1. vivax or benign tertian malaria
Malaria is a mosquito-borne infectious disease affecting humans and other animals caused by parasitic protozoans (Plasmodium)
P.vivax:
vivax or benign tertian malaria
Most predominant
P.ovale:
ovale or ovale tertian malaria
Tropics
P.malariae:
malariae or quartan malaria
Temperate zones
P.falciparum:
falciparum or subtertian or malignant malaria
Tropics
Geographical Distribution
Presence of Malaria = Presence of Anopheline mosquito

2. Development of Plasmodium in infected human
Infective♀ Anopheles injects sporozoites in its saliva at the site of bite
I- Liver phase
within 40 min in blood
Liver merozoites
P.vivax P.ovale
hypnozoites
Trophozoite
Schizont
Rupture
II- Blood phase ♂
Blood merozoites
P.v. 3rd d
P.o. 3rd d ♀
P.m. 4th d
Malaria pigment or haemozoin
Ring
Trophozoite
Schizont
Rupture
P.f. irreg.
gametocyte

3. Development in Anopheles Mosquito gut♀ ♂ ♀
gametocytes
Sporozoites in salivary gland
Reduction division ♂ ♀
to form gametes
Infective Stage
Sporocyst
Oocyst
exflagellation
Ookinete
fusion
Female Anopheles Malaria transmitter
Alimentary canal of Anopheles mosquito
Zygote

4. Pathology
Malaria

5. Symptoms of malaria are due to the release of massive number of merozoites into the circulation.
Infection results in the production of antibodies against merozoites and schizonts.
The activated macrophages help in the destruction of infected erythrocytes and antibody-coated merozoites..
Malarial infection is associated with immunosuppression.
Hemolysis of infected and uninfected R.B.Cs

6. In Falciparum malaria, ( adhesion phenomenon) occurs.
Pathology
In Falciparum malaria, ( adhesion phenomenon) occurs.
Merozoites of P. vivax and P. ovale are able to invade only reticulocytes, P. malariae are limited to the old cells while, P. falciparum is able to invade all ages of R.B.Cs indifferently

7. Pathogenesis and Clinical Picture
Incubation period followed by influenza-like symptoms.
Malaria paroxysm (clinical attack):
Coincides with:
Haemozoin
- Rupture of infected and uninfected RBCs.
- Release of parasite metabolites.
- Host immunologic response.
Metabolites
Includes:
- Cold stage
Lasts about 15 min.
- Hot stage
Lasts 2-6 hours
- Sweating stage
Lasts for hours

8. Pathogenesis and Clinical Picture
Malarial paroxysmal attacks recur at the following intervals:-
P. vivax and P. ovale attack occurs every 48 hours (tertian malaria).
P. malariae attack occurs every 72 hours (quartan malaria).
P. falciparum attack occurs from hours (malignant or irregular malaria).

9. Pathogenesis and Clinical Picture
Patients also complain from headache, fatigue, dizziness, anorexia, arthralgia, abdominal pain, diarrhea and vomiting. There is anemia, splenomegaly and hepatomegaly.
Between paroxysms, the patient may be tired but otherwise feel fairly good.

10. Pathogenesis and Clinical Picture
Enlargement of liver and spleen.
occurs due to enhanced phagocytosis of remnants of ruptured red cells and debris of schizont.
Remnants

11. Anaemia: haemolytic anaemia
Relapse (in P.vivax and P.ovale infection)
due to presence of hypnozoites in the liver.
Recrudescence (All species may recrudesce, especially P.malariae and P.falciparum infection)
persistent low-grade parasitaemia due to incomplete treatment or failure of immune system to destroy the parasite .
Anaemia: haemolytic anaemia
Plasmodium parasite invades:
- Reticulocytes only (in P.vivax and P.ovale).
Restricted anaemia
- Old RBCs only (in P.malariae).
- RBCs at any age (in P.falciparum).
Severe anaemia

12. MALARIA MALIGNANT
P.falciparum

13. The most dangerous type, may be severe and fatal.
Paroxysms are less well defined and fever may be continuous or irregular.
In non-immune, the primary attack can be fatal whereas in endemic areas in immune adults it leads to parasitemia with no fever or illness.
Recrudescences may occur up to 1 to 2 years, rarely longer.

