Supplemental Readings and References
hydrolyzes the lactam ring of penicillin and inactivates its
therapeutic effect. In addition, highly ^-lactam-resistant
enterococcal bacteria strains may overexpress penicillin-
binding proteins and/or reduce their affinity to /f-lactam
antibiotics. Resistance to vancomycin may be more diffi-
cult to achieve because it involves binding of the bulky in-
hibitor to substrate outside the membrane so that the active
sites of two enzymes cannot align themselves correctly. It
has been found that enterococci can express an inducible
resistance to high levels of the glycopeptides vancomycin
and teicoplanin. This resistance is due mainly to synthesis
of altered peptide sequences that reduce vancomycin affin-
ity. Because /3-lactam antibiotics, such as penicillin, also
trigger the production of autolytic enzymes that degrade
the peptidoglycan, another option is to treat with com-
binations of drugs; the /3-lactam antibiotics can weaken
the cell wall and provide “holes” for the entry of other
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