.

⦿ The first two phases of

trypanosomiasis only show up in
people of non-African decent
(Europeans).
African Trypanosomiasis Course
of Infection
⦿ Phase I: Incubation Period.

⚫ Trypomastigote in skin.
⚫ Red lesion and chancre at site of bite,
painful.
⚫ Itching and inflammation of skin.
⚫ Duration one to two weeks.
African Trypanosomiasis Course
of Infection
⦿ Phase II: Trypomastigotes enter
circulation.

⚫ Fever
⚫ Headache
⚫ Skin rash
⚫ Duration is variable
African Trypanosomiasis Course
of Infection
⦿ Phase III: Trypomastigotes collect in
lymph nodes and channels.
⚫ Cells not invaded but there is
proliferation of endothelial cells
⚫ Infiltration of leukocytes
⚫ Enlargement of lymph nodes
Phase III

Enlargement of lymph nodes in cervical triangle

(on back of neck) Winterbottom’s Sign one of the
cardinal signs of African Trypanosomiasis.
African Trypanosomiasis Course
of Infection
⦿ Phase III: Trypomastigotes collect in
lymph nodes and channels.
⚫ Fever, headache, and delayed sensation
to pain
⚫ General weakness
⚫ Duration many years with T. b.
gambiense; less than 1 year and usually
less than 4 mo for T. b. rhodesiense
African Trypanosomiasis Course of
Infection
⦿ Phase IV: Invasion of Central Nervous
System-African Sleeping Sickness.
African Trypanosomiasis Course
of Infection
⦿ Phase IV: Invasion of Central Nervous
System-African Sleeping Sickness.
⚫ Headaches are severe
⚫ Emaciation
⚫ Mental dullness
⚫ Apathy; disinclination to work
⚫ Drowsiness and coma
⚫ Death from asthenia, heart failure,
meningitis, severe fall, etc.
African Trypanosomiasis Course
of Infection
⦿ Phase IV: Invasion of Central Nervous
System-African Sleeping Sickness.
⚫ Duration variable with T. b. gambiense;
usually does not occur with T. b.
rhodesiense.
Pathology
1) Parasites themselves are toxic.
-Their by products are toxic and end up
circulating in the blood stream.
Pathology
1) Parasites themselves are toxic.
-Their byproducts are toxic and end up
circulating in the blood steam.
2) Hyper stimulated immune system.
-Parasite has variable antigenic types (VATs)
which are constantly changing.
-This compromises our immune system, and
those infected can be susceptible to other
bacteria and virus infections.
Pathology
3) Host lyses its own erythrocytes
(RBCs).
-This is why anemia is a symptom of
this disease.

So why does this happen?

Diagnosis
⦿ Can find Trypanosomes in plasma.
⦿ Concentrated in lymph nodes.
⚫ Treatment differs if there has been
invasion of CNS
⦿ If questionable do a lumbar puncture.
Treatment
⦿ Drug of choice 🡪 Suramin (Bayer 205)
⚫ Not affected against CNS forms!
Treatment
⦿ Drug of choice 🡪 Suramin (Bayer 205)
⚫ Not affected against CNS forms!
⦿ Melarsoprol (and arsenical; toxic) is
used with Bayer 205 to treat CNS
forms.
⚫ Vomiting, and kidney damage.
⚫ 10% of patients will die from treatment.
Treatment
⦿ Drug of choice 🡪 Suramin (Bayer 205)
⚫ Not affected against CNS forms!
⦿ Melarsoprol (and arsenical; toxic) is used with
Bayer 205 to treat CNS forms.
⚫ Vomiting, and kidney damage.
⚫ 10% of patients will die from treatment.
⦿ Ornidyl (DFMO)🡪 Current drug of
choice.
⚫ Tolerated well; effective against CNS,
expensive
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