Trypanosoma

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1. TRYPANOSOMIASISTRYPANOSOMIASIS

GUIDE:DR. MRS.VAIDYAGUIDE:DR. MRS.VAIDYA

2. TRYPANOSOMIASIS TRYPANOSOMIASIS
IINTRODUCTION:- NTRODUCTION:-
 Human trypanosomiasis is endemic in Africa Human trypanosomiasis is endemic in Africa
and South America. In Africa the disease is known and South America. In Africa the disease is known
as Human African Trypanosomiasis (HAT) or as Human African Trypanosomiasis (HAT) or
sleeping sicknesssleeping sickness. Whereas American . Whereas American
trypanosomiasis is known as trypanosomiasis is known as Chaga’s disease.Chaga’s disease.
 Trypanosomes are haemoflagellates. Trypanosomes are haemoflagellates.
 Disease caused by pathogenic types is called Disease caused by pathogenic types is called
trypanosomiasis. trypanosomiasis.

3. Genus Trypanosoma Genus Trypanosoma
Exist as trypomastigotes in vertebrate hosts and some Exist as trypomastigotes in vertebrate hosts and some
assuming amastigote forms. assuming amastigote forms.
Pass their life cycle in two hosts Vertebrate and insectPass their life cycle in two hosts Vertebrate and insect
( amastigote, promastigote, epimastigote and ( amastigote, promastigote, epimastigote and
metacyclic trypomastigote). metacyclic trypomastigote).
Transmission is effected from one vertebrate to Transmission is effected from one vertebrate to
another by blood sucking insects.another by blood sucking insects.

Types of Development :- Types of Development :-
1. 1. Anterior station Anterior station
2. 2. Posterior station Posterior station

4. Morphology of Trypomastigotes Morphology of Trypomastigotes
Method of reproduction – binary longitudinal fission. Method of reproduction – binary longitudinal fission.

5. Classification of TrypanosomiasisClassification of Trypanosomiasis
Two British scientists (Forbe and Two British scientists (Forbe and
Dutton) discovered trypanosomes in Dutton) discovered trypanosomes in
1901 in Gambia 1901 in Gambia
 T. Brucei- T. Brucei-
a) T. Brucei Gambiense a) T. Brucei Gambiense
b) T. Brucei Rhodesiense b) T. Brucei Rhodesiense
c ) T. Brucei brucei c ) T. Brucei brucei
 T. Cruzi- T. Cruzi-
 T. Rangeli- T. Rangeli-
 Found in peripheral blood of man in Found in peripheral blood of man in
venezuela. venezuela.
 Non pathogenic for man. Non pathogenic for man.
Trypanosomiasis Seen in Animals Trypanosomiasis Seen in Animals
1)1) NON PATHOGENICNON PATHOGENIC- - T. LewisiT. Lewisi
 Life cycle passes in to two hosts -rat Life cycle passes in to two hosts -rat
and rat flea and rat flea
 Shriwastava et al. reported Shriwastava et al. reported
Trypanosome resembling T. Lewisi in Trypanosome resembling T. Lewisi in
peripheral blood of 2 cases suffering peripheral blood of 2 cases suffering
from short febrile illness in Raipur M.P.from short febrile illness in Raipur M.P.

6. 2)2) PATHOGENIC – PATHOGENIC –
T. Brucei brucei- T. Brucei brucei-
Transmitted by G. Morsitans Transmitted by G. Morsitans
T. Evansi – ( Causes ‘Surra’ in horses, T. Evansi – ( Causes ‘Surra’ in horses,
mules, camel, elephants) mules, camel, elephants)
T. Equiperdum- Stallions diseaseT. Equiperdum- Stallions disease
T. Equinum T. Equinum
T. Vivax T. Vivax
T. Congolense T. Congolense

7. African Trypanosomiasis African Trypanosomiasis
The parasite discovered by David Bruce in The parasite discovered by David Bruce in
1890.He suggested it to be the cause of 1890.He suggested it to be the cause of
NaganaNagana
Trypanosoma BruceiTrypanosoma Brucei
Based on host specificity, clinical features, Based on host specificity, clinical features,
geographical distribution and geographical distribution and
epidemiological features originally classified epidemiological features originally classified
into into
1)1)The animal strain – The animal strain –
T. Brucei brucei T. Brucei brucei

8. 2) Human strain 2) Human strain
1)1)Gambian Gambian
2)2)RhodesianseRhodesianse
3)3)Zambezi Zambezi
Morphologically the strains are indistinguishable Morphologically the strains are indistinguishable
Blood incubation infectivity test Blood incubation infectivity test

9. African Trypanosomiasis African Trypanosomiasis
Trypanosoma infection is Trypanosoma infection is
confined to a particular area confined to a particular area
due to vector species being due to vector species being
confined to these places confined to these places
alone. alone.
 Tsetse belt of tropical central Tsetse belt of tropical central
Africa is the one where Africa is the one where
several species of the fly several species of the fly
(Glossina sp.) breed.(Glossina sp.) breed.
Most of them feed on wild Most of them feed on wild
animals and they transmit animals and they transmit
enzootic trypanosomiasis. enzootic trypanosomiasis.

