trypanosoma

Trypanosoma

IntroductionIntroduction

1- Extracellular in BLOOD & TISSUES2- West African Trypanosomiasis: West African Trypanosomiasis: “ West African Sleeping Sickness” caused by T. brucei gambiense.

3- East African Trypanosomiasis: East African Trypanosomiasis: “ East African Sleeping Sickness” caused by T. brucei rhodesiense.

4- Chronic form: Chronic form: caused by T. brucei gambiense. While Acute Form Acute Form is caused by T. brucei rhodesiense.

5- African Sleeping SicknessAfrican Sleeping Sickness is the 3rd important parasitic disease globally after Malaria & Schistosomiasis

6- West African Sleeping SicknessWest African Sleeping Sickness is in regions along riverside while East African Sleeping Sickness East African Sleeping Sickness is in Forest regions (Savannas).

Dr. RAAFAT T. MOHAMED

Trypanosoma

Trypanosomiasis

American Trypanosomiasis

East African Trypanosomiasis

Transmitted byTransmitted by

Causes

T.brucei rhodesienseT.brucei gambiense T.cruzi

Sleeping sickness Chagas’ disease

West African Trypanosomiasis

Glossina (tsetse fly) Triatoma (winged bug)


Trypanosoma

Morphology

Exist into 2 interchangeable forms:

TrypomastigoteTrypomastigote in Blood/ Lymph / tissue space of various

organs& C.N.S is terminal & fatal EpimastigoteEpimastigote in salivary gland of vector & Culture media.

TrypomastigoteTrypomastigote (Polymorphic Trypanosomes

Spindle shaped – Central nucleus – free flagellum – undulating membrane. 3 forms

1 -long Slender Form (30µ): active motile with free flagellum.

2 -Short stumpy Form (15µ): sluggish without free flagellum.

3 -Intermediate Form (20µ): with a short free flagellum.Dr. RAAFAT T. MOHAMED

Geographical Distribution of African Trypanosomiasis

G.palpalis G.morsitansIn West Africa In East Africa


Trypanosoma brucei causing Sleeping Sickness

West Africa East AfricaT.brucei gambiense T.brucei rhodesiense

Less plentiful More plentifulCannot live in lab animals Can live in lab animals

Reservoir host: goats, cattle & pigs

Reservoir host: wild game animals

Transmitted by: G.palpalis Transmitted by: G.morsitans

Nucleus is shifted posteriorly


Mechanism of disease transmission by Glossina

Bite of ♂ & ♀ Glossina

Trypomastigotes (polymorphic trypanosomes)

Diagnostic stage

12-42µ

Epimastigote

Full of short stumpy metacyclic

Trypomastigote

3 weeks

Infective stage

Biological transmission

Salivary gland


African Trypanosomiasis life cycleAfrican Trypanosomiasis life cycle

Life cycle of Trypanosoma brucei gambiense & T. b. rhodesiense



t-brucei-human-hostok.swf



T.Gambiensei (Tse tse).swf


severe headache, mental apathy, slow speech, deep sleep, coma & death

Pathogenesis and Clinical PictureIncubation period (2 weeks)Trypanosoma chancre (at the site of bite)

Via lymphatics: enlarged lymph nodes especially posterior cervical region.

Via blood stream: headache, fever(fluctuating), muscle & joint pain, irregular erythematous rash.Invasion of bone marrow

Enlarged liver & spleen, generalized weakness.

Invasion of CNS:

In East African Trypanosomiasis:Disease runs more rapid & fatal course

(Winterbottom’s sign)

(hypoplastic anaemia)


Winterbottom sign

Coma before death

Trypanosoma chancre

Emaciation على جلد

عظم

Pathogenesis and Clinical PicturePathogenesis and Clinical Picture


Clinical PictureClinical Picture

Progressive disease may lead to the following C.N.S manifestations:-

1- Insomnia أرق

2- Mood changes (dullness بالهة / apathy المباله)

3- Motor & Sensory Disorders: (Hyperesthesia الحس slurred / فرطspeech متداخل طبيعية abnormal gait / كالم غير .(مشيه

4 -Convulsions 5- Epilepsy الصرع داء

Terminal stage:1 -Permanent Sleep.

2 -2ry Bacterial infection.3 -Coma & Death.


Diagnosis

1- Clinical picture

2- Demonstration of trypanosomes:

- Microscopic examination of unstained or

stained blood films- Culture on suitable medium (N.N.N OR Weinmann’s media to detect Epimastigote)

- Animal inoculation

Polymorphic Trypanosomes

N.B. in case of T.brucei rhodesiense injected in labAnimal produce a new form “Posterior Nucleus Shift ”


DiagnosisDiagnosis

C.S.FC.S.F


Diagnosis

3- Serological test:Increased total IgM level in serum due to antigenic variationantigenic variation

of the surface coat of the parasite.

Trypanosome posses genes that code for about 1000 variant forms of their surface glycoproteins (SVG). Switch to a different variant produces a new generation not susceptible to attack by

immune factors specific to the previous generation.Trypanosomes can evade(تهرب) the immune system


مطرده Why in African Trypanosomiasis infection, thereزيادةis a sustained elevated IgM level???????

