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![Definitive Host
•Female Anopheles
mosquito [sexual phase]
Intermediate Host
•Man [ asexual phase]](https://image.slidesharecdn.com/malaria-211002173958/85/Malaria-5-320.jpg)
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Malaria
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- 2. CASE • A 48year old male presented in the OPD with history of • High grade fever associated with chills • profuse sweating • headache.
- 3. Malaria • Causative agents: • Plasmodium vivax • Plasmodium falciparum • Plasmodium malariae • Plasmodium ovale
- 4. CLASSIFICATION Phylum : Apicomplexa. Class: Haematozoa. Order : Haemosporina Genus : Plasmodium
- 5. Definitive Host •Female Anopheles mosquito[sexual phase] Intermediate Host •Man [ asexual phase]
- 6. Mode of infection • throughbite of infected female anopheles mosquito (vector) Infective form • Sporozoites
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- 8. •Life Cycle ofPlasmodium Vivax
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- 11. Sporozoites which areelongated and spindle shaped become rounded in liver cells, undergo multiple nuclear division to form Schizont .
- 12. In 8-10 days,Merozoites are liberated
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- 15. Early trophozoite isformed
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- 19. The Mosquito Cycle: Sporogony
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- 22. The Human Cycle:Pre-erythrocytic Schizogony In 8 days Merozoites liberated per schizont are 10,000 in number. Some sporozoites go into dormant state, known as Hypnozoites,(clinical relapses)
- 23. (infect reticulocytes andyoung RBCs) Erythrocytic Schizogony (48 hrs) All stages of Erythrocytic Schizogony can be seen in the peripheral blood smear.
- 24. Erythrocytic Stages ofPlasmodium Vivax (12-24 merozoites per Schizont) Trophozoite Malaria pigment Female Male Schuffner's dots
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- 26. The Human Cycle:Pre-erythrocytic Schizogony In 6 days Merozoites liberated per schizont are 30,000 in number. No hypnozoites
- 27. (infect both youngand mature RBCs) (Late trophozoites, schizonts are formed in capillaries of internal organs, and not in peripheral blood) Gametogony after 10 days Female gametocyte Male gametocyte Multiple rings, accole form in normal sized RBCs
- 28. Erythrocytic Stages ofPlasmodium falciparum Trophozoite Malaria pigment Maurer's dots Male Female Gametocytes schizonts multiple rings accole form
- 29. Erythrocytic Stages ofPlasmodium falciparum Peripheral circulation Vascular beds of internal organs Trophozoite Gametocytes schizonts
- 31. Pathogenesis The clinical manifestationsin malaria are due to : • Response of host to parasitic antigens • Anaemia in malaria is due to increased clearance of both parasitized and non parasitized RBCs by the spleen. • Tissue hypoxia due to obstruction of blood flow
- 32. Capillaries of brain pluggedwith parasitized RBCs
- 33. Clinical Features Fever withchills & rigor Anaemia Spleenomegaly
- 34. Fever Sweating stage : 2– 4hours Hot stage : 2–6 hours Cold stage : 15–60 mins
- 35. Types of Malarial Fever Plasmodium vivax:Benign Tertian Plasmodium falciparum: Malignant Tertian Plasmodium malariae: Quartan Plasmodium ovale: Benign Tertian
- 36. Complications of FalciparumMalaria
- 37. 1.Pernicious malaria • Cerebralmalaria • Algid malaria • Septicemic malaria 2.Black water fever
- 38. Cerebral Malaria üP.falciparum incapillaries of internal organs, secrete protein knobs on surface of RBCs. üThis promotes aggregation of infected RBCs to non infected RBCs and capillary endothelial cells, causing capillary plugging in brain. üIt leads to anoxia, ischaemia and haemorrhage in brain. üManifested by headache, hyperpyrexia, coma, paralysis. Capillary plugging
- 39. Algid Malaria •Patient presentswith severe abdominal pain, vomiting, diarrhoea and profound shock. •This syndrome is characterized by peripheral circulatory failure, rapid thready pulse, low BP, cold clammy skin.
- 40. Septicemic Malaria It ischaracterized by high continuous fever with dissemination of the parasite to various organs, leading to multi organ failure. Death occurs in 80% of the cases.
- 41. Blackwater Fever •Seen infalciparum malaria patients on inadequate treatment with quinine. • Development of anti-erythrocyte antibodies. •Massive, sudden, intravascular hemolysis occurs. •characterized by massive absorption of hemoglobin by the renal tubules, leading to haemoglobinuria, excessive pigment in urine gives brown black colour to urine.
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- 43. Peripheral blood smear examination Antigendetection- By rapid immunochromatographic test QBC – Quantitative Buffy Coat Culture Molecular method
- 44. Peripheral blood smearexamination • For Microscopy ü thick and thin blood film. • Romanowsky stain i. Field’s stain ii. Giemsa stain iii. Leishman stain iv. Jaswant Singh and Bhattacharya (J.S.B) stain
- 46. • THICK FILM §Lysed RBCs, many layers § Larger volume (0.25 µl blood/100 fields) § Good screening test • THIN FILM § Single layer of RBCs § Small volume (0.005µl blood/100 fields) § Species differentiation
- 51. Rapid immunochromatography Testfor Antigen detection Histidine- rich protein II (HRP – II) : P. falciparum. Parasite lactate dehydrogenase (pLDH) Parasite aldolase: all Plasmodium spp.
- 55. Culture RPMI 1640 medium:- (RoswellPark Memorial Institute and 1640 denotes the number of passages). Dulbecco’s Modified Eagle Medium(DMEM)
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- 58. Treatment of vivaxmalaria (NVBDCP guideline) • Chloroquine : 25mg/kg divided over three days, i.e.10 mg/kg on day 1and 2 and 5 mg/kg on day 3 • Primaquine: 0.25 mg/kg daily for 14 days
- 59. Treatment of falciparum malaria(NVBDCP guideline,India) • ACT-SP (artesunate- sulfadoxine/pyrimethami ne) • Artesunate (25mg/kg) for 3 days • Sulfadoxine (25mg/kg)/ pyrimethamine(1.25mg/ kg), 1 tablet given on first day • Primaquine
- 60. Prevention • For adult: •Residual spraying: dichlorodiphenyltrichloroethane (DDT) and malathion. • Individual protection: bed nets and protective clothing
- 61. For larva • Larvicide-mineral oil or Paris green • Biological larvicide- Gumbusia affinis (fish) and Bacillus thuringensis (bacteria) • Source reduction ( to reduce the mosquito breeding sites) includes environmental sanitation, water management and improvement of the drainage system.
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