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History of malaria 

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Year Place Event
c 10000 years ago   Virulent malaria evolves although people were almost certainly exposed to less virulent types well before this. The evidence for this relatively recent origin of virulent malaria comes mainly from the analysis of human genes that confer reduced risk from malaria infection. By modelling the spread of the beneficial alleles, it has been worked out that malaria only started having a major impact on human survival from about 10000 years ago which coincides with start of agriculture. However, there are conflicting findings from other studies so with further research this dating might change. See Pennisi (2001) and Tishkoff et al. (2001).
c 6000-5000 years ago east Mediterranean Evidence of malaria from the structure of human bone from east Mediterranean archaeological sites. Populations experiencing a high incidence of Plasmodium falciparum infection have an increased frequency of sickle cell anaemia. One of the side effects of this condition is enlarged marrow spaces in the bone (termed parotic hyperostosis) which is most clearly shown in the skull. By analysing bone from archaeological deposits, it is therefore possible to date the presence of malaria in these ancient populations. 
c 2500 years ago   Hypocrites wrote of malaria and divided the fever into different types: quotidian (daily), tertian (alternate days) and quartan (every fourth day).
c 1500  Central and South America European settlers and slavery are likely to have brought malaria to America. 
1630s   Jesuit missionaries learned of the anti-malarial properties of  the bark of the Cinchona tree (which contains quinine) and introduced it to Europe. For hundreds of years previously, this bark had been used by local people for treating fevers.
1820   Quinine identified as the active agent in the bark of the South American Cinchona tree.  
mid-1800's Java (Indonesia) The Dutch grew Cinchona trees and established virtually a world monopoly in the supply of quinine.
1800s Northern Europe and US Decline in malaria because (1) of drainage of swamps for agricultural use; and (2) better housing and screening. However, in the American Civil War of  1861-1865, it has been estimated that 50% of the white soldiers and 80% of the black soldiers got malaria annually.
1880 Algeria Charles-Louis-Alphonse Laveran observed the malaria parasites in a slide of blood he was viewing under a microscope. His discovery was initially rejected by the medical community and only in 1886 was it accepted
1882   The mosquito transmission hypothesis for malaria was first put forward.
18 December 1897   Dr Ronald Ross reported in the British Medical Journal his discovery of malaria cysts in the stomach wall of Anopheles mosquitoes that had fed on a malaria patient. 
July 1898   Italian scientist Giovanni Batista Grassi proved that malaria was transmitted by Anopheles to people.
post 1918   Germany during and after World War I developed the anti-malarial drug atabrine.
1927   J. Wagner von Jauregg received the Nobel Prize in Medicine for his work in treating syphilis using malaria. Patients were innoculated with the malaria pathogen from which three or four bouts of fever resulting from this infection were enough to burn up the temperature-sensitive syphilis bacteria (Treponema pallidum). Once cured of syphilis, the patient was give quinine to get rid of the malaria. In the 1950s this treatment of syphilis was replaced by the use of antibiotics.
1934 Germany An antimalarial compound called Resochin, belonging to the 4-amino quinoline group of chemicals, was developed by a German pharmaceutical company. A similar compound called Sontochin was later produced.
1943   The Americans acquired Sontochin when Tunis was liberated from the Germans. They changed its composition slightly and called it Chloroquine.
1940s US Large-scale spraying with DDT of breeding areas in the US but probably contributed little to the final disappearance of malaria because competent vectors still remain. There are still occasional outbreaks of malaria in the US, associated with infected people coming back from malaria areas.
1934-1949 Brazil Eradication programme successful
1948 Egypt Eradication programme successful
early 1950s   DDT resistance by Anopheles developed in several countries, prompting renewed efforts to use it on a wide scale before resistance became too widespread.
1955   World Health Assembly launched the malaria eradication initiative. Africa was excluded because of the extent of malaria transmission and because of a lack of infrastructure. The goal was to reduce infected vector populations feeding on humans sufficiently to interrupt parasite transmission, rather than trying to eradicate all vectors. Malaria was eradicated in the temperate zones but in places like Sri Lanka, initial successes were followed by resurgences of the disease.
1960s   Chloroquine resistance developed in Plasmodium falciparum strains from South America and Southeat Asia and spread to most of the world except Africa.
1969   It was recognised that eradication was not achievable in many areas and that instead the goal should be control. Problems with eradication stemmed from geographical differences in behaviour of Anopheles which made a uniform control approach ineffective, and also support from local communities was often lacking.
early 1970's   Resources for malaria control shifted largely to other health needs.
early 1970's   DDT removed from the marketplace in the US because of its environmental effects. Alternative insecticides were more expensive and in some cases were more toxic to people.
1969-1976   World Health Organisation co-ordinated an intensive study of malaria in the Garki district of Northern Nigeria. This study showed the problems that can be encountered in combatting malaria in Africa (e.g. high bite intensity, high proportion of vectors carrying the parasite, mosquitoes resting outdoors after blood meals instead of indoors on insecticide treated walls). It was concluded that the use of drugs and insecticides could markedly reduce the incidence of malaria in the short term but was not enough to break transmission and achieve long-term success.
1980   Chloroquine resistance by P. falciparum appeared in coastal Tanzania and Kenya and spread over most of Africa in the 1980's.



  • Cloudsley-Thompson, J.L. 1976. Insects and History. Weidenfeld and Nicolson, London.

  • Collins, F.H. & Paskewitz, S.M. 1995. Malaria: current and future prospects for control. Annual Review of Entomology 40: 195-219.

  • Pennisi, E. 2001. Malaria's beginnings: on the heels of hoes? Science 293: 416-417.

  • Tishkoff, S.A., Varkonyi, R., Cahinhinan, N. Abbes, S., Argyropoulos, G., Destro-Bisol, G., Drousiotou, A., Dangerfield, B., Lefranc, G., Loiselet, J., Piro, A., Stoneking, M., Tagarelli, A., Tagarelli, G., Touma, E.H., Williams, S.M. & Clark, A.G. 2001. Haplotype diversity and linkage disequilibrium at human G6PD: recent origin of alleles that confer malarial resistance. Science 293: 455-462.

Text by Hamish Robertson  

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