1. MALARIA

2. Malaria Sporozoa belong to the phylum Apicomplex. The parasites of class Haematozoa occur in the blood of their vertebrate hosts. This class contains two orders: -Haemosporida, containing the genus Plasmodium which causes malaria, -Piroplasmida, containing the genus Bebesia.

3. Malaria Malaria parasites infecting humans belong to four species: Plasmodium falciparum, P. vivax, P. malariae and P. ovale. They cause a life-threatening protozoan disease called malaria. It is the most important of all the tropical diseases in terms of morbidity and mortality. More than 300-500 million individuals throughout the world are infected with malaria, and 1.5-2.7 million people a year, most of whom are children, are being killed by the disease.

5. Malaria The incidence of malaria is increasing due to: 1.Resistance of vectors insecticides. 2.Drug resistant parasites. 3.The absence of a potent vaccine. 4.High cost of mass treatment.

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8. Pathogenesis: Man gets infection by the bite of infected female anopheles mosquito. However, infection may also be transmitted by: 1. Transfusion of blood from a patient of malaria. This is known as transfusion malaria. 2. Transfusion of infection to fetus in utero through some placental defect. This is known as congenital malaria. 3. By the use of contaminated syringes particularly in drug addicts. The above conditions are also known as trophozoite induced malaria, in which there is no primary and secondary exo-erythrocytic schizogony, short incubation period, and there is no relapse.

9. Malaria Malaria generally occurs in areas where environmental conditions allow parasite multiplication in the vector. Thus, malaria is usually restricted to tropical and subtropical areas but this distribution might be affected by climatic changes, especially global worming and population movements. Prevalence of malaria parasites according to spp. as the most prevalent one is P. falciparum account for 50% of malaria cases, vivax about 40%, malariae about 7% and ovale less than 3%.

10. Malaria There are certain people, who are resistant to malaria infection, including those with: 1.Duffy antigen blood group negative (esp. for vivax). 2.Sickle cell traits. 3.Thalassemia. 4.Glucose-6-phosphate-dehydrogenase deficiency.

11. Malaria Clinical features: After an incubation period of 12 days for P.falciparum, 13-17 days for P.vivax, and P. ovale, and 28-30 days for P. malariae, patient will develop typical picture of malaria that consists of: Febrile paroxysm, Anaemia, and Splenomegaly.

12. Malaria Febrile paroxysm: It generally begins in the early afternoon and comprises of 3 successive stages; cold stage hot stage sweating stage.

13. Malaria Febrile paroxysm: It generally begins in the early afternoon and comprises of 3 successive stages; cold stage, hot stage and sweating stage. In the cold stage, lasting 15-60 min, the patient experiences intense cold and shivering. This is followed by hot stage, lasting for 2-6 hours, when the patient feels intense hot. Patient develops high fever (40-40.6 C), severe headache, nausea, and vomiting. Then, fever ends by a crisis of profuse sweating.

14. Malaria The periodicity of the attack varies with the species of the infecting parasite. 1)In P. vivax is 48 hrs (benign tertian) 2)In P. ovale is 48 hrs (ovale tertian) 3)In P. malariae 72 hrs (quatrain). 4)In P. falciparum typical tertian is not usual in it, so it is called malignant tertian.

15. Malaria Febrile paroxysms follow the completion of erythrocytic schizogony when the mature schizont ruptures releasing merozoites, malarial pigment and other parasitic debris. Macrophages engulf these and release endogenous pyrogens leading to pyrexia

16. Malaria

17. Anaemia after few paroxysms, anemia of microcytic or normocytic hypochromic type develops as a result of: 1.Mechanical destruction of parasitized RBCs. 2.Reduced erythropoiesis in the bone marrow. 3.Lysis and phagocytosis of uninfected RBCs. 4.In a small number of patients with malignant tertian malaria there is autoimmune destruction of RBCs. 5.Consumption of more than 70% of haemoglobin in RBCs by the parasite. 6.Failure of the liver to convert liberated iron.

18. Malaria Splenomegaly: After few paroxysms, spleen gets enlarged and becomes palpable. Splenomegaly is due to massive proliferation of macrophages which phagocytize both parasitized and non- parasitized RBCs. Jaundice can also occur due to rupture of RBCs.