10. Suffix Suffix demedeme has been has been
employed to refer to employed to refer to
population of population of
trypanosomes that trypanosomes that
differs from others differs from others
belonging to the same belonging to the same
species or subspecies in species or subspecies in
regard to specified regard to specified
properties. properties.
e.g. e.g.
a) a) Nosodeme Nosodeme
b) b) Zymodeme Zymodeme
c) c) Serodemes Serodemes

11. HABITATHABITAT
T. Brucei T. Brucei
Essentially a parasite of connective Essentially a parasite of connective
tissue.tissue.
Consumes enormous amount of Consumes enormous amount of
glucose glucose
Invades regional L.N. & also invades Invades regional L.N. & also invades
blood stream causing parasitemia blood stream causing parasitemia
Finally localizes in brain Finally localizes in brain
Chronic Chronic GambianseGambianse strain is found strain is found
mainly in west and central Africa and mainly in west and central Africa and
scattered areas of East Africa scattered areas of East Africa
RhodesienseRhodesiense- East Africa - East Africa
ZambeziZambezi- East Africa which - East Africa which
botswana, Rhodesia, Zambia botswana, Rhodesia, Zambia

12. Polymorphism Polymorphism
 Trypomastigotes- polymorphicTrypomastigotes- polymorphic
Two main forms Two main forms
1)1)Short, thick, stumpy form Short, thick, stumpy form
2)2)Other long slender form Other long slender form
ANTIGENIC VARIANT ANTIGENIC VARIANT
 A succession of variants occur A succession of variants occur
in T. Brucei infection both in in T. Brucei infection both in
animals and in man animals and in man
 Each new variant emerges at Each new variant emerges at
3-4 days intervals possibly by 3-4 days intervals possibly by
selection of mutants. selection of mutants.
 This appears to depend upon This appears to depend upon
the ability of the host’s defence the ability of the host’s defence
mechanism. mechanism.

13. Outer proteinaceous coat may protect the Outer proteinaceous coat may protect the
organism in escaping from the host’s defence organism in escaping from the host’s defence
mechanism. mechanism.
Also Ab develop to a series of Also Ab develop to a series of
immunologically distinct type of variant in the immunologically distinct type of variant in the
serum of host.serum of host.
 Each rise in antibody titre coincides with the Each rise in antibody titre coincides with the
disappearance of the homologous variant and disappearance of the homologous variant and
when this has been eliminated, a new antigenic when this has been eliminated, a new antigenic
type immediately arises.type immediately arises.

14. TRYPANOSOMA BRUCEI LIFE TRYPANOSOMA BRUCEI LIFE
CYCLE CYCLE
T. Brucei passes its life cycle in two different T. Brucei passes its life cycle in two different
hosts hosts
Definitive host Definitive host
Intermediate host - insect Intermediate host - insect

15. Infective from is metacyclic Infective from is metacyclic
trypomastigote trypomastigote
Metacyclic trypomastigotes are Metacyclic trypomastigotes are
inoculated through the skin when a tsetse inoculated through the skin when a tsetse
fly takes a blood meal. Initially they fly takes a blood meal. Initially they
proliferate at site of inoculation and then proliferate at site of inoculation and then
through lymphatics, enters blood streamthrough lymphatics, enters blood stream

16. It takes about 3 wks from the time of blood meal for fly to become It takes about 3 wks from the time of blood meal for fly to become
infective. Then it remains infective for life (6Months) infective. Then it remains infective for life (6Months)

17. Clinical DiseaseClinical Disease
Pathogenesis Pathogenesis
1.1.Mode of infection Mode of infection
2.2.Trypomastigotes introduced by the fly with saliva into the Trypomastigotes introduced by the fly with saliva into the
S.C. pool of blood S.C. pool of blood
3.3.Majority get entangled in the tissue spaces Majority get entangled in the tissue spaces
4.4.Initial growth occurs in tissue spaces which form a more Initial growth occurs in tissue spaces which form a more
favourable nidus favourable nidus
5.5.It is also suggested that connective tissue damage caused by It is also suggested that connective tissue damage caused by
trypomastigotes may be due to exaggerated immune trypomastigotes may be due to exaggerated immune
response rather than any direct effect response rather than any direct effect
6.6.Trypomastogotes in tissue excites host’s response in two Trypomastogotes in tissue excites host’s response in two
ways ways
a) Producing large amount of nonspecific a) Producing large amount of nonspecific
immunoglobulins immunoglobulins
b) By heavily infilltrating the site of infection with b) By heavily infilltrating the site of infection with
macrophages. macrophages.

