Acacia xanthophloea is a tree in the Fabaceae family and is commonly known in English as the Fever Tree (local East African names include Olerai, Kimwea, Murera, and Mwelele). This species of Acacia is native to eastern and southern Africa. It can be found in Botswana, Kenya, Malawi, Mozambique, Somalia, South Africa, Swaziland, Tanzania, Zambia and Zimbabwe. It has also become a landscape tree in other warm climates, outside of its natural range.
The trees grow to a height of 15–25 m. The characteristic bark is smooth, powdery and greenish-yellow in colour. It is one of the few trees where photosynthesis takes place in the bark. Straight, white spines grow from the branch nodes in pairs. The leaves are twice compound, with small leaflets (8 x 2 mm). The flowers are produced in scented pale cream spherical inflorescences, clustered at the nodes and towards the ends of the branches.
Fever trees are fast-growing and short-lived. They have a tendency to occur as single-aged stands, and are subject to stand-level diebacks that have been variously attributed to elephants, water tables, and synchronous senesce
A Fever tree planted outside of its natural range at Ilanda Wilds
Planted at Umdoni Bird Sanctuary
Foliage and branches
Quinine: The original antimalarial agent, quinine took its name from the Peruvian Indian word "kina" meaning "bark of the tree" referring to the cinchona tree. From this tree, quinine was first obtained. The Peruvian Indians called it "the fever tree."
Quinine, a large and complex molecule, is the most important alkaloid found in cinchona bark. Until World War I, it was the only effective treatment for malaria. In fact, quinine was the first chemical compound to be successfully used to treat an infectious disease.
Quinine was isolated in crystalline form in 1820 by J.B. Caventou and P.J. Pelletier. In one of the classical achievements of synthetic organic chemistry, R.B. Woodward and W. Doering first made synthetic quinine in 1944.
Quinine acts by interfering with the growth and reproduction of the Plasmodium, the malarial parasite that lives within the victim's red blood cells. Quinine causes the parasites to disappear from the blood and the symptoms of the disease are thereby alleviated. However, when quinine treatment ends, many patients relapse. They suffer another attack of malaria due to the failure of quinine to kill the malarial parasites in cells of the body other than the red blood cells. These parasites persist and, after a time, they reinvade the red blood cells and precipitate the relapse.
Since quinine does not permanently cure malaria, better drugs were sought. A number were discovered that replaced quinine during and after World War II. Some of these drugs (such as chloroquine and chloroguanide) are more effective than quinine in suppressing the growth of the blood forms of the malarial parasite. Others (such as primaquine and pyrimethamine) act upon both the blood and tissue phases of the parasite, producing a complete cure and preventing a relapse.
Quinine has been used outside of malaria as a remedy for fever and pain and to treat and prevent leg cramps. Prolonged administration of quinine may produce toxic symptoms such as deafness, disturbances in vision, skin rashes, and digestive upsets.