19. Malaria

20. Complications: In case of P.vivax and P.ovale some sporozoites enter the hepatocytes and become dormant (resting) known as hypnozoite. After a period of time, up to two years, hypnozoites are reactivated to become secondary exo-erythrocytic schizonts and release merozoites that infect RBCs producing malaria relapse.

21. Malaria There is a situation in which the infected RBCs are not eliminated by immune system or by therapy and the number of parasites increases inside these RBCs, with subsequent clinical symptoms, this is called malaria recrudescence. All spp. of Plasmodium may cause a recrudescence.

22. Malaria Complications: Pregnant women have an increased risk of abortion, stillbirth, premature delivery and of low birth weight of their infants.

23. Malaria P. falciparum is the most pathogenic of the 4 species. It causes a high level of parasitemia with parasite density exceeding 250,000-300,000 /ml of blood. Nearly 30- 40% of RBCs may be infected. In contrast to other species, it invades erythrocytes of all ages (old and young).

24. Malaria Erythrocytic schizogony in P. falciparum takes place in the capillaries of the internal organs (spleen, bone marrow, brain, kidney, intestine, heart and placenta) Membrane protuberances (knobs) appear on the surface of infected red cells, they mediate attachment of parasitized cells to each other and to the lining of the capillaries and venules as the parasites (except gametocytes) get older (sequestration). Thus only young ring and gametocytes are typically found in peripheral blood. Therefore, parasites may not be found in a blood film at the time when clinical picture is most suggestive. The characteristic lesions are due to blockade of small vessels by sticky parasitized erythrocytes. This leads to tissue hypoxia.

25. Malaria Pernicious malaria: It is a complex of life-threatening complications that sometimes supervene in acute falciparum malaria. It is due to heavy parasitization and is of 3 types: 1.Cerebral Malaria 2.Algid Malaria 3.Septicemic Malaria.

26. Malaria Cerebral Malaria is characterized by hyperpyrexia, coma and paralysis. Capillaries of the brain are plugged with parasitized RBCs, each cell containing malaria pigment. In highly endemic area of malaria, C.M. occurs in children between 6 months and 5 years, most commonly at 3-4 years of age. Algid Malaria resembles surgical shock with cold clammy skin, peripheral circulatory failure and profound shock. Patient may develop vomiting and dysentery. Septicemic Malaria is characterized by high degree of prostration; there is high continuous fever with involvement of various organs.

27. Malaria Blackwater fever is a manifestation of repeated infections with P. falciparum which were inadequately treated with quinine. Sometimes resumption of quinine for new attack is followed by massive destruction of RBCs, fever, haemoglobinuria and renal failure. The exact mechanism of this fever is not known but an autoimmune mechanism has been suggested. Parasitized and quininized RBCs, during previous infection, act as Ag against which Abs are formed. With subsequent infection and treatment with quinine, there is a massive destruction of both infected and uninfected RBCs. As other anti- malarial drugs have been replaced quinine, blackwater fever is now rare.

28. Malaria Complications of P. vivax malaria include splenomegaly (rarely splenic rupture), and P. malariae include nephrotic syndrome.

29. Malaria Diagnosis : 1. Clinical picture is highly suggestive, esp. the characteristic paroxysm. 2. Microscopic identification of parasite (stages) in blood film is the method most frequently used to demonstrate an active infection. 3. Ab detection can detect past (not active) infections. 4. Rapid Diagnostic tests (RDTS) are based on detection of Ag derived from lysed blood cells using immunochromatographic methods. 5. Molecular diagnostic techniques can complement other tests, esp. in species identification.

30. Blood film parasite stages

31. Malaria Treatment: Chloroquine was the standard treatment for many years but resistance has made a problem so quinine is an alternative. Primaquine is used to eliminate the exo- erythrocytic phase. However, this drug may precipitate hemolysis in individuals who are deficient in the enzyme glucose-6-phosphate dehaydrogenase. Supportive measures and blood transfusion may be necessary.

32. Malaria Prophylaxis: 1. Spraying insecticides. 2. Spraying larvicides in breeding sites. 3. Using biological larvicides by using spore forming bacterium that produces a crystal of toxic protein (endotoxin). When spores and crystals are ingested by larvae, the mouthparts and gut are paralysed and the gut epithelium is destroyed, leading to death.

33. Malaria 4. Wearing long sleeve clothing and trousers to avoid bites. 5. Using bet nets. 6. Taking prophylactic treatment (Chemoprophylaxis). 7. Early diagnosis and prompt treatment of patients.

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