18. Pathogenic Lesion Pathogenic Lesion
1.1.CNS - CNS -
2.2.LN – Congestion, LN – Congestion,
haemorrhage, proliferation haemorrhage, proliferation
of macrophages. of macrophages.
3.3.Spleen Spleen
4.4.Liver Liver
5.5.Heart Heart
6.6.Kidney Kidney
7.7.Bone Marrow Bone Marrow
8.8.Lungs Lungs
9.9.Localized edema of eyelid, Localized edema of eyelid,
perineum, skin of back perineum, skin of back

19. Clinical Features Clinical Features
The disease occurs in The disease occurs in
two stages. Incubation two stages. Incubation
period – 2-3 weeksperiod – 2-3 weeks
1st stage1st stage
Enlarged post Enlarged post
cervical L.N. cervical L.N.
Winterbottom’s Winterbottom’s
sign sign
Pruritus ,Transient Pruritus ,Transient
edema edema
Papuloerythematous Papuloerythematous
eruption eruption
Endocrine dysfunction Endocrine dysfunction

Profound anaemia Profound anaemia

20. 22
ndnd
Stage – Stage –
HeadacheHeadache
Impaired motor functionImpaired motor function
Slurred speech,Slurred speech,
Abnormal movements, Abnormal movements,
tremors tremors
Mental Changes – Mental Changes –
Generalised pruritis, Generalised pruritis,
bedsores, wt. loss, bedsores, wt. loss,
wasting. wasting.
Coma followed by death if Coma followed by death if
untreated. untreated.

21. T.B. RhodesienseT.B. Rhodesiense
11
stst
Stage Stage
1.1.Chancre Chancre
2.2.Painful, indurated, red Painful, indurated, red
papule 2-5 cm papule 2-5 cm
3.3.Regional Regional
lymphadenitis, lymphadenitis,
adjacent cellulitis adjacent cellulitis
4.4.Fever, parasitaemia Fever, parasitaemia
22
ndnd
Stage Stage
1.1.Rapid progress to Rapid progress to
death.death.

22. Lab Diagnosis African Trypanosomiasis Lab Diagnosis African Trypanosomiasis
1.1.Examination of blood Examination of blood
2.2.Examination of aspirates from Examination of aspirates from
enlarged lymph glands enlarged lymph glands
3.3.Examination of CSF Examination of CSF
4.4.Detection of trypanosomal antibody Detection of trypanosomal antibody
in serum in serum

23. 11. . Examination of Blood Examination of Blood
1. Thick and thin films, Wet 1. Thick and thin films, Wet
preparation preparation
2. Concentration method 2. Concentration method
a. Triple centrifugation a. Triple centrifugation
technique technique
b. Miniature anion- b. Miniature anion-
exchange centrifugation technique exchange centrifugation technique
c. Buffy coat preparation c. Buffy coat preparation
22. . Examination of Aspirates in Examination of Aspirates in
lymph nodes lymph nodes
3. Examination of CSF 3. Examination of CSF
4. Detection of trypanosomes 4. Detection of trypanosomes
antibody in serum antibody in serum
- CATT - CATT
- Direct agglutination, indirect - Direct agglutination, indirect
haemagglutination, gel haemagglutination, gel
precipitation, ELISA , PCRprecipitation, ELISA , PCR

24. Also animal Also animal
inoculation of inoculation of
mice, rat, guinea mice, rat, guinea
pig can be done . pig can be done .
ProphylaxisProphylaxis
1.1.Attack on parasite Attack on parasite
2.2.Attack on vector Attack on vector
3.3.Personal Personal
prophylaxis prophylaxis

25. South American Trypanosomiasis South American Trypanosomiasis
History History
Habitat Habitat
Muscular and nervous Muscular and nervous
tissues, RES. tissues, RES.
Exists in the amastigote Exists in the amastigote
form form
Morphology Morphology

