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Twin tests for malaria control

- Scan on mutations, absence of symptoms

New Delhi, Feb. 24: Novel genetic mutations in malaria parasites and an infected population without symptoms observed for the first time in Bengal may hamper efforts to control a lethal form of malaria, researchers have said.

The genetic mutations appear linked to drug resistance in malaria parasites and highlight the need to revise the existing primary treatment strategy, said scientists at Vidyasagar University, Midnapore, who spotted the mutations have.

In an independent study, researchers at the Calcutta School of Tropical Medicine have detected a tribal population in Purulia district infected with the malaria parasite, Plasmodium falciparum, but without any symptoms whatsoever of the disease.

While doctors have sporadically reported cases of such asymptomatic infections earlier from states with high malaria prevalence, such as Chhattisgarh, Jharkhand and Orissa, scientists say this is the first report from Bengal.

“Asymptomatic infected persons remain a hidden reservoir of the parasite,” said Swagata Ganguly, a medical researcher and a member of the CSTM team. “They don’t seek treatment and facilitate transmission of the parasite.”

The CSTM team led by Ardhendu Maji examined about 1,040 members of a tribal population in a forested area of Purulia in June 2012 and found that about eight per cent of the population had Plasmodium falciparum without symptoms. The findings are published this week in the Journal of Clinical Microbiology. Maji said the CSTM hopes to conduct similar studies in other parts of Bengal.

The findings come at a time when Vidyasagar University microbiologists have reported what they say are novel mutations in the parasite that seem associated with resistance to sulfadoxine and pyrimethamine, a drug combination used to treat malaria.

Their study suggests that a mutation in a gene called dhfr is associated with the parasite’s resistance to pyrimethamine, and a set of quadruple mutations — at four points on the parasite’s genome — in another gene called dhps seem strongly linked to resistance to sulfadoxine. Their study is also published this week in the International Journal of Antimicrobial Agents.

“The parasite is changing — it is quickly adapting to our medicines,” said Amiya Kumar Hati, a medical entomologist and former director of the CSTM who has collaborated with the Midnapore team.

India’s malaria control programme had recommended in 2009 the use of a combination of drugs — artemisinin with sulfadoxine and pyrimethamine — to treat malaria caused by Plasmodium falciparum, the most dangerous of malaria parasites.

The decision to introduce this artemisinin-combination therapy (ACT) was taken amid concerns about the emergence of Plasmodium falciparum parasites resistant to the standard anti-malarial drug, chloroquine, used for decades earlier.

The new results signalling the emergence of mutations associated with resistance to sulfadoxine and pyrimethamine imply that the government should reconsider the current ACT policy in some regions, Hati told The Telegraph.

The studies led by Somenath Roy, professor of physiology at Vidyasagar University, were aimed at understanding the genetic mechanisms underlying parasite resistance to chloroquine and sulfadoxine and pyrimethamine.

Roy and his colleagues isolated Plasmodium falciparum from dozens of patients with malaria from Calcutta and Purulia and examined the parasite’s genetic material. They found that mutations in dhfr and dhps were linked to resistance and treatment failure.

“The results suggest that artemisinin should be used in combination with drugs different from sulfadoxine and pyrimethamine,” said Sabyasachi Das, a research scholar at Vidyasagar University.

India’s malaria control programme estimates that some 1.5 million persons fall ill with malaria each year, and nearly 50 per cent of these infections are caused by Plasmodium falciparum, most of them in eastern India. This parasite has the ability to cause life-threatening complications that involve the brain.

Drug resistant parasites and asymptomatic infections both represent a challenge to malaria control, Maji said. Scientists still do not understand the exact mechanisms that prevent some infected persons from showing symptoms.

“It has something to do with the (host) immunity,” Ganguly said. “This should be investigated in detail.”

The Vidyasagar scientists have also found that genetic mutations underlying resistance appear to vary from place to place. Studies in the past have indicated that Plasmodium falciparum’s resistance to chloroquine across the country emerges from a mutation in a gene called Pfcrt.

But the Vidyasagar researchers have discovered that while chloroquine resistance in Calcutta appears linked to Pfcrt, chloroquine resistance in Purulia is associated with a mutation in another gene called Pfmdr1. This study has been accepted for publication in the

The Vidyasagar scientists have also found that genetic mutations underlying resistance appear to vary from place to place. Studies in the past have indicated that Plasmodium falciparum’s resistance to chloroquine across the country emerges from a mutation in a gene called Pfcrt.

But the Vidyasagar researchers have discovered that while chloroquine resistance in Calcutta appears linked to Pfcrt, chloroquine resistance in Purulia is associated with a mutation in another gene called Pfmdr1. This study has been accepted for publication in the American Journal of Tropical Medicine and Hygiene.

“The Pfmdr1 has been observed earlier in Madagascar,” Das said. The researchers believe the different mutations emerge from differences in the drugs used in the two sites. “The anti-malarial drugs in Calcutta have changed over the year, new drugs introduced every five or ten years,” said Roy. “But in Purulia, chloroquine has been the main drug for decades.”