malaria Flashcards
intro
over 87 endemic countries - over half in SSA
2.4 billion at risk
219 million clinical episodes each year
43500 deaths annually
25% of child mortality in Africa
low birthweight, preterm delivery, cerebral malaria, severe malarial anaemia
disease of the poor
species of plasmodium
P. falciparum P. vivax (relapsing) P. ovale (relapsing and 2 species) P. malariae P. knowlesi
Vector
female anopheline mosquitos
Life cycle
gametocytes ingested in blood meal and microgametes (male) penetrate macrogametes to form diploid zygotes
zygote becomes motile and elongated (ookinete), invades midgut and develops into oocyst
oocyst ruptures and sporozoites make way into salivary glands
human bitten and sporozoites into the liver and mature to schizonts which rupture to release merozoites
in relapsing hypnozoites produced
merozoites invade RBC and develop by digesting haemoglobin
schizonts rupture releasing merozoites
some parasites develop into gametocytes which are taken back up by mosquito
asexual cycle
leads to clinical symptoms of disease and key stage for diagnosis and therapy
chemotherapy targets
intraerythrocytic cycle to relieve clinical symptoms
liverstages for prophylaxis
gametocytes to reduce transmission
uncomplicated malaria
fever every other day
severe complicated malaria in P. falciparum
cerebral coma anaemia pulmonary edema renal failure shock lactic acidosis hypoglycaemia tropical splenomegaly maternal death stillbirth low birthweight pregnancy anaemia
severe complicated malaria in P vivax and ovale
splenic rupture
anaemia
debilitating fevers
higher TNF alpha per parasite
severe complicated malaria in p. malariae
immune complex
glomerulonephritis leading to nephrotic syndrome
what happens to rbc with p. falciparum
remodels both outside and inside of erythrocyte which increases cytoadherence and causes sequestration of parasites in capillaries
sequestration allows parasite to escape the removal by the spleen and is associated with severe malaria
what happens in cerebral malaria
sequestration causes blocked vessels in the neuroectoderm which causes haemorrhages - can be modelled in the retina as derived from same neuroectoderm as the brain
malaria sequelae
cognitive impairment, behavioural disturbances, spasticity, epilepsy, vision, hearing and speech impediment
25% of children suffering cerebral malaria develop neurological sequelae
acquired immunity
as age increases, pathology decreases as immunity develops which is why children under 5 most likely to be effected
innate immunity
haemoglobinopathies e.g. thalessemia
RBC enzyme deficiency e.g. glucose 6 phosphate dehydrogenase
RBC surface components e.g. duffy blood group
sickle cell (>20% in Nigeria)
thought to include o2 and reactive oxygen species
