Final answer:
Bacteria become resistant to antibiotics through various means such as drug modification or inactivation, target modification, decreased permeability or prevention of cellular uptake, efflux pumps, and the use of alternate metabolic pathways. These mechanisms impair the efficacy of the antibiotic by altering its interaction with the bacterial cell.
Step-by-step explanation:
Antibiotic resistance mechanisms can be broadly categorized into several types:
- Drug Modification or Inactivation: Enzymes produced by bacteria can chemically modify or hydrolyze the antibiotic, as in the case of ß-lactamases breaking the ß-lactam bond in penicillins.
- Target Modification: Bacteria may alter the binding site of antibiotics through mutations or acquisition of alternative binding proteins, thus preventing the drug from interacting effectively.
- Decreased Permeability or Prevention of Cellular Uptake: Alterations in membrane lipids or porins can reduce drug entry into the bacterial cell. Similarly, the thick, waxy cell envelope of Mycobacterium species naturally inhibits antibiotic entry.
- Efflux Pumps: Bacteria may use membrane proteins to expel antibiotics from the cell, sometimes involving multidrug resistance (MDR) efflux pumps.
- Use of Alternate Metabolic Pathways: Bacteria can bypass the metabolic steps inhibited by antibiotics, thus rendering the drugs ineffective.
These resistance mechanisms can be transmitted between bacteria through horizontal gene transfer or may develop through mutation. The emergence of multidrug-resistant pathogens poses a significant challenge in the treatment of infectious diseases.