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TRYPANOSOMIASIS
DR.FARIA ASHRAF
Introduction
 The name is derived from Greek word,
 Trypano means (borer)
 Soma means (body)
 They are unicellular flagellate protozoa.
 Have corkscrew like motion.
 transmitted by a vector.
Tsetse fly
Reduviid
(Triatomine) bug
Trypanosoma (Trypanes- to bore, Soma- body)
Trypanosoma species infecting human:-
Parasite Vector Disease
1 T. brucei Tsetse fly African Trypanosomiasis ( sleeping sickness)
T. brucei gambiense
T. brucei rhodesiense
T. brucei brucei Not infective to human.
2 T. cruzi Triatomid bug American Trypanosomiasis ( Chagas disease)
3 T. rangeli Triatomid bug Non pathogenic ( in south America)
African sleeping sickness
 Trypanosoma brucei
gambiense: West
and Central Africa,
mainly human
infection
 Trypanosoma brucei
rhodesiense: East
Africa, wild and
domestic animal
reservoirs
Trypanosome forms
Epimastigotes:
flagellum anterior to
the nucleus. Present
in the insect vector. T.
brucei and T. cruzi
Trypomastigotes: 15-80
m single flagellum
posterior to the nucleus.
Found in the mammalian
host in the blood. Also as
metacyclics in the insect
vector. Undulating
membrane. T. cruzi and T.
brucei
Promastigotes:
short flagellum. No
undulating
membrane.
Extracellular form
in the insect vector.
Leishmania
parasites
Amastigotes: short or no
flagellum. Intracellular
form in mammalian cells.
T. cruzi and leishmania.
 Life cycle-
 Vertebrate host- man, domestic animals
 Invertebrate host- tsetse fly of genus Glossina
(G.palpalis, G. fuscieps, G.tachinoides)
 Both male and female fly bite, usually early
morning and evening
Tsetse fly
African Trypanosomiasis
 Pathogenicity- African
trypanosomiasis or West African
sleeping sickness
 Chronic in nature
 Chancre develops at the site of
bite, hard, painful and fluid filled
 Trypomastigotes move through
blood and lymphatic vessels
 Lymph nodes in posterior cervical
region are involved-
Winterbottom`s sign
Pathogenesis of African Trypanosomiasis
Tsetse fly bite
Chancre resolve in 7-10 days
Asymptomatic weeks  months
Blood
Fever alternating with a febrile period
Lymphatics
CNS Involvment
Death
Cure
Winterbottoms
sign (posterior
cervical
lymphadenopathy)
Leptomeningitis
Keranders sign
positive
Pathology and clinical picture
1. Skin stage: chancre.
2. Haematolymphatic stage:
generalized lymphadenopathy,
anaemia, liver and kidney
generalized organ involvement.
3. Central nervous system stage
(CNS): Meningoencephalitis.
(Development of the disease more
rapid in Trypanosoma brucei
rhodesiense)
 Lab Diagnosis-
 Blood, LN aspirate, CSF,
sternal bone marrow, fluid
from chancre
 M/E, culture and animal
inoculation
 Trypomastigote forms are
seen in largest number during
febrile periods, so multiple
daily blood samples
 Serology- IF, CFT, ELISA and
card agglutination test
Trypanosoma brucei rhodesiense
 East and central Africa
 When inoculated in to guinea pig, rat or mice-
posterior nucleate forms are more common
 Reservoir host are mainly animals
 More virulent
 Trypomastigotes are more in blood
 East african sleeping sickness
 Acute form
 Febrile paroxysms are more
 Fever, oedema, weakness, rapid loss of
weight, myocarditis
 Marked CNS symptoms are lacking or not
much evident
 Treatment and prophylaxis-
 Suramin and pentamidine for primary stage
 Melarsoprol for CNS infection.
TRYPANOSOMA CRUZI
South American Trypanosomiasis
(Chagas disease)
 Central and south America
 Carlos Chagas discovered the parasite
 Named T.Cruzi after his mentor Oswaldo Cruz
 Morphology
 Trypomastigote  peripheral blood of humans
and does not multiply in humans. C- shaped
 Amastigote- muscles of heart and skeletal
system, neurological cells and RES. It is a
multiplying form.
Trypanosoma cruzi
 T. cruzi causes chagas disease
 Found in the vector reduviid bug & humans
 It is zoonosis
 May serve as reservoirs of infection
 Blood transfusion accounts for 5% cases
Epidemiology
 Distribution- Central & South
America.
 Reservoirs- Reduviid bug &
animals (dogs, cats, armadillos,
raccoons).
 Transmission-
Invertebrate host : Reduviid
bug.
