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Mutation for drug resistance in Indian malaria identified

T. V. Padma

13 January 2005 | EN

Aedes aegypti (a vector of Dengue) taking a blood meal through human skin. (Courtesy of the Dept. of Medical Illustration, Liverpool School of Tropical Medicine, Liverpool, UK).

Aedes aegypti (a vector of Dengue) taking a blood meal through human skin. (Courtesy of the Dept. of Medical Illustration, Liverpool School of Tropical Medicine, Liverpool, UK).

WHO\TDR\LSTM

[AHMEDABAD] Scientists have identified the genetic mutation allowing the parasite that causes fatal cerebral malaria in India to resist a widely used drug. They warn that India could be becoming a new centre for the spread of such resistance, and that it needs to reassess the way it treats the disease. 

The scientists, based at the Indian Institute of Science (IISc) in Bangalore, studied the genetic make-up of the malaria parasites in the blood of 200 people with cerebral malaria — the form of the disease affecting the brain that accounts for almost 60 per cent of the 2.3 million cases of malaria in India each year.

The researchers found that in 95 per cent of those infected, the parasite had a mutation — termed SVMNT — in one of its genes. Malaria parasites with the mutation are not affected by chloroquine, a drug commonly used to treat the disease.

Govindrajan Padmanabhan, scientist emeritus at IISc, told the 92nd Indian Science Congress in Ahmedabad last week that until now the mutation had not been reported outside South America, including in India's neighbouring South-East Asia, or in Africa where malaria is rampant.

Resistance to chloroquine is spreading fast in India — increasing from 30 per cent before 1996 to 91 per cent in 2000-2001, according to studies by IISc and the All India Institute of Medical Sciences in Delhi.

"We need to redefine chloroquine therapy in India," said Padmanabhan.

Nicholas White at the Faculty of Tropical Medicine at Mahidol University in Bangkok agrees. He told delegates at last week's meeting there is increasing criticism of some of the drugs recommended for malaria treatment. Discussing the Roll Back Malaria Initiative, whose goal is to halve the global burden of malaria by 2010, White added: "Things have not been going well. We are using lousy drugs."

The number of children under the age of five dying from malaria has doubled in eastern and southern Africa in the past few years, whereas deaths from other causes are falling. The main problem, said White, was that scientists were wrongly assessing the effectiveness of a potential malaria drug in people after just 14 days instead of waiting for 28 days before testing it.

The World Health Organization now recommends artemisinin — derived from the shrub Chinese wormwood — used in combination with other drugs as a malaria treatment. This approach has halved drug resistance rates in Thailand and increased cure rates in Africa, said White.

Padmanabhan's group has also found that curcumin, a component of the Indian spice turmeric, can reduce the number of chloroquine-resistant parasites. When artemisinin was given in combination with curcumin, a low concentration was enough to kill all resistant parasites.

Padmanabhan suggested that India should consider using a combination of artemisinin with other compounds. Such a combination strategy was also advocated by White who pointed out it was being used to control HIV, tuberculosis and leprosy.

Using a single drug no longer works, he said.

According to the US Centers for Disease Control and Prevention, malaria kills one million people — mostly children — every year. Ninety per cent of malaria deaths are in sub-Saharan Africa.

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