TRYPANOSOMIASISTRYPANOSOMIASIS

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

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.

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

Morphology of Trypomastigotes Morphology of Trypomastigotes

Method of reproduction – binary longitudinal fission. Method of reproduction – binary longitudinal fission.

Classification of TrypanosomiasisClassification of TrypanosomiasisTwo British scientists (Forbe and Dutton) Two British scientists (Forbe and Dutton) discovered trypanosomes in 1901 in discovered trypanosomes in 1901 in Gambia 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 and Life cycle passes in to two hosts -rat and

rat flea rat flea Shriwastava et al. reported Trypanosome Shriwastava et al. reported Trypanosome

resembling T. Lewisi in peripheral blood resembling T. Lewisi in peripheral blood of 2 cases suffering from short febrile of 2 cases suffering from short febrile illness in Raipur M.P.illness in Raipur M.P.

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

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 BruceiBased 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

2) Human strain 2) Human strain 1)1) Gambian Gambian 2)2) RhodesianseRhodesianse3)3) Zambezi Zambezi Morphologically the strains are indistinguishable Morphologically the strains are indistinguishable Blood incubation infectivity test Blood incubation infectivity test

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.

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

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

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.

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.

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

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

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)

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 response trypomastigotes may be due to exaggerated immune response rather than any direct effect 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 immunoglobulins a) Producing large amount of nonspecific immunoglobulins b) By heavily infilltrating the site of infection with b) By heavily infilltrating the site of infection with macrophages. macrophages.

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

Clinical Features Clinical Features The disease occurs in The disease occurs in

two stages. Incubation two stages. Incubation period – 2-3 weeksperiod – 2-3 weeks1st stage1st stage Enlarged post Enlarged post

cervical L.N. cervical L.N. Winterbottom’s sign Winterbottom’s sign

Pruritus ,Transient Pruritus ,Transient edema edema

Papuloerythematous Papuloerythematous eruption eruption

Endocrine dysfunction Endocrine dysfunction Profound anaemia Profound anaemia

22ndnd Stage – Stage – HeadacheHeadacheImpaired motor functionImpaired motor functionSlurred 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.

T.B. RhodesienseT.B. Rhodesiense 11stst 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 22ndnd Stage Stage 1.1. Rapid progress to Rapid progress to

death.death.

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

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

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

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

Vectors and Life Cycle Vectors and Life Cycle

Hosts Hosts Vertebrate Vertebrate Insect – Bugs- Reduviidae family, subfamily- Insect – Bugs- Reduviidae family, subfamily-

Tritominae Tritominae

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 .

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 tissue Gross lesions mainly in heart, skeletal muscle and nervous 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, chronica)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 enlargement. Signs of cardiac muscle damage, edema, heart enlargement. Dilatation of tubular organs- Due to degeneration of intramural Dilatation of tubular organs- Due to degeneration of intramural autonomic nerve plexus. autonomic nerve plexus. Chaga’s Cardiomyopathy (10%) Chaga’s Cardiomyopathy (10%)

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 xenodiagnosis4) 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

11stst 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.

REFERENCESREFERENCES

Medical parasitology – Rajesh KaryakarteMedical parasitology – Rajesh KaryakartePaniker’s medical parasitologyPaniker’s medical parasitologyK.D Chatterjee’s human parasites & parasitic K.D Chatterjee’s human parasites & parasitic

diseasesdiseasesHarrison’s internal medicineHarrison’s internal medicineInternet Internet