1. Clinical features (fever) Cold stage: rigor (cold and shivers)
headache (half-1hour)
Fever (hot) stage:
temperature rises to maximum ,sever headache pain in back and joints vomiting and diarrhea (1-4h)
Sweating stage patient perspires temperature fall and patient relieved until the next rigor (1-4h).
Cold- hot- sweating - normal

2. Incubation period Primary attack Repeated attack Malarial paroxysm
cold -hot –sweating normal
Repeated attack
Relapse (P.vivax & P.ovale)
recrudescence

3. Malarial relapse due to delayed development of hypnozoites in liver
Recrudescence of falciparum it is caused by parasites persisting in circulation at sub clinical level following previous attack.
Malarial relapse due to delayed development of hypnozoites in liver
There is no hypnozoites in falciparum

4. Plasmodium falciparum

5. Erythrocytic cycle takes 36-48 hours
IN life cycle of P.falciparum
There is No hypnozoite stage
no relapse.
Erythrocytic cycle takes hours
Schizont contain 8-32 merozoites .
Large number of RBCs infected and
many cell contain more than one
trophozoite.
only ring stage and gametocyte
in peripheral blood.

6. Mainly due to mechanical distraction of parasitised RBCs.
Anemia can be sever and rapid
Mainly due to mechanical distraction of parasitised RBCs.
RBCs Phagocytosed in spleen and destroyed Due to lose of deformability .
Aplastic anemia due to effect of malarial toxins on B.M.
Hemolytic destruction (immune sensitization).

7. Erythrocytic schizogony take place in capillaries of deep organs.
(Ring and gametocyte only that appeared in blood film).
Adhererance phenomena lead to congestion ,hypoxia ,blockage and rupture of small blood vessels, (DIC) disseminated intravascular coagulation.
High level of parasitaemia up to % of RBCs infected (5% considers sever).
Cerebral malaria :parasitized RBCS and fibrin block capillaries and small bl. Vessels (may causing un-arousable coma)

8. Black-water fever :rapid and massive intravascular hemolysis of both parasitized and non-parasitized RBCs
Urin appears dark red to brown-black Renal failure hemoglbinurea
Diarrhea and vomiting
Pulmonary edema
Hypoglycemia
Hyperpyrexia
Pregnant women

13. Child with severe malaria, anemia, acidosis and respiratory distress

14. P. ovale and P. vivax infect immature red blood cells
P. malariae infects mature red cells.
P. falciparum infects both.

15. Serologloy used in epidemiology.
Laboratory Diagnosis
microscopic identification of parasites in blood is most certain method of confirming infection with plasmodium.
Examination of thick (large amount) and thin blood film relation of parasite to RBCs and rate of infection
Serologloy used in epidemiology.

17. Thick smear should be examined in all suspected cases of malaria because of its ability to detect parasites even when the parasitemia is low.
A thin film is used for species and stage identification and to provide information regarding erythrocytes, leukocytes, and platelets.

18. High parasitemia, growing stages of parasites (trophozoites and schizonts) and pigment-laden neutrophils indicate poor prognosis.
In case of uncertainty in identification of the species in severe malarial patients, it should always be considered as
P. falciparum.

19. P.f. ring

20. Plasmodium falciparum schizonte

21. Plasmodium falciparum gametocyte

23. P. falciparum

24. Plasmodiun vivax infected RBC usually not exceed 2%
- infection less sever than P.f.
P.v synchronized :regular 48h pattern of fever
All form of parasites trophozoites ,schizontes and gametocyte can be found in blood films.
enlargement of RBCS, schuffner`s dotes
Spleen enlargement and anemia
Relapse are feature of P.vivax
Patient must receive treatment both for attack and against relapsing form. (primaquine)

25. Plasmodium vivax ring stage of trophozoite

26. Plasmodium vivax schizontes

27. Plasmodium vivax gametocyte

29. Plasmodiun vivax

30. Plasmodium malariae
Cycle synchronized every 72 h.(quarten)
Spleen enlarge early.
Nephrotic syndrome which progress to renal failure caused by damage to kidney following deposion of antigen-antibody complex on glomerular membrane of kidney (proteinuria ,low serum albumin oedema)
Recrudescence can occur.

