What causes antibiotic resistance in common bacterial infections?

Short answer: antibiotic resistance arises when bacteria acquire or develop traits that let them survive exposure to antibiotics. Those traits come from random mutation or from receiving resistance genes from other bacteria, and antibiotic use creates strong selection that lets resistant strains multiply and spread.

More detail — what causes resistance
- Natural mutation + selection: bacteria randomly mutate; when antibiotics are present, susceptible cells die and resistant mutants survive and multiply.
- Horizontal gene transfer: resistance genes move between bacteria by
- conjugation (transfer of plasmids),
- transduction (bacteriophages),
- transformation (uptake of free DNA).
Many clinically important resistance genes are carried on mobile plasmids or transposons.
- Overuse and misuse of antibiotics:
- unnecessary prescriptions (e.g., for viral infections),
- too broad-spectrum drugs when a narrow agent would do,
- wrong dose or too short/too long courses,
- not finishing prescribed courses (which can favor selection of resistant survivors).
- Agricultural and environmental use: routine antibiotic use in livestock and aquaculture and release of antibiotics into the environment select for resistant bacteria that can transfer to people.
- Poor infection control and sanitation: allows spread of resistant strains in hospitals and communities.
- Lack of rapid diagnostics: empirical broad use while waiting for test results increases selection.
- Limited development of new antibiotics: reduces treatment options for resistant infections.

How bacteria resist antibiotics (mechanisms)
- Enzymatic drug inactivation (e.g., beta-lactamases that destroy penicillins/cephalosporins).
- Alteration of the antibiotic target (e.g., mecA gene in MRSA produces altered PBP2a; mutations in ribosomal proteins or DNA gyrase).
- Reduced drug uptake or increased efflux (porin loss, efflux pumps).
- Biofilm formation: communities embedded in a matrix that limit antibiotic penetration and slow growth.
- Metabolic changes or bypass pathways that make the drug ineffective.

Examples in common infections
- Urinary tract infections (E. coli): increasing rates of extended-spectrum beta-lactamases (ESBLs) and plasmid-mediated resistance to fluoroquinolones, trimethoprim-sulfamethoxazole.
- Respiratory infections (Streptococcus pneumoniae): altered penicillin-binding proteins causing penicillin and some cephalosporin resistance; macrolide resistance via methylation of ribosomal targets or efflux pumps.
- Skin and soft tissue (Staphylococcus aureus): MRSA has mecA-mediated resistance to nearly all beta-lactams; some strains have additional resistance to macrolides, tetracyclines, etc.
- Gonorrhea (Neisseria gonorrhoeae): accumulated mutations and plasmid-mediated enzymes causing resistance to penicillins, tetracyclines, fluoroquinolones, and reduced susceptibility to extended-spectrum cephalosporins.
- Tuberculosis (Mycobacterium tuberculosis): resistance usually from chromosomal mutations selected during inadequate or incomplete therapy (multidrug-resistant TB, extensively drug-resistant TB).

What helps prevent/slow resistance
- Appropriate prescribing: only when needed, using narrow-spectrum agents guided by culture when possible.
- Stewardship programs in hospitals and clinics to optimize antibiotic choice, dose, and duration.
- Patient adherence: take antibiotics exactly as prescribed; do not share or save antibiotics.
- Vaccination, hygiene, and infection control to reduce infections and antibiotic use.
- Reducing non-therapeutic antibiotic use in agriculture.
- Improved rapid diagnostics and surveillance to detect resistance early.
- Research and incentives for new antibiotics and alternative therapies.

Takeaway: resistance is driven by bacterial evolution plus human practices (overuse, misuse, spread). Reducing unnecessary antibiotic exposure, improving infection control, and better diagnostics/stewardship are the main ways to limit it.