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.