14. Complications of falciparum malaria
1- Knobs develop on surface of infected RBCs
Knobs are parasite antigens expressed on the surface of infected red cells containing trophozoites and schizont stages.
They adhere to receptors found on endothelium of blood capillaries of internal organs blood supply
anoxia and necrosis.
Parasite antigens
Normal RBC
Blood capillary
Infected RBC

15. In the lung : blood flow in pulmonary circulation.
In brain :
In the lung : blood flow in pulmonary circulation.
In liver : impaired glycogenolysis
In the kidney : acute renal failure.
cerebral malaria.
Headache, drowsiness, convulsions & coma
Pulmonary oedema, difficulty in breathing
Hypoglycemia: This is common in severe malaria, particularly in pregnancy.

16. In Gastrointestinal tract:-
ischaemia in capillary bed of intestinal wall.
An acute hepatitis with enlarged tender liver and jaundice.
(b) Dysentery, which is very similar to acute bacillary dysentery.
(c) Cholera-like, profuse diarrhea watery diarrhea, vomiting, dehydration and muscular cramps.
Algid malaria:
It resembles acute adrenal insufficiently with low blood pressure, collapse and peripheral vascular failure.

17. Tropical splenomegaly syndrome (Hyperactive malaria splenomegaly)
Massive persistent splenomegaly in individual living in endemic area.
A non transient reduction in spleen size
upon antimalarial treatment.
Lymphocytic infiltration of the liver.
Anemia.
Increased serum polyclonal IgM and antimalarial antibodies and immune complexes.

18. Anaemia, haemoglobinuria, jaundice.
Black water fever
(Malarial haemoglobinuria):
Occurs: when?
- Repeated attacks of P.falciparum infection.
- The trigger mechanism is irregular dosage of Quinine with exposure to cold or exercise.
Pathogenesis
intravascular hemolysis, hemoglobinuria, and renal failure that affects only none or semi-immune individuals
Anaemia, haemoglobinuria, jaundice.
This is autoimmune with development of antibodies to infected red blood cells.

19. Pathogenesis of Black Water Fever
Blood Vessel of the infected patient
Auto-antibodies
Normal RBCs
Infected RBCs
Normal urine
Jaundiced patient
Haemoglobinuria

20. Parasitological examination
Diagnosis
Clinical diagnosis
Characteristic fever, enlarged tender spleen, anemia (microcytic hypochromic) and leucopenia or pancytopenia.
Parasitological examination
Blood film (thin and thick) stained by Giemsa or Leishman stains

21. Diagnosis 1- Thin and thick blood films to demonstrate the parasite.
Thin blood film
One drop of blood spread on a slide
Finger prick
Thick blood film
4 drops of blood spread in a small circle on a slide
Giemsa stained blood films

22. X X P. vivax P. ovale P. malariae P. falciparum Infected RBC
Enlarged, rounded
Enlarged, oval
Normal size & shape
Ring 1/3 RBC size
Ring 1/3 RBC size
Ring 1/3 RBC size
Ring 1/6 RBC size
Ring
Multiple rings
Malaria pigments (Haemozoin) X
Trophozoite
Band-shaped
Ziemann’s dots
Maurer’s clefts
Schuffner’s dots
Schizont X
Not seen in peripheral blood
Gametocyte ♀ ♂ ♀ ♂ ♀ ♂ ♀ ♂

23. Malaria pigments = Haemozoin It is the remnants of haemoglobin that was digested by Plasmodium parasite
Schuffner’s dots
Ziemann’s dots
Maurer’s clefts Called: Stippling It is degeneration process occurring in Plasmodium infected RBCs

24. Diagnosis
Provocative test (Ascoli test)
By injection of 1/2 cc adrenaline solution 1/1000 subcutaneously to stimulate the parasite to appear in peripheral blood in chronic cases (with no parasites in blood). Also, cold shower may be useful.

25. Serological Diagnosis
2- Detection of circulating parasite antigen using monoclonal antibodies. C T
3- Detection of parasite DNA and RNA in patient’s blood using DNA and RNA probes.

26. Treatment
Radical cure drugs: Drugs acting on pre-erythrocytic and tissue forms and prevent relapses e.g. primaquine
Suppressive drugs: Act on erythrocytic stages to terminate acute attack, but relapses may occur e.g. Quinine, atebrine, chloroquine, comaquin and mefloquine.
Gametocidal drugs: Destroy gametocytes, prevent infection of mosquito e.g. primaquine, pyrimethamine and proguanil.

27. Control Treatment of cases. Mosquito control. Chemoprophylaxis.
Vaccination: Many methods of vaccination against malaria are now investigated, aiming either to prevent any infection or to alleviate clinical picture or to stop transmission to mosquito. None has been approved as effective vaccine for humans.