1. HEMOFLAGELLATES WINIFREDA U. DE LEON ASMPH YL6

2. HEMOFLAGELLATES BLOOD AND TISSUES TRYPANOSOMA LEISHMANIA ARTHROPOD BORNE KINETOPLASTIDA- differ from other protozoan because they provide with DNA in their nuclues EXTRA NUCLEAR DNA KINETOPLAST

3. STAGES OF DEVELOPMENT CURRENT OLD AMASTIGOTE - LEISHMANIA PROMASTIGOTE LEPTOMONAD EPIMASTIGOTE CRITHIDIA TRYPOMASTIGOTETRYPANOSOME

4. STAGES OF DEVELOPMENT

5. audio Amastigote stage: –Different because they are providedof Kinetoplast which is composed axonem, blepharoplast, and para basal body –Intracellular in location –Most of the time invade the cells of reticuloendothelial system –These amastigote multiply and Continue to multiply until the cell is filled by amastigote –Amastigote will be released once the host cell is filled up with the stage of development and will eventually released amastigote into the circulation –The amastigote is supposed to develop and become promastigote Promastigote stage –From promastigote there is epimastigote stage which is an elongated organism with nucleus and kinetoplast –In this stage: –Epimastigote differs in the sense promastigote stage that it does not carry the undulating membrane Epimastigote stage –From the epimastigote it willbecome trypomastigote, there is nucleus and flagellum –Longer undulating membrane How does trypomastigote differes: -Very long undulating membrane connected to the kinetoplast -The kinetoplast moved posterior to the nucleus in this stage

6. TRYPANOSOMA CRUZI- SOUTH AMERICA

7. Audio Tryponosoma cruzi –Prevalence in human has infection rate of 7/100 people

8. TRYPANOSOMA CRUZI

9. VECTOR REDUVIID BUGS 3 genera identified: TRIATOMA PANSTRONGYLUS RHODNIUS Common names: -KISSING BUG- habit of biting in the face mainly near the mouth -ASSASIN BUG- neck -CONE NOSED BUG- latest board exam for pharmacy Are these bugs exclusive to south america ?No -Bed bugs localy; but are smaller -Causes nuisance bites on humans and causes allergic reaction due to sensitivity to the bite of these bugs -Amastigote stage are found on the tissues of the patient -If the cell ruptures trypamastigotes develops -Animal reservoir: epimastigote develops until they become metacyclic trypomastigotes  infective stage -Infective stage passed out with the feces due to metacyclic trypanosomes’ posterior method of development -Bad habit: biting while defecating

10. VECTOR

11. LIFE CYCLE

12. If it is cruzi or Chagas disesase by dr carlos chagas Amastigotes are found inside the cell and when the host cells burst that is when they are releases and developed into trypomastigote stage Palpebral edema- romana sign Both young and old populatios are equally affected

14. ROMANA SIGN

15. MAIN PATHOLOGY DECREASES NERVE GANGLIA- supplying HOLLOW ORGANS when it relaxed it causesENLARGEMENT  MEGA DISEASE There is involvement of: ESOPHAGUS INTESTINES HEART

16. MEGA- ESOPHAGUS

17. PATHOLOGY

18. Enlarged intestines Cardiomegaly- in chronic chagas disease –Enlargement of the ventricles –Apical aneurysm is pathognomonic of chagas involving the heart

19. HEART IN CHAGAS DISEASE

20. DIAGNOSIS BLOOD, LYMPH FLUID, BUFFY COAT TRYPOMASTIGOTES C OR S SHAPED PROMINENT KINETOPLAST Characteristic feature: prominent kinetoplast

21. TISSUES - AMASTIGOTES

22. A heart muscle filled up with amastigotes Audio for next slide: –They have to be fed with patients blood –In africa, when there is high susp[icion, bug will be fed with patients blood and after 3 weeks, bugs will be dissected.

