=plymorphic Trypanosomes Trypanosoma Gambiense + Trypanosoma Rhodesiense

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=Plymorphic Trypanosomes Trypanosoma gambiense + Trypanosoma rhodesiense

Disease

African trypanosomiasis =Sleeping sickness

West African trypanosomiasis =Gambian trypanosomiasis

Geographi cal distributio n

(sub-Saharan Africa

(West and central Africa (river sides

Morpholog y

Trypomastigote :in man blood, lymph, CSF, tissue spaces of the RES, endocrine system, CNS

Trypanosoma gambiense

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

Intermedi ate H

Metacyclic trypomastegote

Infective :Stage

.metacyclic trypomastigote

Mode ,infect

Bite of infected glossina inoculating Metacyclic trypomastegote, blood transfusion

Diagnosti

Trypomastigote & epimastigote

cS

Pathogen ic S

trypomastigotes Pathogenesis Acute (early) stage

A- Skin lesions :(Chancre) Bhemolymphat ic stage

At the site of bite Multiplying trypomastigotesinflammatory cellular infiltrate (Skin lesions (Trypanosomal Chancre ParasitaemiaThen the parasite escape the immune system through 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

CPerivascular tissue :spaces

Multiplication in the perivascular tissue spaces of— variuos organs 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͵ —

Complication s

Intercurrent infections͵ Heart failure͵ Endocrinology : amenorrhea, impotence͵ —

Diagnosis

Clinical picture: history of residence or travelling to-(1 endemic areas Laboratory-(2 :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

EAR LY stag e

LAT E stag e

Suramin͵ Pentamidine͵

Tryparsamide : the drug of choice͵ Melarsoprol ͵

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