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  1. 1. ,
  2. 2.  Malaria is a mosquito-borne infectious disease of humans and other animals caused by protists (a type of microorganism) of the genus Plasmodium. It begins with a bite from an infected female mosquito (Anopheles Mosquito), which introduces the protists via its saliva into the circulatory system.
  3. 3.  Five species of Plasmodium can infect and be transmitted by humans. The vast majority of deaths are caused by P. falciparum while P. vivax , P. ovale and P. malariae cause a generally milder form of malaria that is rarely fatal.
  4. 4.  Headache , fever ,shivering ,arthralgia (joint pain), vomiting hemolytic anemia jaundice hemoglobinuria retinal damage and convulsions.
  5. 5.  The pathological changes in malaria are related to the development of asexual parasites in the blood.  The release of malaria antigens, pigment and toxins gives rise to a cascade of pathological events.
  6. 6.  Cytokines,  Tumour necrosis factor (TN fd),  The effects of other circulating “endogenous pyrogens” such as interlukin-1 (IL-1) and IL- 6. TNF
  7. 7. 1. Individual organs 2. Central nervous system 3. Anaemia 4. Bone marrow 5. The spleen 6. The kidneys
  8. 8. 1. Adrenals 2. The lungs 3. The cardiovascular system 4. Gastro-intestinal tract 5. Placenta
  9. 9. Cerebral malaria and coma. Hyperpyrexia. Haemolytic Anaemia. Non cardiogenic pulmonary oedema (ARDS ) Acute tubular necrosis and renal failure Acute Hepatomegaly and centrilobular necrosis Hypoglycaemia An adrenal insufficiency like syndrome Cardiac dysrhythmias Lactic acidosis.
  10. 10. a. Primaquine b. Artemisinin c. Quinine d. Chloroquine e. Pyrimethamine f. Proguanil g. Sulfonamides h. Mefloquine i. Atovaquone j. Doxycycline k. Clindamycin
  11. 11.  Primaquine is a highly active 8- aminoquinolone that is used in treating all types of malaria infection. It is most effective against gametocytes but also acts on hypnozoites, blood schizonticytes and the dormant plasmodia in P. vivax and P. ovale.
  12. 12.  Metabolites of primaquine are believed to act as oxidants that are responsible for the schizonticidal action as well as for the hemolysis and methemoglobinemia encountered as toxicities.
  13. 13.  Drug-induced hemolytic anemia in patients with genetically low levels of glucose-6- phosphate dehydrogenase  Ethemoglobinemia  Granulocytopenia  Agranulocytosis  Primaquine is contraindicated during pregnancy. All plasmodium species may develop resistance to primaquine.
  14. 14.  Artemisinin (or one of its derivatives) is available for the treatment of severe, multidrug-resistant P. Falciparum malaria.  Artemisinin is extracted from a herb,qing hao  Also called sweet wormwood or annual wormwood.
  15. 15.  Extensive structure-activity studies have confirmed the requirement for an endoperoxide moiety for antimalarial activity these compounds act rapidly against the asexual erythrocytic stages of P. Vivax and P. Falciparum.
  16. 16.  Artemisinin action involves two steps  First, heme iron within the parasite catalyzes cleavage of the endoperoxide bridge. This is followed by rearrangement to produce a carbon-centered radical that alkylates and damages macromolecules in the parasite, likely including the ortholog of sarco/endoplasmic reticulum ca2+-atpase
  17. 17.  Chloroquine [klor-oh-kwin] is a synthetic 4- aminoquinoline that has been the mainstay of antimalarial therapy, and it is the drug of choice in the treatment of erythrocytic P. Falciparum malaria, except in resistant strains. Chloroquine is less effective against P. Vivax malaria. It is highly specific for the asexual form of plasmodia.
  18. 18.  Asexual malaria parasites flourish in host erythrocytes by digesting hemoglobin in their acidic food vacuoles,  it generates free radicals and heme (ferriprotoporphyrin IX) as highly reactive by-products. Perhaps aided by histidine-rich proteins and lipids,  heme is sequestered as an insoluble unreactive malarial pigment termed hemozoin.  Chloroquine concentrates in the food vacuoles of susceptible plasmodia, where it binds to heme as it is released during hemoglobin degradation and disrupts heme sequestration.  Failure to inactivate heme or even enhanced toxicity of drug- heme complexes is thought to kill the parasites via oxidative damage to membranes, digestive proteases, and possibly other critical biomolecules. Other quinolines such as quinine, amodiaquine, and mefloquine, as well as other aminoalcohol analogs (lumefantrine, halofantrine) may act by a similar mechanism, although differences in their actions have been proposed
  19. 19.  At higher doses, many more toxic effects occur, such as gastrointestinal upset, pruritus, headaches, and blurring of vision  An ophthalmologic examination should be routinely performed.  Discoloration of the nail beds and mucous membranes may be seen on chronic administration.  Chloroquine should be used cautiously in patients with hepatic dysfunction or severe gastrointestinal problems or in patients with neurologic or blood disorders.  Chloroquine can cause electrocardiographic changes, because it has a quinidine-like effect.
  20. 20.  Quinine is the chief alkaloid of cinchona  Quinine acts primarily against asexual erythrocytic forms; it has little effect on hepatic forms of malarial parasites. The alkaloid also is gametocidal for P. vivax and P. malariae but not for P. falciparum.
  21. 21.  Quinine is more toxic and less effective than chloroquine against malarial parasites susceptible to both drugs. However, quinine, along with its stereoisomer quinidine, is especially valuable for the parenteral treatment of severe illness owing to drug-resistant strains of P. falciparum, even though these strains have become more resistant to both agents in certain parts of Southeast Asia and South America. Because of its toxicity and short half-life, quinine generally is not used for prophylaxis.