Malaria Flashcards
Pathogens Responsible For malaria
Plasmodium falciparum
Plasmodium vivax
Plasmodium malariae
Plasmodium ovale
Incidence of malaria in the world
214 million cases
Percentage of malaria cases from Africa
88 percent
Why is there a resurgence of malaria since 1970
Plasmodium falciparum became resistant to chloroquine and sulfadoxine-pyrimethamine
People at risk of malaria
Children
pregnant women
travelers
migrants from endemic countries who have been a long period of time in an endemic countries and go back to their home country
People living near airport
Life cycle of malaria parasites
Female anopheline becomes infected by feeding on human blood containing gametocytes
Developments of gametocytes to sporozoites in 7 to 20 days
Sporozoites Accumulates in the salivary glands and get inoculated into human bloodstream
After Half an hour , sporozoites get to the liver (primary exo-erythrocytic)
If P.ovale or vivax, can stay long in the liver as hypnozoites and induce clinical illness months later
After some days , merozoites leave liver and invade red blood cells
Asexual cycle of multiplication in RBC producing shizonts
Schizont rupture producing more merozoites into blood -> fever
Pathology of malaria
Infected red blood cell prone to hemolysis.
Why is hemolysis of red blood cell worse in plasmodium falciparum
Because it infects red cells of all ages especially young cells
Peridiocity of fever in the different type of plasmodium
Alternate days in plasmodium vivax and ovale
Every three days in plasmodium Malariae
No periodicity in plasmodium falciparum
Type of red cell invaded by plasmodium vivax an ovale
Reticulocytes
Type of red cell invaded by plasmodium Malariae
Normoblasts
What happens in plasmodium falciparum infection when the red cell contain trophozoites
Form knob proteins which adhere to vascular endothelium in post capillary venules in the brain the kidney liver lungs and gut
Form rosettes and rouleaux with infected red cells
Leads to vessel congestion with organ damage
What are some protective mutation in the human against plasmodium falciparum
Sickle cell
thalassemia
glucose 6 phosphate dehydrogenase deficiency
HLA-B53
Which human evolution protects against plasmodium vivax
Red cell lacking Duffy blood group
Clinical features of plasmodium falciparum infection
Insidious onset -Malaise headache vomiting
Cough, mild diarrhea common
Fever with no particular pattern
jaundice common
enlargement / tenderness of the spleen and liver