notypes are prevalent in India (Mishra et al. 2012). Apart from this, mutations at codon 51 and 164 are also responsible for increasing the tolerance of parasite towards the drug (Lumb et al. 2009). Pf showed variable levels of resistant to sulphdoxine with sequence variation in dhps gene at codon S436 to A436, A437 to G437, K540 to E540, A581 to G581 and A613 to S/T613. High frequency of mutation in pfdhps gene was observed in Cor-Nicobar Island (Lumb et al. 2009). In Northeastern region of Indian, where witness of treatment failure in AS+ SP regimen, with high prevalence of mutations in dhps gene at codon 436, 437 and 540 (Mishra et al.,2014). Factors influencing emergence and spread resistant parasite Spread of drug resistance rapidly in area of high transmission intensity of malaria incidence because clonal multiplicity increased the level of sexual recombination. If more than one gene is required to encode drug resistance, then recombination slows the evolution of resistance by breaking apart the resistant gene combinations (Hastings & D’Alessandro, 2000). In malaria endemic areas therapeutic responses vary with age as young children have little or no immunity compared with older children and adults. Immunity is play important role to decreases the chance of an infection becoming patients and also better therapeutic responses for any level of resistance [Hastings & Watkins, 2005]. The mutation rate in parasites have influence of the frequency of emerging drug resistance, higher mutation rates facilitate a faster emergence of resistance. An increased mutation rate is advantageous for the adaptation to quickly changing environments [Hastings & Watkins, 2005]. Mutation was associated with drug resistance often impart a fitness cost, the selective advantage to biological cost arising from the altered function of the mutated protein. Irrational use of antimalarials>