1. 疟原虫 Plasmodium

4. Plasmodium (Malaria Parasite)
Species susceptible to human:
1.Plasmodium vivax(Pv):
Cause tertian malaria.
2.P.falciparum (Pf):
Cause malignant malaria.
3.P.malariae (Pm):
Cause quartan malaria.
4.P.ovale (Po):
Cause benign malaria.

5. Prevalence:
Malaria is the most important parasitic disease in the world.
300 million cases with one million deaths world wide in 1999;
30 million cases before liberation and cases reported with 39 death in 2000 in china;

6. Distribution of Malaria in the World

7. The vector – female mosquito

8. Life Cycle

10. Life Cycle

11. Life Cycle

12. Morphology & Life Cycle (Biology Features)
1.Asexual development(in human host):
(1)Exo-erythrocytic stage -EE forms (in liver cells),
Sporozoite(Tachysporozoite
& Bradysporozoite)-schizont-merozoites.
One generation results in numerous.

13. 红外期 exo-erythrocytic stage—merozoites in liver cells肝细胞内裂殖体

14. Morphology
Plasmodium is the one-cell parasite, so the basic morphology is a nucleus , cytoplasma and cell membrane
Wright or Giemsa stain gives the Cytoplasm – blue; nucleus - red , while the malarial pigments are yellow-brown
There are three stages and six main forms of plasmodium in RBC

15. P.vivax in RBC three stages and six main forms
滋养体期(trophozoites)：ring form and developing trophozoites
裂殖体期(schizonts)：immature and mature schizont-- merozoites
配子体期(gametocyte)： Microgametocytes and macrogametocytes

16. Ring form of P.v.

17. Amoeboid form of P.v.

18. Schizonts
Figs.： increasingly mature schizonts

19. Immature schisont of P.v.

20. merozoite
hemozoin
Mature schizont: nucleus divided into (16), cytoplasm divided,
each nucleus surrounded by a portion of cytoplasm to form merozoites,
hemozoin clumped

21. Female gametocyte of P.v
Oval in shape, light blue cytoplasm is abundant
compact nucleus, usually at edge of the parasite
scattered pigment granules
The gametocyte is completely filling its host cell

22. Male gametocyte of P.v Oval in shape, blue cytoplasm is abundant;
Loose and large nucleus (chromatin), central in position
Malarial pigments diffuse
Infected RBC enlarged and became pale with red Schüffner‘s  dots

23. Female gametocyte of P.v.

24. Male gametocyte of P.v.

27. P.falciparum ring form

28. P.f ring form Fine ring , smaller,about 1/5 of RBC diameter,
Usually multiple infection
1-2 small nucleus
Infected RBC is normal,almost no change

29. P.f. macrogametocyte
Compact nucleus, red, usually at the center of the cell
Malarial pigments around the nucleus
The crescent-shaped gametocytes of P. falciparum are very distinctive, but tend to only appear late in the infection

30. Pf. microgametocyte Large, diffuse nucleus at the center
Sometimes hard to distinguish from the female gametocytes
Sausage-shaped with two blunt end

31. P.f.

32. The Features of Erythrocytic Stage:
a. Repeated generation.
b. Synchronous development.
c. Definite time duration:
Pv 48h; Pf 36h-48.
d. The stage responsible
for pathogenesis.

33. Male gametes

34. ookinetes

35. Oocysts

36. Oocysts of P. falciparum in midgut of an infected mosquito
Oocysts of P. falciparum in midgut of an infected mosquito. Oocysts appear as circular bodies. Fresh preparation. ×100. Enlarged by 5.4.

37. Sporozoites

38. Malarial paroxysm (疟疾发作)
An attack occurs because of the sudden liberation of merozoites, malarial pigment and RBC debris into the blood stream.

39. Clinical features Pathogenesis Typical malaria paroxysm
symptom for erythrocytic phase
shaking chill （寒战） followed by fever （高热） (2-20 hrs)
RBCs rupture releasing merozoites, malarial metabolites, endotoxin in blood, the pyrogens
profuse sweating when fever breaks （出汗退热）
repeated characteristic cycle for each species

40. Scanning electron micrograph of Plasmodium-infected red blood cells
Scanning electron micrograph of Plasmodium-infected red blood cells. One cell has burst open, releasing merozoites

41. Recrudescence(再燃)
It is a recurrence of symptoms in a patient whose blood stream infection has previously been at such a low level as not to be clinically demonstrable or cause symptoms.

42. Relapse(复发)
It is a recurrence that taken place after complete initial clearing of the erythrocytic infection and implies reinvation of the blood stream by merozoites from activated hypnozoites in liver.

43. Complications Anemia Splenomegaly Malarious nephrosis
Hemolysis of infected erythrocytes
Hypersplenism
Autoimmunization of uninfected erythrocytes
supression of blood production in marrow
Splenomegaly
Malarious nephrosis
fatal malaria-cerebral malaria caused by P.f. (small vessels are plugged)

44. typical splenomegaly syndrome

45. Cerebral malaria

46. Diagnosis
Travel history to endemic area & presence of symptoms, e.g., fever and chills
Etiological- Microscopic examination of blood
Thin and Thick film (Giemsa's stain)
To master the morphology of parasites and changes of infected red cells
Immune probe-Species McAb based assays.
DNA probes- hybridization

47. 实验诊断 Laboratory diagnosis
1．病原检查
（1）Thin film Thick film
Question: Which stages are there in the blood film of P.v. or P.f. ?

48. Epidemiology Distribution: Africa, Asia, Latin America Endemic factors
(1)Source of infection: Patients and carriers.
(2)Vector host: mosquito
(3)Susceptible population
(4) resistance of plasmodium to antimalarial drugs.
(5) Other transmission mode: by transfusion, congenital transmission

49. Treatment Antimalarial drugs: (1)Anti-attack drugs: Kill
E-forms-Quinine,Chloroquine.
(2)Anti-recurrence drugs:
Kill EE-forms-Primaquine.
(3)Chemoprophylaxis:
Kill sporozoite & EE-forms with long shelf life-pyrimethamine 乙胺嘧啶.
affect parasite in different ways depending on stage when administered
emergence of drug-resistant malaria

50. Prevention and control
Control of the source of infection by chemotherapy
Prevention: breaking the human-mosquito-human cycle
mosquito control or eradication - not easy
Personal protection- netting, repellents, etc. avoidance of infected mosquitoes (bed nets , mosquito repellents)

51. Insecticide impregnated bednet
Permethrinn合成除虫菊脂treated, a synthetic pyrethroid除虫菊素类,合成除虫菊酯, ~ 200 mg/sq m.