Malaria Flashcards
What is malaria?
- causative species
- transmission by
Tropical parasitic red blood cell infection caused by protozoal Plasmodium spp. transmitted by female anopheles mosquitoes.
Which Plasmodium spp. cause human malarial disease?
P. falciparum P. vivax P. ovale P. malariae P. knowelsi
Transmission of Malaria
Transmission by female anopheles mosquitoes. Have dusk to dawn activity (i.e. evening and night)
Other routes of transmission: congenital, blood transfusion
Concept of Stable Transmission
Stable transmission happens in a popn. that is continually exposed causing high background immunity in adults
Downside is the burden of disease is greater in children, who will suffer from acute illness and complications
Epidemics are less likely in such popn.
Concept of Unstable Transmission
This happens in popn. exposued to fluctuating rates of disease
Everyone has low background immunity so everyone (adult and children) are susceptible to disease
Epidemics happen b/c of sudden increase in mosquito vector densities
Malaria in UK
1 in 5 febrile returning travellers from sub-Saharan Africa has malaria; 1 in 100 from Asia and Latin America
P. falciparum responsible for majority of cases and deaths
Biggest risk factor: failure to take prophylaxis (more likely in travellers visiting family and friends)
Airport Malaria
Mosquitoes stowed away in luggage or in aircraft infect people who have not travelled abroad
Malaria Life Cycle
1) Blood Meal by infected female anopheles mosquito, injects sporozoites into blood
EXO-ERYTHROCYTIC CYCLE
2) Sporozoites infect hepatocytes
3a) P. vivax and P. ovale enter dormant stage = hypnozoites
3b) Asexual reproduction = schizogony, schizonts form
4) Schizont rupture releases merozoites into blood stream
ERYTHROCYTIC CYCLE (2-3 day cycles)
5) Merozoites infect RBCs
6) Immature trophozoite (ring stage)
7) Mature trophozoite
8) Schizogony forms schizonts
9) Schizont rupture and cycle repeats
Some immature trophozoites (6) transform into gametocytes
1) Form macrogametocyte and microgametocyte (female and male)
2) Mosquito takes blood meal and ingests gametocytes
Sporogenic Cycle
3) In mosquito gut, gametocytes fuse= zygote
4) Ookinete
5) Oocyst
6) Oocyst rupture in saliva, release of schizonts
Symptoms of Malaria
Cytokines like TNF-alpha are released corresponding to rupture of infected RBCs –> paroxysms of fever
Haemolytic anaemia: fatigue, headaches, jaundice, splenomegaly
P. falciparum and Sequestration Process
Mature falciparum trophozites espress PfEMPI receptor on RBCs. This causes infected cells to vind other RBCs or endothelial cells in capillaries of brain, gut, spleen and other organs.
Process of sequestration into deep tissues prevents removal by spleen.
Consequences of Sequestration in P. falciparum infection
- Cerebral Malaria
- Bilious Malaria
Microvascular occlusion –> local ischaemia
Cerebral malaria:
-altered mental status, seizures, coma
Bilious malaria:
- diarrhoea, vomiting, jaundice and liver failure
Other features: acidosis, renal failure, respiratory distress, DIC, shock, hypoglycaemia
Diagnosis of Malaria
Light microscopy (gold standard) w/ thick and thin blood smears.
Thich is more sensitive and allows greater vol. to be examined. Shows parasites in RBCs
Thin directly identifies the plasmodium species
Rapid Diagnostic Tests
RDTs inv. antigen detection or other enzymatic activities
1) detect of histidine rich protein-2 (HRP-2) in P. falciparum
2) detection of plasmodium lactate dehydrogenase (pLDH)
General Management of Malaria
Seek expert advice
Anti-pyretic therapy
Careful rehydration (risk of pulmonary oedema)
Inform local public health team
Treatment of Uncomplicated P. falciparum
Oral therapy w/ one of
1) Malarone (atovaquone-proguanil)
2) Riamet (artemether with lumefantrine)
3) Quinine and doxycyline