 Blood Transfusion- Prominent in
urban areas. Reduviid (Triatomine) bug
trypanosomiasis-sleepin sickness & chagas dise
trypanosomiasis-sleepin sickness & chagas dise
 Culture- NNN medium and epimastigote forms
are seen
 Life cycle- two hosts
 Humans are definitive host
 Triatomine bugs or reduvid bug - intermediate
host
AMERICAN TRYPANOSOMIASIS
trypanosomiasis-sleepin sickness & chagas dise
 Infective form- metacyclic trypomastigote
 Discharge of infected faecal material near bite
wound
 Infected faeces rubbed in to wound by bitten
person
 Abraded skin, oral and nasal mucosa may also be
infected
 Metacyclic trypomastigotes invades the RES
 Converted to amstigote, promastigote and than
trypomastigotes
 Pathogenesis  American
trypanosomiasis or Chaga`s
disease
 IP- 1-2 wks
 Due to multiplication of
amastigotes and causes
damage to cells and tissues
 Myocardium, skeletal muscles,
neurological cells and RES are
affected
 Subcutaneous inflammatory
nodule develop at the site of
entry, Chagoma
 If entry through conjuctiva-
unilateral, painless, oedema
and conjuctivitis- Romana`s
sign
Ocular (Romana sign)
 Acute and chronic form
 Acute form in children
 Fever, generalised oedema and patient dies of
acute myocarditis and meningoencephalitis
 Chronic form in adults and cardiac symptoms
are more
 Lab diagnosis-
 Blood
 CSF
 Aspirate from chagoma
 Tissue specimens
 Microscopy- trypomastigotes in blood
 Culture on NNN medium
 Antigen detection in urine and sera in chronic
form
 PCR
C-shape
 Animal inoculation- I/P in mice,
trypomastigotes appear in blood
 Serology- antibodies detected by ELISA, CFT,
IHA, IFAT, Card agglutination test
 I/D test  the extract of T.cruzi culture CRUZIN
 Biopsy  LN or tissues show amastigote form
 Treatment and prevention- Nifurtimox and
benznidazole
Control
1. Construction of concrete houses.
2. Use DDT.
3. No antigenic variation
4. Development of vaccine for chagas
disease.
Differential features of T.cruzi & T. rangeli
Characteristics T. cruzi T. rangeli
Illness Symptomatic(pathogenic) Asymptomatic(non-pathogenic)
Vector Reduviid bug Reduviid bug
Primary reservoir Oppoums, dogs,cats, wild
rodents
Wild rodents
Diagnostic stage
(blood)
Trypomastigote Trypomastigote
Tissue Amastigote None
Trypomastigote 15- 20um Avg. 30um
Shape C or U shaped None
Recommended
specimen
Blood,lymph node
aspirate, chagoma
Blood but parasites are rarely
recovered
THANK YOU

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BALAJI SOMA

trypanosomiasis-sleepin sickness & chagas dise

  • 2. Introduction The name is derived from Greek word, Trypano means (borer) Soma means (body) They are unicellular flagellate protozoa. Have corkscrew like motion. transmitted by a vector. Tsetse fly Reduviid (Triatomine) bug
  • 3. Trypanosoma (Trypanes- to bore, Soma- body) Trypanosoma species infecting human:- Parasite Vector Disease 1 T. brucei Tsetse fly African Trypanosomiasis ( sleeping sickness) T. brucei gambiense T. brucei rhodesiense T. brucei brucei Not infective to human. 2 T. cruzi Triatomid bug American Trypanosomiasis ( Chagas disease) 3 T. rangeli Triatomid bug Non pathogenic ( in south America)
  • 4. African sleeping sickness Trypanosoma brucei gambiense: West and Central Africa, mainly human infection Trypanosoma brucei rhodesiense: East Africa, wild and domestic animal reservoirs
  • 5. Trypanosome forms Epimastigotes: flagellum anterior to the nucleus. Present in the insect vector. T. brucei and T. cruzi Trypomastigotes: 15-80 m single flagellum posterior to the nucleus. Found in the mammalian host in the blood. Also as metacyclics in the insect vector. Undulating membrane. T. cruzi and T. brucei Promastigotes: short flagellum. No undulating membrane. Extracellular form in the insect vector. Leishmania parasites Amastigotes: short or no flagellum. Intracellular form in mammalian cells. T. cruzi and leishmania.
