Drug resistance in plasmodium species
has seriously hampered the successful treatment of malaria. The progressive
increase in the degree and distribution of resistance to chlroquine by P. falciparum has led to recent
increases in malaria morbidity and mortality in poor endemic countries (Trigg
and Kondrachine, 1998).Resistance to chloroquine and amodiaquine have been
reported in almost all geographical areas where malaria is endemic (Winstanley,
1990).
Resistance to antifolate combinations in
Africa is less common, but is now developing rapidly. It is common both in
South-East Asia and South America. Resistance to quinine is uncommon in both
Africa and South America, but increasingly recognized in parts of south Asia
(Adepoju-Bello and Ogbeche, 2003).
In parts of South Asia, resistance to mefloquine
and halofantrine has been reported. However, this is uncommon in other endemic
areas. Resistance to atovaquone-proguanil, a new formula, has not been reported
(Winstanley, 1990). Also Eckstein-Ludwig (2003) has reported a possible
development of resistance to the new and efficacious artemisinin based
combination by malaria parasite. This resistance can be produced by the
mutation of SERCA, a calcium pump in the endoplasmic reticulum of the parasite
(Eckstein-Ludwig et al., 2003).
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