For example, in E. coli or S. aureus, rifampin resistance is mediated by a chromosomal mutation in the structural gene for the RNA group such that it no longer effectively binds rifampin. Parallel chromosomal mutations are responsible for pneumococci developing resistance to penicillin and the sulfonamides, as well as streptomycin resistance in the enterococci and gram-negative resistance to fluoroquinolones. If this genetic material includes a gene for resistance, a newly infected bacterial cell may become resistant to a drug and be capable of passing the trait of resistance on to its offspring. Transduction is particularly important in the transfer of antibiotic resistance among strains of S. aureus, where some bacteriophages can carry plasmids that code for penicillinase. This confers resistance to similar macrolide antibiotics in succeeding generations of the bacteria.
Transformation involves incorporating DNA that is roaming free in the environment into bacteria.
Some bacterial cells are capable of excreting transforming DNA during certain phases of growth. Conjugation, the passage of genes from cell to cell by direct contact through a sex pilus or bridge, is an extremely important mechanism for the spread of antibiotic resistance, particularly since DNA that codes for resistance to multiple drugs is transferred via this method. The transferable genetic material consists of two different sets of DNA sequences contained in plasmids. The first set of sequences codes for the actual resistance and is termed the R-determinant plasmid. The second plasmid, termed the resistance transfer factor or RTF, contains the information needed for bacterial conjugation to occur.