31. Plasmodium malariae trophozoit

32. Plasmodium malariae schizont

33. Plasmodium malariae gametocyte

34. Plasmodium malariae

35. Plasmodium oval ring, ameboid, schizont

36. Plasmodium oval gametocyte

37. Disease Severity and Duration
vivax
ovale
malariae
falciparum
Initial Paraoxysm Severity
moderate to severe
mild
severe
Average Parasitemia (mm3)
20,000
9,000
6,000
50, ,000
Maximum Parasitemia (mm3)
50,000
30,000
2,500,000
Symptom Duration (untreated)
3-8+ weeks
2-3 weeks
3-24 weeks
Maximum Infection Duration (untreated)
5-8 years
12-20 months
years
6-17 months
Anemia ++ +
++++
Complications
renal
cerebral
Modified from Markell and Voge's Medical Parasitology

38. Exoerthrocytic shizogony ( Liver) Primary hepatic form and hypnozoites
Clinical symptoms
Patent parasitemia
Subpatent parasitemia
Exoerthrocytic shizogony ( Liver) Primary hepatic form and hypnozoites

39. Diagnosis history of being in endemic area
symptoms: fever, chills, headache, malaise
splenomegaly, anemia
microscopic demonstration of parasite (blood smear)
antigen detection PCR amplification of parasite DNA

40. Treatment Chloroquine Quinine pyrimethamine +sulfadoxine (fansidar)
Blood stages:
erythrocytic stages (Asexual schizogony)
Chloroquine
Quinine
pyrimethamine +sulfadoxine
(fansidar)
Mefloquine, halofantrine
Gametocytes: primaquine
Liver stages (in vivax, ovale species)
primaquine

41. In malignant malaria all is right except:
black water fever.
Relapse .
disseminated intravascular coagulation (DIC).
Adhesion phenomena.
Cerebral malaria.
Acute renal failure

42. In benign tertian malaria all can occur except :
attack every 48 hours.
Relapse
Splenomegaly
Un arousable coma

43. In Erythrocytic cycle of P.vivax:
Enlargement of RBCs.
schuffner`s dots.
DIC.
Splenomegaly+ anaemia
Black water fever

44. Erythrocytic tertian or sub tertian schizogony. Maurer`s dots
In P.falciparum
High parasitemia
Multiple infection.
Enlargement of RBCs
Erythrocytic tertian or sub tertian schizogony.
Maurer`s dots
Adhesion phenomena (DIC)

45. In P. malariae: Splenomegaly Band shape trophozoites. Recrudescence
Antigen antibodes complex depostion in glomeruli with nephrotic syndrome
relapse

46. الحمد لله

47. High parasitemia, growing stages of parasites (trophozoites and schizonts) and pigment-laden neutrophils indicate poor prognosis.
In case of uncertainty in identification of the species in severe malaria,it should always be considered as P. falciparum.

48. Inoculation of the sporozoites into a new human host lead to inchoation of:
1 Exo-erythrocytic cycle (Tissue cycle) Pre-erythrocytic cycle
2 -Erythrocytic cycle.
3 -Sporogonic cycle.
4 -Sexual cycle.

49. Malarial releapse is due to
Merozoite.
Sporozoite.
Hypnozoite.
trophozoite
schizonte

50. The clinical manifestations of the disease is due to:
Erythrocytic cycle.
Exo-erthrocytic cycle.
Sporogonic cycle.
Rupture of infected RBC and release malarial pigments and toxin.

51. Infective stage in saliva of female Anopheles is:
Merozoite.
Schizonte.
Trophozoite.
Sporozoite.

55. Geographical Distributions
p.vivax widespread in tropical and subtropical areas
range extends into temperate areas
relatively uncommon in Africa
P falciparum. widespread, but primarily in tropics and subtropics
P malariae broad, but spotty geographical distribution
P. ovale
primarily tropical Africa, especially western coast