Trypanosoma cruzi causing Chagas’ disease

Triatoma or Rhodnius

Prominent kinetoplastKissing bugWinged bug

Trypanosoma cruzi

C-shaped


Trypanosoma cruziTrypanosoma cruzi

Morphology TrypomastigoteTrypomastigote (Monomorphic)

Slender shaped (20µ) – Central nucleus – C or U-shaped –Free flagellum 1/3 body-Large bulging peripheral kinetoplast

AmastigoteAmastigote

Obligatory intracellular – mainly in cardiac & Skeletal muscles – Brain meninges – Nerve ganglia – cells of GIT …. etc

Epimastigote Epimastigote (Vector only)

Spindle shape– Kinetoplast anterior to central nucleus– Undulating membrane is short – terminal free flagellum


Mechanism of disease transmission by winged bug T.cruzi in human blood

Epimastigote form

Short stumpy metacyclic

trypomastigote (infective stage)

Pass out with faeces

Cyclopropagative transmission

Alimentary canal of

bug


AMERICAN TRYPANOSOMIASISAMERICAN TRYPANOSOMIASIS

LIFE CYCLE OF Trypanosoma cruziDr. RAAFAT T. MOHAMED

Mode of infection

Contamination of skin abrasion ( بالجلد (خدوش

by winged bug faecesCone nose Bug – kissing Bug –Assassin bug

Mainly by

Rarely by

Through the placenta

Through infected mother’s milk

Through infected blood transfusion


Life cycle of Life cycle of Trypanosoma cruziTrypanosoma cruzi

t-cruzi-human-host (Man).swf


Life cycle of Life cycle of Trypanosoma cruziTrypanosoma cruzi

T.cruzi (in Tritoma).swf


To

Pathogenesis and Clinical Picture

I- Acute FormI- Acute FormChagomaChagoma occurs at the site of bite.Parasite reaches regional lymph nodes

Blood

Organs and tissuesTo

Fever, enlarged lymph nodes, skin rash, enlarged liver & spleen.

Meningoencephalitis, heart failure

Romana’s signRomana’s sign (Unilateral conjunctivitis appear suddenly

together with oedema of upper & lower eye lids & cheek)

Death or pass to Chronic formDr. RAAFAT T. MOHAMED

Pathogenesis and Clinical Picture

II- Chronic formII- Chronic formParasite produces antigens similar to

patient’s self antigens:

Heart muscle fibres:

Amastigote form of T.cruzi

congestive heart failure.

Oesophageal muscle fibres: البلع عصرmegaoesophagus and dysphagia.

Destruction of Auerbach’s plexus Colon muscle fibres:

megacolon and constipation.

CNS or thyroid glandExacerbation of infection in

immunosuppressed patients.

The body produces auto-antibodies that cause damage to:


Diagnosis

Finding the parasite in:

Blood film (C-shaped T.cruzi)

Biopsy from lymph node, liver or spleen (amastigotes)Culture (Epimastigotes)

Xenodiagnosis

Serological tests

Cruzin test (I.D.)

Molecular techniquesDr. RAAFAT T. MOHAMED

Diagnosis (Xenodiagnosis)Diagnosis (Xenodiagnosis)

Highly efficient – demonstrate low level of parasite in blood

Method:

A Laboratory bred winged bug is starved for 2 weeks then fed on suspected patient’s blood – 30 days later, it faeces & gut examined for trypanosomes.


DiagnosisDiagnosis

Romana’s sign

Chagoma

Trypomastigote

Amastigote

Winged Bug


Treatment

In early stage of the disease:

Pentamidine OR Suramin

In late stages of the disease:

Tryparsamide

For both early and late stages of the disease:

Eflornithine (DFMO) Ornidyl

Nifurtimox - inhibits intracellular

development .- Drug of choice in acute and

early chronic

OR

Primaquinedestroys Trypanosoma in blood

Sleeping Sickness Chagas Disease


Control

Treatment of patients

Control of vectors (Glossina)

Pentamidine as prophylactic drug

Treatment of patients

Control of vectors (Triatoma)

Elimination of reservoir hosts

Sleeping Sickness Chagas’ disease


M.C.Q.

a- Visceral leishmaniasis

b- African trypanosomiasis (sleeping sickness)

c- American trypanosomiasis (Chagas’ disease)

d- Non of the above

e- All of the above

Smear taken from the edge of oriental sore reveals:

Protozoal infections that may cause fever and hepatosplenomegaly

a- promastigote

b- epimastigote

c- amastigote

d- trypomastigote


M.C.Q.

Protozoa causing conjunctivitis include:

a- Trypanosoma cruzi

b- T.brucei gambiense

c- T.brucei rhodesiense

d- Leishmania donovani

Winterbottom’s sign is seen in:

d- American trypanosomiasis

c- African trypanosomiasis

b- Visceral leishmaniasisa- Cutaneous leishmaniasis


M.C.Q.

In African trypanosomiasis, the infective stage is found in:

a- Saliva of Triatoma c- Stool of Triatoma

b- Saliva of Glossina d- Stool of Glossina

Posterior nuclear shift occurs in:a- Trypanosoma cruzi

b- Trypanosoma gambiense

c- Trypanosoma rhodesiense

d- Trichomonas vaginalis

Short stumpy metacyclic trypanosomes


M.C.Q.

In chronic Chagas’ disease, the main lesions are in:

a- Digestive and respiratory tracts.

b- Heart and liver.

c- Heart and digestive tract.

d- Liver and spleen.

Megacolon associated with Chagas’ disease:

a- Is manifested by diarrhoea.

b- Occurs early in the disease.

c- Is due to oedema of the mucosa.

d- Is associated with constipation.


Compare betweenRomana’s sign Acanthamoeba affection

of the eyeInflammation of the conjunctiva Inflammation of the cornea

Occurs through corneal trauma

Exposure to contaminated water

Wearing contaminated contact lenses

Mode of infectionContamination of skin

abrasions by winged bug (Triatoma) faeces

Short stumpy metacyclic

trypanosomes

Ulceration

Perforation

Ocular pain & affection of vision


trypanosoma

Documents

east african sleeping

west african sleeping

brucei gambienset

brucei rhodesienset

mohamedtrypanosoma brucei

short free flagellum

short stumpy form

slender form