trypanosomiasis-sleepin sickness & chagas dise
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Jun 25, 2024
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About This Presentation
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.
Trypanosoma brucei gambiense: West and Central Africa, mainly human infection
Trypanosoma brucei rhodesiense: East Africa, wild ...
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.
Trypanosoma brucei gambiense: West and Central Africa, mainly human infection
Trypanosoma brucei rhodesiense: East Africa, wild and domestic animal reservoirs
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
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 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
Size: 2.5 MB
Language: en
Added: Jun 25, 2024
Slides: 30 pages
Slide Content
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 Winterbottom’s sign (posterior cervical lymphadenopathy ) Leptomeningitis Kerander’s sign positive
Pathology and clinical picture Skin stage : chancre. Haematolymphatic stage : generalized lymphadenopathy , anaemia , liver and kidney generalized organ involvement. 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
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
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 Construction of concrete houses. Use DDT. No antigenic variation 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