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Parasite Plymorphic Trypanosomes=

Trypanosoma gambiense + Trypanosoma rhodesiense

Disease African trypanosomiasis =Sleeping sickness

West African trypanosomiasis =Gambian trypanosomiasis

Geographical sub-Saharan Africa)


distribution Trypanosoma gambiense
West and central Africa (river sides)

Morphology Trypomastigote :in man blood, lymph, CSF, tissue spaces of the RES,
endocrine system, CNS
Plymorphic: Found between RBCs in 3 forms (long , sort , intermediate )
Epimastigote: Vector( salivary G) +culture
Life cycle Alternates Between: Vector = glossina spp. (Tsetse flies) and MAN & R.H
͵ Biological transmission
͵ Anterior station development

Habitat Extracellular (blood, lymph, CNS)

Defen. H man
Vector Glossina spp. (Tsetse flies)
Intermediate Metacyclic trypomastegote
H
Infective metacyclic trypomastigote.
Stage:
Mode infect, Bite of infected glossina inoculating Metacyclic
trypomastegote, blood transfusion
Diagnostic S Trypomastigote & epimastigote

Pathogenic S trypomastigotes
Pathogenesis
Acute (early) stage
A- Skin lesions At the site of bite Multiplying trypomastigotesinflammatory
(Chancre): cellular infiltrate Skin lesions (Trypanosomal Chancre)
B- hemolymphatic ParasitaemiaThen the parasite escape the immune system through
stage 'Antigenic Variation‘ of surface antigens  fluctuating Parasitaemia
& progressive Toxaemia.
CP:
- General effects:
Fever 'fluctuating' Anorexia, headache, malaise Rash, Myalgias,
arthralgias
- Organs (RES mainly)
Splenomegaly Hepatomegaly Lymphadenopathy =Winterbottom’s Sign
Enlargement of LN of the posterior triangle of the neck, Anaemia.
C- Perivascular — Multiplication in the perivascular tissue spaces of variuos organs
tissue spaces: Slowly Progressive Pathological Lesions Heamorrage, edema &
effusion.
— CP: Facial edema. Pleural effusion ,Pulmonary edema, Pericardial
effusion ,Edema.

— Chronic stage: CNS stage: occurs at the end of the 1st year and takes several years in
duration
—
Pathogenesis — Trypomastigotes  cross the blood Brain Barrier, invade the CNS and
multiply causing perivascular lymphatic infiltration of cerebral
vesselsGeneralised meningoencephalitis Prostaglandin D2 & kinin
Increased somnolence
Clinical picture — Headache,Apathy , fatigability,Confusion
— Motor changes (slurred speech),Sensory changesMood changes
— Kerandel’s sign(Pressure on the palm or over the ulnar nerve then
releasing pressure causes severe pain)
— Terminal Stage
͵ Permanent Sleep
͵ 2ry Bacterial Infection
͵ Coma & Death ( from disease or bacteria )
—
Complications ͵ Intercurrent infections
͵ Heart failure
͵ Endocrinology : amenorrhea, impotence
—
Diagnosis 1)-Clinical picture: history of residence or travelling to endemic areas
2)-Laboratory
Direct parasitological:
Specimen is taken from:
͵ Blood (the best) = Anemia , Thrombocytopenia
— Hypergammaglobulinemia ,Elevated serum IgM level
͵ Chancre aspirate.
͵ Lymph node aspirate.
͵ BM
͵ C.S.F. = Trypomastigotes IgM in CSF is diagnostic
— Increased protein level, Increased WBCs
— Sediment shows: lymphocytes and morula cells 
Examined by:
— Smear (Polymorphic Trypomastigotes)
— Culture on N.N.N. (Epimastigote)
— Animal inoculation (Polymorphic Trypomastigotes)
Indirect methods
 Seological tests (CATT)=card agglutination test for trypanosomes
 Serum IgM

Treatment EARLY ͵ Suramin


stage ͵ Pentamidine

LATE ͵ Tryparsamide : the drug of choice


stage ͵ Melarsoprol
East African trypanosomiasis
Forest (Savannas), bush
Rh: wild game animals
Vector: Glossina mrositans

More parasites in blood


Acute course (CNS invasion early but death
before the full development of
meningeoencephalitic stage=sleeping
sickness stage

Sleeping sickness is rare

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