Trypanosomiasis

1. Trypanosomiasis Lecture with Dr. Balsam Mahdi Nasir MBBS/YEAR1/SEM2/2012

2. African trypanosomiasis (sleeping sickness) • Definition: • It is a vector-borne disease. • Endemic to sub-Saharan Africa. • It is caused by the single cell flagellate protozoan Trypanosoma brucei. • Geographic distribution: • Trypanasoma brucei gambiense(West African sleeping sickness or Gambian trypanasomiasis). • Trypanasoma brucei rhodesiense(East African sleeping sickness or Rhodesian trypanosomiasis). Dr. Balsam

3. Geographic distribution Dr. Balsam

4. Mode of transmission • Via the bite of an infected tsetse fly. Dr. Balsam

5. Morphology • In the vertebrate it exists as a TRYPOMASTIGOTE. • Elongated rather flattened. • Spindle shaped organism. • Blunted posterior end. • Finely pointed anterior end. • Central large oval nucleus. • Kinetoplast is small and is situated at the posterior end. • Undulating membrane. • Flagellum. Dr. Balsam

6. Blood forms 1. Trypomastigote (long slender)→ dividing form. 2.Trypomastigotes (short broad stumpy form with or without attenuated flagellum)→ non dividing form → infective to tsetse fly. 3. Intermediate form. Dr. Balsam

7. Tsetse fly procyclic trypomastigote Metacyclic trypomastigote Epimastigote Infective stage to human Human Trypomastigotes Long slender form Short stumpy form Intermediate form Infective stage to tsetse fly

8. Life cycle 8 Dr. Balsam 12/20/2019

9. Life cycle • Definitive host • Man, game and domestic animals. • Intermediate host • Tsetse fly (both male & female flies) • Reservoir of infection • Man (Trypanosoma brucei gambiense)→West African trypanosomiasis. • Animals (Trypanosoma brucei rhodesience)→ East African trypanosomiasis. • Infective stage to man • Metacyclic trypomastigotes Dr. Balsam

10. Pathogenesis and symptomatologyGambian disease Bite of infected tsetse fly • Inoculation of trypomastigotes. • Subcutaneous nodules→ 5-15 days → painless chancre→ resolve in 2-3 weeks. Incubation period • Asymptomatic • several weeks to months up to a year. Stage 1Blood dissemination • Intermittent fever pattern, chills, headache, myalgia, arthralgia..etc Stage 1Lymphatics • Lymphadenopathy, especially in the posterior cervical nodes (on the back of the neck) →Winterbottom’ssign. Stage 2 CNS invasion • Occur at the end of 1st year or the beginning of the 2ndyear • Daytime sleeping, mental dullness, apathy, tremors, convulsions and coma followed by death from asthenia during the 2nd or 3rd year. Dr. Balsam

11. Winterbottoms sign CDC  DPDx Parasite Image Library Dr. Balsam

12. RHODESIAN SLEEPING SICKNESSclinical features Dr. Balsam

13. Dr. Balsam

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15. Diagnosis • Clinical • Patient from endemic area, irregular fever, palpable lymph nodes (post. cervical). • Chronic disease with somnolence, personality changes and neurological symptoms. • Laboratory • Direct microscopy of a wet smear of unstained blood or Geimsa-stained thick smear→ trypmastigote. • Chancre, lymph node, bone marrow and CSF aspirate→ wet preparation. • Culture methods • The standard serologic assay to diagnose West African trypanosomiasis is the card agglutination test for trypanosomiasis (CATT). • Serological tests ELISA. Dr. Balsam

16. Trypanosomabrucei Dr. Balsam

17. Dr. Balsam

18. TREATMENT Dr. Balsam

19. PREVENTION AND CONTROL • Elimination of the reservoir: • Early Diagnosis and Treatment to reduce the reservoir of infection. • Breaking the channel of transmission: • Vector control. • Protection of susceptible: • Persons visiting endemic areas should wear protective clothing and apply repellents. Dr. Balsam

20. Chagas’ disease American trypanosomiasis • Definition • It is a vector-borne disease • It is prevalent throughout South and Central America • It is caused by the flagellate protozoan Trypanosoma cruzi. Dr. Balsam

21. Geographic distribution Dr. Balsam

22. Mode of transmission • Contamination of wound site, conjunctiva, or mucosa by infected feces of insect (reduviid bugs) Dr. Balsam

23. Morphology • Trypomastigote • The same as Trypanosoma brucei. • Long thin form • Short stumpy form • In blood film they appear C or U or S shape. • Amastigote form • Oval bodies. • Nucleus. • Kinetoplast. • Habitat: Striated muscle in heart, skeletal, neurological cells and cells of reticuloendothelial system. Blood Tissue Dr. Balsam

24. Morphology Dr. Balsam

25. Trypomastigote Epimastigote Metacyclictrypomastigote Reduviid bug Human Trypomastigote Amastigote Trypomastigote Dr. Balsam

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27. Life cycle • Definitive host • Man, wild and domestic animals. • Intermediate host • Triatomine bugs (reduviid bugs) • Reservoir of infection • Besides humans, the parasite infects a variety of wild and domestic animals. • Infective stage to man • Metacyclic trypomastigotes Dr. Balsam

28. Clinical features • Acute • In less than 50% of people bitten by a triatomine bug, characteristic first visible signs can be a skin lesion (chagoma ) or a purplish swelling of the lids of one eye (Romana sign) • After 1-2 weeks→ fever, headache, malaise, muscle pain, generalized lymphadenopathy and hepatosplenomegally. • Cardiac abnormalities followed by meningoencephalitis. • Chronic • The parasites are hidden mainly in the heart and digestive tract muscle. • Up to 30% of patients suffer from cardiac disorders. • Up to 10% suffer from digestive (megaesophagus or megacolon), neurological or mixed alterations. • In later years the infection can lead to sudden death or heart failure caused by progressive destruction of the heart muscle.

29. Romana sign Dr. Balsam

30. Megacolon in patient with Chagas disease Dr. Balsam

31. Diagnosis • Clinical may be suspected when general, cardiac or GIT symptoms are present in patients lived under low SES in endemic regions. • Laboratory • Demonstration of the parasitic agent is the diagnostic procedure in acute Chagas'' disease. 1.Microscopic examination • of fresh anticoagulated blood for detecting motile trypanosomes. • of thin and thick blood smears stained with Giemsa for identification of parasites. Dr. Balsam

32. Trypanosomacruziamastigotes in heart tissue Trypanosomacruzitrypomastigote in a thin blood smear stained with Giemsa Dr. Balsam

33. Laboratory diagnosis 2. If the parasites are scanty in blood • Culture of the blood or suspected tissue specimen. • xenodiagnosis, where clean lab-reared reduviid bugs are fed on the patient's blood, and their gut contents examined for parasites 4 weeks later. • Demonstration of antibodies to T. cruzi are required to diagnose chronic Chagas disease by serology –complement-fixation, direct agglutination and indirect haemagglutinatin and ELISA.

34. Treatment • Nitrofurans and benzidazoles have been used in acute disease. • Neither drug is expected to cure established chronic disease. • It is unsatisfactory since the organisms are within cells in established infections. Dr. Balsam

35. Prevention and control • Elimination of reservoirs: • Control and elimination of domestic and peridomestic animals. • Early diagnosis and treatment of infected cases. • Vector control: • Triatomine bugs are highly susceptible to chlorinated hydrocarbon insecticides which form the major weapon for their control. • Protection of susceptible: • Provision of better housing would prevent transmission because most human infections are transmitted by bugs living in cracks and crannies in the walls of ill kept tenement dwellings. Dr. Balsam