26. Vectors and Life Cycle Vectors and Life Cycle
 Hosts Hosts
Vertebrate Vertebrate
Insect – Bugs- Reduviidae family, subfamily- Insect – Bugs- Reduviidae family, subfamily-
Tritominae Tritominae

27. Life Cycle Life Cycle
 Metacyclic trypomastigotes are deposited on skin Metacyclic trypomastigotes are deposited on skin
Trypomastigotes become amastigotes in localized RE Trypomastigotes become amastigotes in localized RE
cells and multiply by longitudinal fission . cells and multiply by longitudinal fission .
After passing through promastigote and epimastigote After passing through promastigote and epimastigote
forms are transformed into trypomastigote forms forms are transformed into trypomastigote forms
Taken up by bug during act of biting Taken up by bug during act of biting
In midgut- transformed to amastigote forms In midgut- transformed to amastigote forms
Amastigote forms later transformed into epimastigote Amastigote forms later transformed into epimastigote
forms which migrate backwards to hindgut and forms which migrate backwards to hindgut and
multiply by longitudinal fission. multiply by longitudinal fission.
In 8-10 days time metacylic forms of trypomastigotes In 8-10 days time metacylic forms of trypomastigotes
appear and are excreted in faeces of bug . appear and are excreted in faeces of bug .

28. Pathogenicity Pathogenicity
a.a.Chagoma Chagoma
b.b.Romana’s Sign Romana’s Sign
c.c.Gross lesions mainly in heart, skeletal muscle and nervous Gross lesions mainly in heart, skeletal muscle and nervous
tissue tissue
Clinical Features Clinical Features
1)1)Incub period 7-14 days Incub period 7-14 days
2)2)Infection - asymptomatic, acute, chronicInfection - asymptomatic, acute, chronic
a)a)Acute stage – Fever, conjunctivitis , unilat edema of face, Acute stage – Fever, conjunctivitis , unilat edema of face,
enlargement of spleen and L.N., anaemia, lymphocytosis. enlargement of spleen and L.N., anaemia, lymphocytosis.
b)b)Chronic – Chronic –
Signs of cardiac muscle damage, edema, heart Signs of cardiac muscle damage, edema, heart
enlargement. enlargement.
Dilatation of tubular organs- Due to degeneration of Dilatation of tubular organs- Due to degeneration of
intramural autonomic nerve plexus. intramural autonomic nerve plexus.
Chaga’s Cardiomyopathy (10%) Chaga’s Cardiomyopathy (10%)

29. Lab Diagnosis Lab Diagnosis
1)Examination of Blood 1)Examination of Blood
a)a)Thick, thin film, Wet preparation Thick, thin film, Wet preparation
b)b)Buffy coat examination Buffy coat examination
2) Xenodiagnosis 2) Xenodiagnosis
3) Blood Culture -3) Blood Culture - As sensitive as xenodiagnosis As sensitive as xenodiagnosis
4) Serology 4) Serology
a)a)Indirect fluorescence Ab test Indirect fluorescence Ab test
b)b)CFT CFT
c)c)IHAT IHAT
d)d)ELISA ELISA
Other tests like intradermal test, biopsy from involved L.N. or muscle. Other tests like intradermal test, biopsy from involved L.N. or muscle.
Other findings are increased ESR; marked lymphocytosis Other findings are increased ESR; marked lymphocytosis
Prophylaxis Prophylaxis

30. 11
stst
case of Trypanosomiasis in India case of Trypanosomiasis in India
45 yrs old man 45 yrs old man
Farmer from Chandrapur dist in Maharashtra Farmer from Chandrapur dist in Maharashtra
Came with fever associated with chills and Came with fever associated with chills and
sweating for 15 days. Then he developed signs of sweating for 15 days. Then he developed signs of
sensory deficit sensory deficit
In GMC Nagpur- Blood smear showed presence of In GMC Nagpur- Blood smear showed presence of
parasites with morphology typical of monomorphic, parasites with morphology typical of monomorphic,
slender, flagellated, dividing trypomastigote form slender, flagellated, dividing trypomastigote form
of trypanosoma of trypanosoma
Later on PCR based methods confirmed diagnosis Later on PCR based methods confirmed diagnosis
of T. evansi. of T. evansi.

31. REFERENCESREFERENCES
Medical parasitology – Rajesh KaryakarteMedical parasitology – Rajesh Karyakarte
Paniker’s medical parasitologyPaniker’s medical parasitology
K.D Chatterjee’s human parasites & parasitic K.D Chatterjee’s human parasites & parasitic
diseasesdiseases
Harrison’s internal medicineHarrison’s internal medicine
Internet Internet