23. DIAGNOSIS CULTURE- jews doctor Dr warman who cul;tures organism in the philippines XENODIAGNOSIS- animal inoculation test PATIENT’S BLOOD BUG METACYCLIC TRYPANOSOMES (INFECTIVE STAGE)

24. CONTROL/ PREVENTION TREATMENT NIFURTIMOX BENZNIDAZOLE PREVENTION PROPER BLOOD DONOR SCREENING BETTER HOUSING

25. HOUSING CONDITION

26. AFRICAN TRYPANOSOMES TRYPANOSOMA BRUCEI COMPLEX 3 species: T. b. BRUCEI- non pathogenic 8in humans, only in animals  NAGANA CAUSATIVE: SLEEPING SICKNESS T. b. RHODESIENSE T. b. GAMBIENSE

27. RHODISIENCE- occur only in mid-eastern part of africa Gambiense- western hemisphere Derived where they were identified Rhodiseince-rapid and fatal Gambiense- chronic form Few cases now identified

28. OCCURENCE TRYPANOSOMA RHODESIENSE MID EASTERN AFRICA RAPID FATAL FORM TRYPANOSOMA GAMBIENSE WESTERN HEMISPHERE CHRONIC

31. OCCURENCE FLY BELT TSE TSE FLIES ( GLOSSINA) -Fly belt of africa -African tryponosomiasis occur -No amastigote stage -Only trypomastigotes- pleomorphic

32. What they found are that trypomastigotes are pleomorphic: –Some are short, some are long, static when recovered from patient –Infective stage: metacyclic trypomastigote –Have anterior stage of development: salivary gland –Introduced when they bite the host

33. LIFE CYCLE

35. PATHOLOGY WINTERBOTTOM’S SIGN KERANDEL’S SIGN PROGRESSIVE CNS INVOLVEMENT SOMNOLENT APATHETIC COMA

36. Winterbottom sign- At the site of the bite there could also be lesion There is a delayed response to pain- kerandel’s sign Progressive CNS involvement and detected by doctor when the patient becomes somnolent, they are apathetic  coma  death

37. SITE OF TSE TSE BITE

38. Site of Tse tse fly Site of the bite  toxic products by the tsetse fly Increasing involvement of the CNS They can fall asleep in the street while walking Medical movie: while patients are dining they could simply fall asleep  the patient was already in deep coma

39. Immune evasion There are spikes which correspond sto fever, acts when glycoproteins are released, numbered 1, 2, 3. Actually there are hundred released Hypergammaglobulinemia Another surface glycoproteind will be in circulation Even the patient have high titer of Ab, stil its not protective When antigen have different codes, The parasites are able to hide sndevade from the protective nature of the antibodies

41. PATHOLOGY

44. IMMUNE EVASION – VARIANT SURFACE GLYCOPROTEIN

45. Immune evasion There are spikes which correspond to fever, acts when glycoproteins are released, numbered 1, 2, 3. Actually there are hundred different glycoproteins when they released in circulation Hypergammaglobulinemia When there are released, Another surface glycoprotein will be in circulation Even the patient have high titer of Antibody, still it’s not protective When antigen have different codes, even antibodies developed they are not protective The parasites are able to hide and evade from the protective nature of the antibodies

47. In Africa they believe they thought they actually decreased the number of cases but in this figure, 1999, re-emergenvce  environmental changes worldwide

48. DIAGNOSIS BLOOD, LYMPH FLUID, BUFFY COAT CSF only the trypomastigotes SEROLOGY - CATT Card agglutination test for trypanosomiasis- rapid dx’c procedure to identify the condition Lumbar tap- should be in strict aseptic technique

49. TRYPOMASTIGOTES- pleomorphic (short, long, or longitudinal)

50. TREATMENT PENTAMIDINE- first line of drug MELARSOPROL EFLORNITHINE- widely use now in africa

51. LEISHMANIA L. TROPICASKIN CUTANEOUS ORIENTAL SORE L. BRAZILIENSESKIN/ MUCOUS MEMBRANE MUCO-CUTANEOUS ESPUNDIA L. DONOVANIVISCERAL ORGANS LIVER/ SPLEEN KALA AZAR

