The mechanism by which MRSA has evolved from Staph. aureus could be described as adding "information" to the genome, depending on how you define "information".
The mechanism is that an alternative penicillin binding protein (PBP2a), is produced in addition to the usual penicillin binding proteins. The protein is encoded by the mecA gene, and because PBP2a is not inhibited by antibiotics such as flucloxacillin the cell continues to synthesise peptidoglycan and hence has a structurally sound cell wall.
Note that there is no loss of function, no loss of information. The opposite is true: the bacterium has evolved the ability to survive flucloxacillin therapy, by acquiring a new gene (extra "information").