Is Russellâs argument for the view that our ideas are vague and confused acceptable?
Sample Solution
ccording to WHO, resistance to antimalarial drugs can be defined as âthe ability of a parasite strain to survive and/or to multiply despite the administration and absorption of a drug given in doses equal to, or higher than, those usually recommended, but within the limits of tolerance of the subjectâ (WHO). Chloroquine CQ resistance is associated with a decrease accumulation of CQ concentration in the food vacuole of parasites, which is the site of action for C (Fidock et al., 2000.). The substitution of lysine to threonine (K76T) at codon 76 of the pfcrt gene is associated with in vivo and in vitro CQ resistance in Africa, South America, and Southeast Asia (Anvikar et al., 2012; Garcia et al., 2004; Ojurongbe. et al., 2007). Sulphadoxine-pyrimethamine(SP) SDX and PYR is inhibiting to the DHPS and DHFR enzymes, respectively, specific point mutations in Pfdhps & Pfdhfr gene encoding these enzymes lead to a lower binding affinity for sulphadoxine-pyrimethamine drugs. High frequency of mutations in codon S108N followed by codon C59R and double mutant (S108N+C59R) genotypes 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 & DâAlessandro, 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 >
ccording to WHO, resistance to antimalarial drugs can be defined as âthe ability of a parasite strain to survive and/or to multiply despite the administration and absorption of a drug given in doses equal to, or higher than, those usually recommended, but within the limits of tolerance of the subjectâ (WHO). Chloroquine CQ resistance is associated with a decrease accumulation of CQ concentration in the food vacuole of parasites, which is the site of action for C (Fidock et al., 2000.). The substitution of lysine to threonine (K76T) at codon 76 of the pfcrt gene is associated with in vivo and in vitro CQ resistance in Africa, South America, and Southeast Asia (Anvikar et al., 2012; Garcia et al., 2004; Ojurongbe. et al., 2007). Sulphadoxine-pyrimethamine(SP) SDX and PYR is inhibiting to the DHPS and DHFR enzymes, respectively, specific point mutations in Pfdhps & Pfdhfr gene encoding these enzymes lead to a lower binding affinity for sulphadoxine-pyrimethamine drugs. High frequency of mutations in codon S108N followed by codon C59R and double mutant (S108N+C59R) genotypes 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 & DâAlessandro, 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 >