52. Leishmania 3 species –L. tropica Affects only the skin Cutaneous leishmaniasis Oriental sore in India –Braziliense Skin/mucous membrane Initially not only the mouth also, ears, nose –Donovani Viceral leishmaniasis Liver and spleen

53. VECTOR SANDFLIES- under phlebotomous species -In Phil there are about a hundred species of phlebotomous flies PHLEBOTOMINE FLIES

54. TERMITE HILLS

55. Vector –Sandflies Phlebotomous In Phil there are about a hundred species of phlebotomous flies –Termite hills Host –Rats –There are rat holes under the termite hills Other hosts –Canid families –Not only humans are infected but also the family canidae –Infected individual has amastigotes in tissues—they are found Inside the macrophages, once it is filled it will bvurst and release amastigotes –When sandflies bite the patoient, it will get the promastigote  promastigote 2 stages Promastigote in sandflies Promastigote in patient

56. Is it only acquired thru bite of cutaneous leishmaniasis? Mechanical vectors may transmit parasite to other Our overseas Filipino workers are going to these countries where Leishmaniasis are rampant Cutaneous lesion- weeping lesions These are typical lesions and dermatologist are not yet so much familiar from these lesions

57. HOSTS

58. OTHER HOSTS FOX JACKAL WOLVES DOGS

60. LEISHMANIASIS AFRICA CHINA SOUTHERN EUROPE SOUTH AMERICA Brazil/ Honduras MIDDLE EAST

61. SITE OF BITE

62. CUTANEOUS

63. CUTANEOUS LESIONS

64. Muco-cutaneous –Not only the mouth but also the nose –Highly disfiguring Visceral leismani Kala-azar: hepatosplenomegaly –Post kala-azar –Post kala-azar dermal lesion Amastigotes onside the lesion Initially diagnosed as leprosy When pricked the lesion found to have amastigotes of leishmania Histoplasma are also occupying macrophages

65. MUCO-CUTANEOUS

66. VISCERAL

67. POST KALA AZAR

68. DIAGNOSIS NEEDLE ASPIRATION SMEAR – GIEMSA CULTURE Novey MCNeal Nicolle LEISHMANIN SKIN TEST

69. TREATMENT ANTIMONY COMPOUNDS STIBOGLUCONATE AMPHOTERICIN B GLUCANTINE PENTAMIDINE MILTEFOSINE CRYOTHERAPY

70. Diagnosis Smear stained with giemssa Cultuire What is the choice of culture medium for leishmania –Novey, mcneal, Nicole NMN Leishmanin skin test Treatment Antimony compounds Amphotericin B: Glucatine Arytherapy- like cold compress—freeze and kill the organisdm

71. PUBLIC HEALTH CONCERNS HEAVY INTERNATIONAL TRAFFIC OFWS PHILIPPINE SPECIES OF PHLEBOTOMINES PHILIPPINE SPECIES OF REDUVIID BUGS POSSIBILITY OF LOCAL TRANSMISSION??

72. Public health concerns Everybody are going out of the country, however, t may also be good to find out that majority of Flipino csn be found to the contries where these [parasoites are endemic—thay can be infected Phlebotomins- vectrors of leishmania American t: reduvid bugs

73. FINGER PRICK BLOOD SAMPLE

75. THIN BLOOD FILMS

76. audio –Select the finger to puncture (usually the third or fourth finger) (Maam prefers the ring finger) –Puncture the side of the ball of the finger. Do not make the puncture too close to the nail bed. If the blood does not well up immediately, put pressure. Normally, it should well up immediately. Not too much since it will be plasma. –Touch the blood with the slide – THIS IS VERY IMPORTANT. –To conserve glass slides, prepare thick and thin smears on the same slide. –For thin blood film, hold another slide about 30 degrees on the blood drop. Gently press then push to the other side of the slide. –Thick smear – for rapid diagnosis –Thin smear – to know the species of the filarial; usually the hemoglobin is removed first but this is already not the concern of the doctor.

77. BLOOD SMEARS THICK/ THIN

78. AFTER STAINING

80. THANK YOU AND GOOD DAY

81. THANK YOU