Not true about bacterial drug resistance mechanism:
High-Yield Explanation
Complete removal of target is cause of resistance to Vancomycin is not true. There is alteration of the target site, and not complete removal. Drug Resistance Option a Most common mechanism of resistance: b-lactamase enzymes are capable of hydrolysing the b-lactam rings. Option b If resistance is chromosomally mediated, it is usually transferred veically from parent to daughter bacteria. If resistance is plasmid mediated, it is usually transferred by horizontal route mainly by conjugation. Option c Penicillin-resistant pneumococcal strains: Resistance to penicillin and other beta-lactam antibiotics is not mediated by production of beta-lactamase enzymes, but is due to the modifications of proteins, such as penicillin-binding proteins (PBPs) found on the cell wall. These penicillin-resistant strains are also resistant to multiple drugs, such as cefotaxime, ceftriaxone, erythromycin, tetracycline, macrolides, and trimethoprim-sulfamethoxazole (TMP-SMX). Resistance is seen most often in S. pneumoniae serotypes 6, 9, 14, 19, and 23. Option d Vancomycin resistant Enterococcus (VRE): VRE is mediated by van gene, which alters the target site for vancomycin present in cell wall. D-alanyl-D-alanine side chain of peptidoglycan layer is altered to D-alanyl-D-serine or D-alanyl-D-lactate. This altered side chains have very less affinity for binding to vancomycin.