Nearly all deaths from severe malaria result from infections with P. falciparum. P. falciparum is the most prevalent malaria parasite on the African continent. It is responsible for most malaria-related deaths globally.
Severe P. vivax malaria may present with some symptoms similar to those of severe P. falciparum malaria and can be fatal. Severe anaemia and respiratory distress occur at all ages, although severe anaemia is particularly common in young children. For more information on P. vivax malaria visit the P. vivax information hub.
The criteria for severe P. vivax infections are the same as for adults and children with severe P. falciparum malaria but with no parasitaemia density thresholds and without the criterion of hyperparasitaemia. Primary symptoms include severe anaemia, respiratory distress and acute lung injury (ALI), acute kidney injury (AKI), splenic rupture, metabolic acidosis, jaundice, multiorgan dysfunction, morbidity and shock, but rarely coma.
Parasite densities in P. vivax are usually lower than P. falciparum andmay cause severe anaemia at lower parasitaemia levels.
In P. vivax, contrary to P. falciparum, all stages of parasite development may be seen in the peripheral blood film. Note that the currently available RDTs are slightly less sensitive for detecting P. vivax than for P. falciparum.
For more information on the diagnosis of severe malaria, visit the diagnosis page.
Following parentarel artesunate, treatment can be completed with a full treatment course of oral ACT or chloroquine (in countries where chloroquine is the treatment of choice). A full course of radical treatment with primaquine should be given after recovery.
Groups at risk
The risk of developing severe disease is especially associated with young age, higher transmission intensity, early and frequent relapse, less access to early diagnosis and treatment and/or greater prevalence of co-morbidities including bacterial co-infections and malnutrition. Severe disease is rare in temperate areas and in returned travelers. It occurs in relatively high-transmission areas with chloroquine resistance, such as Indonesia and Papua New Guinea, as well as in low-transmission areas, including India and South America.
The monkey parasite P. knowlesi can cause malaria in humans living in close proximity to macaque monkeys (particularly on the island of Borneo). P. knowlesi replicates every 24h, which can result in rapidly increasing parasite densities, severe disease and death in some cases, and have a threefold higher risk of developing severe malaria than P. falciparum. Early diagnosis and treatment are therefore essential.
Epidemiologically, criteria for severe P. knowlesi have lower parasitaemia cut-offs for hyperparasitaemia and jaundice than P. falciparum:
Hyperparasitaemia: Parasite density >100 000/ll
Jaundice and parasite density >20 000/ll
Any patient with a P. knowlesi parasitaemia of >20 000/ll needs to be observed very carefully.
As P. knowlesi and P. malariae are similar in the peripheral blood film, microscopy alone is insufficient to diagnose P. knowlesi. Polymerase chain reaction (PCR) is required to confirm P. knowlesi infection, but should not delay treatment. A high parasite density (> 0.5% parasitaemia) with P. malariae-like parasites should be treated for P. knowlesi infection.
For more information on the diagnosis severe malaria, visit the diagnosis page.
P. knowlesi malaria occurs mainly on the island of Borneo but has been reported in other South-East Asian countries. Local residents and travelers to or from this region are at risk for infection. It is transmitted mainly in forests and along forest fringes.