Abstract
The treatment of bacterial illnesses is a complicated task because this mi-cro-organism has the ability to de-velop a wide spectrum of antibiotic resistance and in different mecha-nisms. Antimicrobial drugs are typi-cally categorized according to their primary mode of action, for example β-lactams and glycol-peptide agents may interfere with cell wall synthesis, while macrolides and tetracycline disturb bacterial protein synthesis, another group (fluoroquinolones and rifampin) can inhibit nucleic acid and genetic material synthesis, while inhibition of a metabolic pathway is a mechanism of trimethoprim-sulfamethoxazole agents, interfer-ence with the structure of bacterial membranes and function is a char-acteristics of polymyxins and dap-tomycin. Antibiotic resistance can develop in bacteria in a variety of ways. They may be naturally re-sistant to antimicrobial treatments, or they may be resistant due to ge-netic alterations or the transmission of a resistance allele from another species. The development of efflux-ing systems that prevent the medi-cine from accomplishing its aim in-tracellularly, adapting the medica-tion's area of action, or providing a substitute biosynthetic activity that avoids the drug's effects could all be possible with a new resistant allele. By conjugation, transformation, or transduction, antimicrobial-inclined microorganisms can gain current genetic material from resistant bacte-ria, with transposons commonly as-sisting the inclusion of multiple re-sistance genes into the host's genome or plasmids. Antibacterial therapies provide selection stress, which allows new bacteria to emerge.