How big of problem is malaria?
The World Health Organization (WHO) estimates that more than 3 million people die each year from vector-borne diseases. Annually there are over 250 million new malaria cases with the majority due to infection with the most dangerous parasite Plasmodium falciparum, yet despite decades of research, there is still no vaccine against malaria. The complexity of the malaria parasite’s life cycle coupled with its ability to hide within host cells and avoid clearance by the host immune response have made it an elusive target for vaccine development. Current vaccines only offer partial protection in large scale efficacy trials. In 1955 the WHO launched the Global Malaria Eradication Campaign and by 1967 malaria was eradicated from many countries where the disease was endemic. However, the program ultimately failed due to the rapid appearance of pesticide and drug resistance.
The heavy use of antimalarials, such as chloroquine, led to the emergence and spread of drug resistant parasites, and without a replacement drug having the same low cost and reliability of chloroquine, the number of malaria cases increased. There is now some level of parasite resistance to all commercially available anti-malarial drugs. Concurrent with the rise in drug resistance in parasites there has been a marked increase in pesticide resistance in the mosquito vectors of malaria parasites. In the absence of more effective and longer lasting insecticides the WHO has reintroduced the use of DDT, despite its known adverse health and environmental effects. There has been a movement to distribute pyrethroid-impregnated bed nets for mosquito control, however, pyrethroid-resistant mosquitoes have already been observed. Climatic and ecological factors have also contributed to the spread of malaria. The rate of malaria parasite development is dependent on ambient temperature, with accelerated development occurring at higher temperatures. Mosquito reproduction also depends on climatic conditions, such that increased temperatures can allow for habitat expansion. Therefore, changes in climate may lead to the further spread of malaria.
The heavy use of antimalarials, such as chloroquine, led to the emergence and spread of drug resistant parasites, and without a replacement drug having the same low cost and reliability of chloroquine, the number of malaria cases increased. There is now some level of parasite resistance to all commercially available anti-malarial drugs. Concurrent with the rise in drug resistance in parasites there has been a marked increase in pesticide resistance in the mosquito vectors of malaria parasites. In the absence of more effective and longer lasting insecticides the WHO has reintroduced the use of DDT, despite its known adverse health and environmental effects. There has been a movement to distribute pyrethroid-impregnated bed nets for mosquito control, however, pyrethroid-resistant mosquitoes have already been observed. Climatic and ecological factors have also contributed to the spread of malaria. The rate of malaria parasite development is dependent on ambient temperature, with accelerated development occurring at higher temperatures. Mosquito reproduction also depends on climatic conditions, such that increased temperatures can allow for habitat expansion. Therefore, changes in climate may lead to the further spread of malaria.
SOURCE: Kaiser Family Foundation, based on WHO, World Malaria Report 2014
what is malaria?
Malaria is a disease caused by protozoan parasites in the genus Plasmodium. Malaria symptoms include fever, fatigue, vomitting, and in severe cases seizures, coma and death. Malaria is transmitted by the bites of female Anopheles mosquitoes. The malaria parasite life cycle involves development in both mosquito and mammalian hosts (for a great video reviewing the life cycle go here). Development of Plasmodium parasites in Anopheles mosquitoes begins with the ingestion of blood containing male and female gametocytes by the mosquito. These gametocytes fuse within minutes of ingestion to form mobile ookinetes that penetrate the midgut epithelium and transform into vegetative oocysts. After growth and development for 10-12 days, hundreds to thousands of sporozoites are released from each oocyst into the hemolymph, the open circulatory system of the mosquito. These sporozoites invade the salivary glands, where they are released into the saliva and injected into a human host during a subsequent blood feeding. Shortly after an infected female mosquito feeds on a human host, the injected sporozoites migrate to the liver, invade hepatocytes and undergo multiple rounds of asexual development. Ultimately, liver-derived merozoites invade red blood cells (RBCs), at which point clinical symptoms develop. RBC development progresses, with cyclical waves of parasite replication, cell lysis and parasite invasion. A fraction of merozoites released from infected RBCs become gametocytes, the parasite stage infectious to mosquitoes.
