Abstract:
Plasmodium falciparum has successfully developed resistance to almost all currently used antimalarials.
A single nucleotide polymorphism in the P. falciparum chloroquine resistance transporter (Pfcrt) gene at
position 76 resulting in a change in coding from lysine to threonine (K76T) has been implicated to be the
corner stone of chloroquine resistance. Widespread resistance to chloroquine in endemic regions led to
its replacement with other antimalarials. In some areas this replacement resulted in a reversion of the
mutant T76 allele to the wild-type K76 allele. This study was conducted to determine the prevalence of the
K76T mutation of the Pfcrt gene eight years after the ban on chloroquine sales and use. A cross-sectional
study was conducted in 6 regional hospitals in Ghana. PCR-RFLP was used to analyse samples collected
to determine the prevalence of Pfcrt K76T mutation. Of the 1318 participants recruited for this study,
246 were found to harbour the P. falciparum parasites, of which 60.98% (150/246) showed symptoms for
malaria. The prevalence of the Pfcrt T76 mutant allele was 58.54% (144/246) and that of the K76 wild-type
allele was 41.46% (102/246). No difference of statistical significance was observed in the distribution of
the alleles in the symptomatic and asymptomatic participants (P = 0.632). No significant association was,
again, observed between the alleles and parasite density (P = 0.314), as well as between the alleles and
Hb levels of the participants (P = 0.254). Notwithstanding the decline in the prevalence of the Pfcrt T76
mutation since the antimalarial policy change in 2004, the 58.54% prevalence recorded in this study is
considered high after eight years of the abolishment of chloroquine usage in Ghana. This is in contrast to
findings from other endemic areas where the mutant allele significantly reduced in the population after
a reduction chloroquine use.
