When advising travellers on malaria prevention it is important to understand some of the basic natural history and epidemiology of the disease. This can help to convince the traveller of the life threatening nature of the illness and make clear, for example, why compliance with prophylaxis is so important. Many travel advisors also see returning travellers, so some knowledge of diagnosis and treatment is important. When emergency standby treatment is prescribed clear instructions as to its use must be given to the traveller.
Malaria is spread by the bite of the female anopheline mosquito. Most anopheline species prefer to feed between dusk and dawn which is when most transmission of malaria occurs.
Malaria is now predominantly a disease affecting Africa, South and Central America, Asia and the Middle East. Travellers from non endemic countries can contract the disease when visiting these areas and become ill while abroad or present with symptoms on return home. When malaria risk varies within a country, those living in non malarious parts can become infected when travelling to malarious areas. In some malarious areas, for example in parts of southeast Asia, there is a seasonal pattern of transmission. Mosquitoes like a humid atmosphere and breed only in fresh water so their numbers usually increase after periods of heavy rainfall or monsoons.
This map is reproduced with permission of and acknowledgement to WHO.
Countries that are not coloured have not reported cases to WHO which does not necessarily mean that no cases are occurring.
There are 5 different species of human parasite. Plasmodium falciparum causes malignant disease and is the predominant species in sub-Saharan Africa, Papua New Guinea and in the Amazon rain forests of South America. P.knowlesi is rarely imported at present but is capable of producing severe illness. It is found mainly in south-east Asia. The other species cause less serious, so-called benign disease. P.vivax predominates in the Indian sub-continent and is rare in sub-Saharan Africa where the predominant benign form of disease is caused by P.ovale. P.malariae occurs rarely in all malarious areas but mostly in Africa.
The mosquito inoculates sporozoites through its salivary ducts as it feeds. These enter the circulation and within a few minutes settle in hepatic parenchyma cells. Asexual reproduction takes place and the hepatic cells then rupture releasing into the blood up to 40 000 merozoites for every sporozoite inoculated. This takes 5-7 days for P.falciparum. P.vivax and P.ovale can cause illness after a similar period but these species can form hypnozoites which persist in the liver and may not become active for many months, sometimes for more than a year. The reason why these hypnozoites develop is not clear but it appears to be seasonal. Chemoprophylaxis with chloroquine or mefloquine, during exposure and for the usual 4 weeks afterwards, may not prevent these delayed illnesses since they only destroy the post hepatic erythrocytic forms of the parasite. Primaquine (often used after treatment of illness to eradicate hypnozoites) and to a lesser degree proguanil can destroy these hepatic forms.
The merozoites invade red blood cells and develop into ring forms or trophozoites. These destroy the contents of the erythrocytes, which eventually rupture releasing parasite and red cell debris plus 6-36 new merozoites (depending on the species), which rapidly invade new erythrocytes. This is when the typical fevers of malaria occur. The number of infected cells increases rapidly as the process repeats itself. Each erythrocytic cycle takes around 24 hours to complete for P.knowlesi, 48 hours to complete for P.falciparum, vivax and ovale and 72 hours for P.malariae.
Fevers may not be at regular intervals, particularly with P.falciparum, since several cycles can occur simultaneously. Red cell destruction with P.falciparum is much more rapid and severe than with the other species, which is why it causes more serious, life threatening disease. Death can occur within days.
After several cycles, if the patient survives, a sub-population of sexual forms of parasite called gametocytes, appear which are ready to be ingested by further mosquitoes. The male and female gametes fuse and develop in the gut wall of the mosquito. These oocysts eventually rupture releasing sporozoites, which find their way to the mosquito’s salivary glands, completing the life cycle.