Bacterial resistance to antibiotics develops through several mechanisms, driven by genetic mutations and horizontal gene transfer. The main mechanisms include:

1. Mutations: Spontaneous genetic mutations can occur in bacterial DNA, altering the target sites of antibiotics, reducing their binding efficacy, or modifying metabolic pathways to bypass the antibiotic’s effects.

2. Enzyme Production: Bacteria can produce enzymes, such as beta-lactamases, that deactivate antibiotics by breaking down their molecular structure.

3. Efflux Pumps: Some bacteria develop efflux pumps that actively expel antibiotics from their cells, reducing the intracellular concentration of the drug to sub-lethal levels.

4. Altered Permeability: Changes in the bacterial cell membrane or wall can reduce the uptake of antibiotics, limiting their access to target sites.

5. Target Modification: Bacteria can modify the molecular targets of antibiotics, such as ribosomes or enzymes, so that the drugs can no longer bind effectively and exert their effects.

6. Biofilm Formation: Bacteria can form biofilms, complex communities that provide a protective barrier against antibiotics and the immune system, making eradication difficult.

7. Horizontal Gene Transfer: Bacteria can acquire resistance genes from other bacteria through transformation, transduction, or conjugation, spreading resistance traits rapidly within and across species.

These mechanisms collectively enable bacteria to survive antibiotic treatment, necessitating the development of new strategies and drugs to combat bacterial infections.