Resistance against the frontline antimalarial, artemisinin, is mediated by mutations of the Kelch 13 (K13) gene. K13 is involved in the formation of the cytostome; the apparatus which brings haemoglobin from the host red blood cell into the Plasmodium parasite. Haemoglobin digestion supplies essential amino acids for parasite growth and releases haem which is required for the activation of artemisinin. Parasites expressing mutant K13 have a slowed rate of parasite feeding which is characterised by a reduction in haem biosynthesis and delayed growth. This reduced level of haem leads to less artemisinin activation, resulting in less parasite death. However, the mechanisms as to how mutation of K13 causes this slowed feeding phenotype remains unclear. We hypothesise that mutation of K13 reduces its stability and abundance, affecting the rate at which new cytostomes are formed and thus parasite feeding. Using expansion microscopy, we have resolved K13 as ring-shaped structures that localise to the periphery of the parasite. We performed expansion microscopy at various timepoints throughout the asexual life cycle and compared the morphology and number of K13 rings present in the mutant vs WT. We found that K13 mutant parasites formed new K13 rings at a slower rate than the wild type. Some K13 mutants also appeared to form cytostomes that were not regulated by a cytostomal ring. These data provide a potential mechanism linking the artemisinin resistance mutations to reduced rate of haemoglobin uptake.