Frontline anti-malaria drugs are failing and
the rapid decline in their effectiveness is directly linked to increasing
parasite mutations, a study released this week has found.
The
mutations to a specific parasite gene, which is particularly prevalent along
the Myanmar-Thailand border, may be responsible for the area’s spike in
drug-resistant strains, according to the 10-year study by the Shoklo Malaria
Research Unit and the Mahidol-Oxford Tropical Medicine Research Unit (MORU).
Researchers
have long known that artemisinin, a Chinese herb derivative used to combat
malaria, was facing growing resistance. But now partner drugs used in
combination treatments are likewise proving impotent.
“This
study demonstrates for the first time that artemisinin resistance leads to
failure of the artemesinin partner drug, in this case, mefloquine. This means
that the first-line artemisinin combination therapy [ACT] introduced here in
1994 has finally fallen to resistance,” said professor Francois Nosten,
director of the Shoklo unit.
In 2003,
100 percent of the malaria patients in the study, conducted at clinics on the
Myanmar-Thailand border, were cured when they took MAS3, a combination of drugs
that had been highly effective in treating the mosquito-borne infectious
disease since it was introduced in 1994.
By 2013,
the drug worked for only 81.1pc of the study’s participants.
The study
was focused on one of the most common types of malaria, called P falciparum.
Over the span of the study, researchers found a more than 12-fold increase in
the percentage of malaria cases that included the genetic mutation K13, which
is more common along that border.
In 2003,
when the drugs were still highly effective, only 6.7 percent of the cases
contained a K13 mutation. But by 2013, 83.4pc of the cases included the
mutation.
This,
combined with a doubling of instances of a more universal mutation, is believed
to be what caused the drug’s declining effectiveness.
When the
K13 mutation is present, the drugs fail more frequently. The same is true of
another mutation, Pfmdr. But when both mutations are present, the negative
effects are multiplied, rather than added.
“Synergy
between these two resistance determinants may help to explain why failure rate
declined precipitously in 2009,” the authors wrote.
The
connection between the appearance of K13 mutations and a strain’s resistance to
artemisinin-based combination treatments, like MAS3, has been alluded to in
past studies but, the MORU authors wrote, the link was not “clearly
established” and some contested the claim.
“This
uncertainty may have contributed to the failure to contain artemisinin
resistance in the greater Mekong area,” the authors wrote in the study.
Malaria
has been adapting to drugs in the area of the Myanmar-Thailand border for
decades. The MAS3 treatment was itself a replacement for a previous drug that
had lost its potency.
The
treatment has had a much longer run than many of its predecessors but the
authors warned that, as MAS3’s effectiveness declines, help, in the form of a
new drug, is not on the way any time soon.
The
spread of the strain needs to be stopped in the region, they said, with
elimination the only option unless new treatments are made immediately
available.
“Alternatives
are needed desperately,” they wrote. “With new antimalarials still years from
deployment, there is an urgent need to eliminate P falciparum from the area
before the recent and substantial gains in malaria control are reversed.”
Reported
deaths related to malaria have declined drastically over the last decade and a
half in Myanmar, according to the World Health Organization.
In the
year 2000, there were more than 2700 reported deaths related to the disease. By
2014 that number was down to 92, though WHO has warned that these totals are
often underreported.
According
to the WHO, Myanmar had 152,195 reported cases of malaria last year.
In 2015,
31.8 million Myanmar people, more than half the population, were at risk for
malaria, and 8.4 million were at high risk.
Dave
Simpson
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