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The gastric disease causing bacteria, Helicobacter pylori utilize flagella driven motility and chemotaxis to detect external signals as they swim away from acid to cross the mucus layer and colonize the epithelial surface of the stomach. The lack of the chemotaxis regulator protein ChePep leads to increased reversal frequency (Howitt et al²). We analyze translational and cell body rotational motility data obtained by phase contrast microscopy to compare the speed and turn angle distribution of the wild type (WT) with the ΔChePep mutant and compare with run-reversal-reorient model and Resistive Force Theory calculations of torque. We observe higher reversal frequency of ΔChePep in agreement with previous observation, however the cell body rotational rate and torque are not influenced by the lack of protein ChePep. Interestingly, both WT and ΔChePep are most likely to maintain their initial run speed after a reorientation or a reversal event, although the distribution of the change in speed indicates that large speed changes by factor of two and beyond are possible.