quinine

/kwuy"nuyn, kwin"uyn/ or, esp. Brit., /kwi neen"/, n. Chem., Pharm.

1. a white, bitter, slightly water-soluble alkaloid, C₂₀H₂₄N₂O₂, having needlelike crystals, obtained from cinchona bark: used in medicine chiefly in the treatment of resistant forms of malaria.

2. a salt of this alkaloid, esp. the sulfate.

[1820-30; < Sp quin(a) ( < Quechua kina bark) + -INE²]

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Alkaloid found in the bark of cinchona trees and shrubs.

The chemical structure of this heterocyclic compound is large and complex, with several rings. For the 300 years preceding the 1940s, when newer antimalarials were developed, quinine was the only drug known to Western medicine for the prevention and treatment of malaria. The first chemical compound ever used successfully against an infectious disease, it has benefited more people than any other such drug in history and is still used to treat malaria, often in combination with other drugs. Quinine is also a flavouring agent in some carbonated beverages, including tonic water.

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▪ drug

      drug obtained from Cinchona bark that is used chiefly in the treatment of malaria, an infection caused by the protozoan parasite Plasmodium, which is transmitted to humans by the bite of various species of mosquitoes. During the 300 years between its introduction into Western medicine and World War I, quinine was the only effective remedy for malaria. As a specific treatment for this disease, quinine has benefited more people than any other drug used thus far to fight infectious diseases. The treatment of malaria with quinine marked the first successful use of a chemical compound in combating an infectious disease. Quinine was first synthesized in a laboratory in 1944; however, synthesis of the drug on a commercial scale is not economically feasible.

      Quinine, an alkaloid, acts by interfering with the growth and reproduction of the malarial parasites, which inhabit the red blood cells (erythrocytes (erythrocyte)). Administration of quinine dramatically improves the condition of a person with malaria; the parasites promptly disappear from the blood, and the symptoms of the disease are quickly alleviated. When quinine treatment is terminated, however, many recovered patients experience another attack of malaria several weeks later. This recurrence stems from 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, reinvade the red blood cells and precipitate the second malarial attack, or relapse.

      Because quinine fails to produce a complete cure of malaria, better antimalarial drugs have been developed. Research during World War II produced a number of antimalarial drugs that almost completely replaced quinine. Some of them, such as chloroquine, are more effective than quinine in suppressing the growth of the blood forms of the malarial parasite; others, such as primaquine, act upon both the blood and tissue stages of the parasite, thus producing complete cures and preventing relapses. All the newer antimalarials, unlike quinine, may be completely synthesized on a commercial scale.

      During the 1960s several strains of the malarial parasite Plasmodium falciparum developed resistance to the synthetic drugs, particularly the highly valued chloroquine. The parasite remained sensitive, however, to quinine, which had to be reinstated in various parts of the world as the drug of choice despite the side effects that sometimes occur when the necessarily large doses of quinine are given. Prolonged administration of quinine may produce toxic symptoms such as deafness, disturbances in vision, rash, and gastrointestinal symptoms.

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