This study examined the compression of solvated polymer brushes on bioengineered surfaces during the initial stages of Staphylococcus Aureus (S. aureus) adhesion from gentle flow. A series of PEG [poly(ethylene glycol)] brushes, 7 to 17 nm in height and completely non-adhesive to proteins and bacteria, were modified by the incorporation of sparse isolated ~10 nm cationic polymer "patches" at their bases. These nanoscale regions, which lacked PEG tethers, were electrostatically attractive towards negative bacteria or proteins. S. aureus drawn to the interface by multiple adhesive patches compressed the PEG brush in the remaining contact region. The observed onset of bacterial or fibrinogen capture with increases in patch content was compared with calculations. Balancing the attraction energy (proportional to the number of patches engaging a bacterium during capture) against steric forces (calculated using the Alexander-DeGennes treatment) provided perspective on the brush compression. The results were consistent with a bacteria-surface gap on the order of the Debye length in these studies. In this limit of strong brush compression, structural features (height, persistence length) of the brush were unimportant so that osmotic pressure dominated the steric repulsion. Thus, the dominant factor for bacterial repulsion was the mass of PEG in the brush. This result explains empirical reports in the literature that identify the total PEG content of a brush as a criteria for prevention of bioadhesion, independent of tether length and spacing, within a reasonable range for those parameters. Bacterial capture was also compared to that of protein capture. It was found, surprisingly, that the patchy brushes were more protein-than bacteria-resistant. S. aureus adhesion driven by patches within otherwise protein-resistant PEG brushes was explained by the bacteria's greater tendency to compress large areas of brush to interact with many patches. By contrast, proteins are thought to penetrate the brush at a few sites of PEO-free patches. The finding provides a mechanism for the literature reports that in-vitro protein resistance is a poor predictor of in-vitro implant failure related to cell-surface adhesion.