**5. Inherent resistance to antibiotics**

Alterations in the Penicillin binding proteins (Pbp, notable Pbp5) are responsible for the resistance seen against, Ampicillin and the Cephalosporins. In addition, some enterococci also express the beta lactamase enzyme.

They are also inherently resistant to Clindamycin, due to modifying enzymes.

Co-trimoxazole is ineffective due to the ability of enterococci to utilise extracellular folate. Hence it may look susceptible in vitro by disc diffusion.

Aminoglycoside resistance is due to poor uptake or covalent modification by intracellular enzymes which prevent binding to the ribosome. Poor uptake is overcome by combination with a beta lactam antibiotic like Ampicillin or cell wall acting antibiotic like Vancomycin. However, high-level aminoglycoside resistance (HLAR) mediated by aminoglycoside destroying enzymes cannot be overcome by combinations.

*van*C that is inherent in *E. gallinarum* and *E. casseliflavus* is a chromosomally encoded gene cluster, unlike *van*A and *van*B, conferring resistance to Vancomycin.
