Malaria Flashcards
What could be making the incidence fall?
Prevention (*Gates foundation)
What could be making the incidence rise?
resistance of parasite to antimalarials/mosquitoes to insecticides
increased travel to endemic areas
what are the 4 species of plasmodia that cause human malarial disease?
P (plasmodium) P. falciparum P. ovale P. vivax P. malariae
Features of infection with P. vivax
incubation 10-17 days
fever spikes every 48hrs
Features of infection with P. ovale
similar to P.vivax
except untreated infection does not last long
Which 2 species are referred to as benign tertian malaria?
P.vivax + p.ovale
what may both of the benign tertian malarias produce?
relapses = invasion of blood by latent hypnozites in liver, up to a few years after complete clearance of parasites from blood
Features of P.malariae
incubation 18-40 days
recurs 72-hrly
can lie low in blood and reappear between 1-52yrs
rarely fatal
may cause glomerulonephritis
Features of p.falciparum
incubation 7-10 days
recurs 36-48hourly
fulminating disease (occurs suddenly)
what are the vectors in malaria?
female anopheles mosquitos
parasite undergoes temp dependent cycle of development in gut of insect
what does the mosquito inject into the human host?
plasmodium protozoa
it multiplies in human RBCs
- -> haemolysis
- -> cytokine release
Human liver stages
-exo-erythrocytic cycle
Mosquito takes blood meal = human bite = injects sporozites (immature parasite)
Protozoa is filtered into liver infected hepatocyte
In the liver sporozites mature exoerythrocytic schizonts
Schizonts escape by rupturing the hepatocyte they matured in
How do p.ovale and p.vixav cause relapse months later?
they lie dormant as hypnozoites in hepatocytes
Human blood stage pathway#1 (leading to ruptured schizont)
- erythrocytic cycle
- forms immature trophozoite (ring stage)
- -> mature trophozoite in RBC
- -> mature into Schizont
- -> rupture RBC it matured in
–> infect more RBCs and erythrocytic cycle continues
Human blood stage pathway#2
(producing gametocytes)
- erythrocytic cycle
- forms immature trophozoite (ring stage)
- -> gametocytes
- -> replicate DNA and produce strains of parasite
Mosquito stage (sporogonic cycle)
mosquito takes a blood meal = bites human = uptaking gametocytes
fertilization + development of sporozites in mosquito gut occurs
–> infective stage –> cycle continues
detail of the fertilization of spopzites in mosquito gut
Flagellated microgametocyte received joins the macrogametocyte → ookinete → oocyte
Oocyte rupture = release of sporozoites
Migration of new sporozoites to mosquito salivary gland
Severe P.falciparum malaria can result in what?
cerebral malaria, fatal infection!!
sequestration of parasitized erythrocytes in microvasculature of vital organs = tissue hypoxia and widespread organ damage
Complications of cerebral malaria
shock metabolic acidosis hypoglycaemia renal failure ARDS
Rx for cerebral malaria
anti-malarials in full dose ASAP
parenteral artesunate > quinine
IV then oral
what are merozoites?
1.any protozoan cell produced by the fission of a schizont, e.g. that of the malaria protozoan
when does the pt become symptomatic?
merozoites/schizonts are released into the bloodstream
fever and haemolysis
Presentation
fever paroxysms (sudden attack) = synchronous release of flocks merozoites from mature schizonts
- shivering
- hot stage (T>41); flushed, dry skin, nausea/vom, headache
- sweats (3hrs) as temp falls
Symptoms
Fever in a recent traveller!!
90% present within 1 month of mosquito bite
- prodromal headache (prodrome = early symptom)
- chills/sweats, rigors
- malaise, fatigue
- myalgia, anorexia
- vom, nausea, diarrhoea
–> may be no pattern to fever spikes initially
