The genetic determinants of antibiotic resistance originate as a result of random events, affected only by those physical and chemical agents that stimulate mutation. It is the selection and spread, within and between species, of new genetic material that is influenced by environmental factors, though the intrinsic antibiotic resistance of many opportunistic pathogens remains to be explained.

Depending on the frequency of genetic change, the biochemical resistance mechanism, the efficiency of selection (including access of antibiotic to relevant bacteria), and the opportunity for person-to-person spread, resistance may present in a number of ways. The use of an antibiotic in any individual may give rise to resistance, among pathogens or normal flora, to that antibiotic alone, to some or all members of its class, or to additional unrelated antibacterials, or to the acquisition of new bacteria, from a variety of sources (humans, animals, inanimate environment). A resistant organism may occasionally have other advantages that enable it to spread in the absence of the initial selective agents.

In the absence of controlled experiments, which are difficult or perhaps impossible, the only evidence of the truth of these hypotheses comes from the clinical use of antibiotics. A wise observer will conclude that the emergence of resistance is a rare event in an individual patient, but is commoner but by no means universal in populations, especially those that are closed. He will note the reports of diminished resistance in the presence of increased usage.

The role of academic infection control is to explain all the phenomena observed, and to formulate methods for identifying and countering the actual as opposed to the imagined hazards.