Modified drug target site: This is a common drug-resistant mechanism and occurs due to spontaneous mutation of bacterial genes and selection in the presence of antibiotics. They can also occur due to enzymatic modification or by replacement of the original target. For instance, modifications in bacterial RNA polymerase and DNA gyrase result in resistance to the rifamycins and quinolones, respectively. Similarly, vancomycin-resistant bacteria typically acquire resistance through modification of the drug's target site in bacterial cell walls, resulting in a reduction in the binding affinity of vancomycin, making it less efficient in disrupting cell walls. Target amplification: It involves increasing the production of target molecules that the antibiotic acts upon. It can be observed in the case of resistance to trimethoprim-sulfamethoxazole (TMP-SMX) due to mutations that can lead to an increase in the production of dihydrofolate reductasedrug target of trimethoprim. Enzymatic degradation/modification: Bacteria produce enzymes that can degrade antibiotics by modifying their structure (mostly through redox reactions or group transfer). For instance, ßlactamases are a group of enzymes that deactivate ß-lactam antibiotics by hydrolyzing the ßlactam ring. ß-lactamases are mostly present in Gram-negative bacteria and a few Grampositive ones such as Staphylococcus aureus, Enterococcus faecalis, etc. In P. aeruginosa beta-lactamases are present in their periplasmic spaces. Carbapenem-resistant Enterobacteriaceae (CRE) possess metallo-beta-lactamases such as New Dehli metallo-betalactamase-1, Klebsiella pneumoniae carbapenemase-2, and other metallo-beta-lactamases encoded by genes such as bla(NDM-1), bla(KPC), bla(IMP), and bla(CMY). Carbapenemresistant Enterobacteriaceae are resistant not only to penicillins and cephalosporins but also to carbapenems, making them a serious global health threat. In certain bacterial species, one or combinations of these factors play a role in developing resistance. For instance, A. baumannii is resistant to carbapenems owing to a combination of decreased expression of porins, increased expression of three RND-type efflux pumps, and the presence of ß-lactamases. Apart from resistance, certain bacteria also show 'tolerance' which is the ability of bacterial cells to withstand antibiotics due to them being in a physiological state of dormancy or slow growth. In addition, certain sub-populations of bacteria, known as 'persisters' are non-growing and transiently tolerate antibiotic treatment. Persistent bacteria are often linked to chronic bacterial infections. Some other mechanisms are used by bacteria to exhibit tolerance and virulence such as biofilm formation, endospores, adopting certain morphologies such as filamentous and L-form (cell wall deficient bacteria), using survival techniques such as quorum sensing, having secretory proteins and toxins such as type III secretion systems (T3SS), siderophores among others.