Haemophilus influenzae responds to the stresses it encounters in the host by utilizing specialised pathways and these define the cell and bacterial lifestyle. We have recently reported that this pathogen harbours a unique nickel uptake system (nikKLMQO-nimR). Unusually, the disruption of the nickel uptake system (nikQ or nimR mutants) resulted in cells that aggregated and formed an increased biofilm compared to the wild type cells. The nikQ mutant also had increased sensitivity to numerous chemical and physical stresses. Using a gloA mutant strain and urease-specific inhibitor we showed that this phenotype is not due to the loss-of-function of these enzymes; there are global effects related to nickel. The nikQ mutant was unable to accumulate nickel but the addition of excess nickel did restore intracellular nickel levels and this resulted in the nikQ mutant returning to the wild type “free-living” phenotype. We used a range of techniques that have shown that the nikQ mutant possesses changes to its cell surface properties. The mutant was more negatively charged than wild type cells as well as being more hydrophobic. We have performed mRNA sequencing with wild type and nikQ mutant cells to define the transcriptomes in these cells. Although the nikQ mutant appears to grow the same as its wild type cell we have shown that there is a change in the “lifestyle” of these nickel limited cells and this induces changes to the surface of the cell to promote cell-cell aggregation and biofilm formation.