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is significantly higher in 2007 than in 2001 for Gem and Karemo areas, whereas in Asembo, the prevalence of parasitaemia was same in 2007 and 2001. Only ITNs were distributed during the mass campaigns between 2004 and 2006 and the increase in parasitaemia prevalence could be caused by two factors: (i) the change in population density of the area as a result of different interventions during the study period, (ii) a possible deteriorating performance of the nets in preventing human-vector contact. To further understand the changes in malaria transmission dynamics due to interventions, the parasite population size and its association with increased morbidity needs to be examined. In the malaria endemic area, the potential role of insecticide resistance is a major threat to malaria control efforts. Malaria is the leading cause of outpatient consultations in Kenya, accounting for 43% of outpatient hospital consultations and 56% of hospital admissions in 2007 [54]. In 2007, 9% of outpatient consultations and 15% of hospital admissions were due to malaria. Prior to 2007, the WHO-recommended first-line anti-malarial treatment in Kenya was chloroquine, which has been slowly replaced by artemisinin-based combination therapies (ACTs) [9]. Standardised, reliable estimates of the prevalence of artemisinin resistance would offer a useful starting point to investigate the possible association of parasite resistance with patient health outcomes. To date, some evidence of reduced susceptibility to artemisinin has been detected. However, the association between the polymorphisms in the artemisinin resistance loci and parasite resistance to artemisinin has not been determined in Kenya. Artemisinin resistance is associated with the loss of Dd2 D1046Y marker and the appearance of the K1276Y marker [55,56] and both markers are found in the Cromer region [57]. In this study, the K76Y mutation was detected in the 2007 population that was tested, suggesting a possible selection pressure on the parasite population as a result of massive distribution of ITNs. Although no genetic polymorphism on P450 is documented in pfmdr1 to date, a K268N polymorphism related to inducible pfmdr1 mutations, which leads to cross-resistance with chloroquine [58] was detected in the same 2007 population. The high prevalence of parasites carrying K268N suggests that enforcement of the malaria treatment policy change to ACTs may be warranted as parents report that their children have recovered from clinical malaria episodes with only ACTs. d2c66b5586