  • 6. Life cycle- Vertebrate host- man, domestic animals Invertebrate host- tsetse fly of genus Glossina (G.palpalis, G. fuscieps, G.tachinoides) Both male and female fly bite, usually early morning and evening Tsetse fly
  • 8. Pathogenicity- African trypanosomiasis or West African sleeping sickness Chronic in nature Chancre develops at the site of bite, hard, painful and fluid filled Trypomastigotes move through blood and lymphatic vessels Lymph nodes in posterior cervical region are involved- Winterbottom`s sign
  • 9. Pathogenesis of African Trypanosomiasis Tsetse fly bite Chancre resolve in 7-10 days Asymptomatic weeks months Blood Fever alternating with a febrile period Lymphatics CNS Involvment Death Cure Winterbottoms sign (posterior cervical lymphadenopathy) Leptomeningitis Keranders sign positive
  • 10. Pathology and clinical picture 1. Skin stage: chancre. 2. Haematolymphatic stage: generalized lymphadenopathy, anaemia, liver and kidney generalized organ involvement. 3. Central nervous system stage (CNS): Meningoencephalitis. (Development of the disease more rapid in Trypanosoma brucei rhodesiense)
  • 11. Lab Diagnosis- Blood, LN aspirate, CSF, sternal bone marrow, fluid from chancre M/E, culture and animal inoculation Trypomastigote forms are seen in largest number during febrile periods, so multiple daily blood samples Serology- IF, CFT, ELISA and card agglutination test
  • 12. Trypanosoma brucei rhodesiense East and central Africa When inoculated in to guinea pig, rat or mice- posterior nucleate forms are more common Reservoir host are mainly animals More virulent Trypomastigotes are more in blood East african sleeping sickness Acute form
  • 13. Febrile paroxysms are more Fever, oedema, weakness, rapid loss of weight, myocarditis Marked CNS symptoms are lacking or not much evident
  • 14. Treatment and prophylaxis- Suramin and pentamidine for primary stage Melarsoprol for CNS infection.
  • 15. TRYPANOSOMA CRUZI South American Trypanosomiasis (Chagas disease) Central and south America Carlos Chagas discovered the parasite Named T.Cruzi after his mentor Oswaldo Cruz Morphology Trypomastigote peripheral blood of humans and does not multiply in humans. C- shaped Amastigote- muscles of heart and skeletal system, neurological cells and RES. It is a multiplying form.
  • 16. Trypanosoma cruzi T. cruzi causes chagas disease Found in the vector reduviid bug & humans It is zoonosis May serve as reservoirs of infection Blood transfusion accounts for 5% cases
  • 17. Epidemiology Distribution- Central & South America. Reservoirs- Reduviid bug & animals (dogs, cats, armadillos, raccoons). Transmission- Invertebrate host : Reduviid bug. Blood Transfusion- Prominent in urban areas. Reduviid (Triatomine) bug
  • 20. Culture- NNN medium and epimastigote forms are seen Life cycle- two hosts Humans are definitive host Triatomine bugs or reduvid bug - intermediate host
  • 23. Infective form- metacyclic trypomastigote Discharge of infected faecal material near bite wound Infected faeces rubbed in to wound by bitten person Abraded skin, oral and nasal mucosa may also be infected Metacyclic trypomastigotes invades the RES Converted to amstigote, promastigote and than trypomastigotes
  • 24. Pathogenesis American trypanosomiasis or Chaga`s disease IP- 1-2 wks Due to multiplication of amastigotes and causes damage to cells and tissues Myocardium, skeletal muscles, neurological cells and RES are affected Subcutaneous inflammatory nodule develop at the site of entry, Chagoma If entry through conjuctiva- unilateral, painless, oedema and conjuctivitis- Romana`s sign Ocular (Romana sign)
  • 25. Acute and chronic form Acute form in children Fever, generalised oedema and patient dies of acute myocarditis and meningoencephalitis Chronic form in adults and cardiac symptoms are more
  • 26. Lab diagnosis- Blood CSF Aspirate from chagoma Tissue specimens Microscopy- trypomastigotes in blood Culture on NNN medium Antigen detection in urine and sera in chronic form PCR C-shape
  • 27. Animal inoculation- I/P in mice, trypomastigotes appear in blood Serology- antibodies detected by ELISA, CFT, IHA, IFAT, Card agglutination test I/D test the extract of T.cruzi culture CRUZIN Biopsy LN or tissues show amastigote form Treatment and prevention- Nifurtimox and benznidazole
  • 28. Control 1. Construction of concrete houses. 2. Use DDT. 3. No antigenic variation 4. Development of vaccine for chagas disease.
  • 29. Differential features of T.cruzi & T. rangeli Characteristics T. cruzi T. rangeli Illness Symptomatic(pathogenic) Asymptomatic(non-pathogenic) Vector Reduviid bug Reduviid bug Primary reservoir Oppoums, dogs,cats, wild rodents Wild rodents Diagnostic stage (blood) Trypomastigote Trypomastigote Tissue Amastigote None Trypomastigote 15- 20um Avg. 30um Shape C or U shaped None Recommended specimen Blood,lymph node aspirate, chagoma Blood but parasites are rarely recovered