Antibiotics

1. Meaning, discovery and public-health importance

Antibiotics are antibacterial medicines that kill bacteria or inhibit their growth. Historically, the term referred to substances produced by microorganisms that inhibited other microorganisms. In present clinical usage, it also covers semisynthetic and synthetic antibacterial medicines. Penicillin originated from a Penicillium mould; several other antibiotics, including streptomycin, were discovered from soil microorganisms. Antibiotics are therefore not necessarily plant products or entirely artificial chemicals.

In 1928, Alexander Fleming observed that a mould contaminating a culture plate inhibited nearby staphylococcal bacteria. Howard Florey, Ernst Boris Chain and collaborators subsequently developed penicillin for therapeutic use. Fleming, Chain and Florey received the 1945 Nobel Prize in Physiology or Medicine. Large-scale antibiotic production transformed the management of previously life-threatening bacterial infections.

Antibiotics also make modern medical procedures safer: surgery, organ transplantation, cancer chemotherapy and intensive care depend on effective infection prevention and treatment. However, they do not cure influenza, dengue, measles or other viral diseases. A clinician may prescribe an antibiotic for a secondary bacterial infection accompanying a viral illness, not to eliminate the virus itself.

2. How antibiotics work and how they are classified

Selective toxicity is the central principle of antibiotic action: the medicine targets features of bacteria that are absent from, or sufficiently different in, human cells. Penicillins and cephalosporins interfere with bacterial peptidoglycan cell-wall synthesis. Human cells lack this wall. Tetracyclines and aminoglycosides act on the bacterial 30S ribosomal subunit, while macrolides act on the 50S subunit, inhibiting protein synthesis.

Fluoroquinolones interfere with bacterial DNA gyrase or topoisomerase IV, enzymes needed for DNA functioning. Rifampicin inhibits bacterial RNA polymerase. Sulfonamides and trimethoprim block different steps in folate metabolism. Polymyxins damage bacterial membranes. These distinct targets explain why one antibiotic cannot be assumed effective against every bacterial species.

Bactericidal antibiotics kill susceptible bacteria, whereas bacteriostatic antibiotics inhibit their growth and allow host defences to help clear infection. This distinction depends partly on the organism, drug concentration and clinical setting. Narrow-spectrum medicines act against a relatively restricted range of bacteria; broad-spectrum medicines cover a wider range. Broad-spectrum does not mean universally stronger or preferable: unnecessary use can disrupt beneficial microbiota and select resistance.

3. Appropriate use, diagnosis and safety

Treatment depends on the likely pathogen, infection site, severity, local resistance patterns and patient characteristics. Where feasible, samples such as blood or urine are collected for culture before treatment begins. Antimicrobial susceptibility testing helps identify which medicines are likely to work. In serious infections, treatment should not be dangerously delayed while awaiting results.

Empirical therapy begins before the causative organism is fully identified, using clinical evidence and local guidance. Once laboratory findings become available, treatment may be narrowed or otherwise adjusted; this is called de-escalation. Prophylactic antibiotics can prevent infection in selected circumstances, such as certain operations, but should not become routine prolonged medication.

Patients should avoid self-medication, sharing medicines and using leftover prescriptions. They should follow the prescribed dose and duration and seek reassessment if symptoms worsen or adverse reactions occur. Potential harms include allergy, organ-specific toxicity, interactions and antibiotic-associated diarrhoea. Destruction of normal gut microbiota can facilitate Clostridioides difficile infection. Antibiotic stewardship means optimising selection, dose, route and duration—not simply reducing all antibiotic use.

4. Antibiotic resistance: evolution and transmission

Resistance is the ability of bacteria to survive or multiply despite an antibiotic that would normally inhibit them. It may be intrinsic to a species or acquired through mutation and gene transfer. Antibiotic exposure creates selection pressure: susceptible bacteria are suppressed while resistant variants can survive and spread. The human body itself does not become antibiotic-resistant.

Bacteria exchange resistance genes through conjugation, often involving plasmids; transformation, involving uptake of free DNA; and transduction, mediated by bacteriophages. Resistance mechanisms include enzymes that destroy drugs, modification of drug targets, reduced drug entry and efflux pumps that expel antibiotics. Beta-lactamases, including some carbapenemases, illustrate enzymatic resistance.

Misuse and overuse accelerate selection, while inadequate sanitation, unsafe water and poor infection control facilitate transmission. Additional drivers include inappropriate veterinary use, substandard medicines, weak diagnostics and poorly managed waste. Resistant infections can cause treatment failure, longer hospital stays, higher costs and mortality. Multidrug-resistant tuberculosis is resistant to at least isoniazid and rifampicin, two important first-line anti-tuberculosis medicines.

5. One Health and the Indian policy response

One Health recognises connections among human, animal and environmental health. Resistant organisms and resistance genes can move between hospitals, households, farms, food systems and water bodies. Consequently, hospital prescribing reforms alone are insufficient. Safe drinking water, sanitation, hand hygiene, vaccination, biosecurity on farms and responsible waste treatment reduce infections and the need for antibiotics.

India launched its National Action Plan on Antimicrobial Resistance in 2017. Its priorities include awareness, surveillance, infection prevention, optimised antimicrobial use, research and coordinated action. The Indian Council of Medical Research’s Antimicrobial Resistance Surveillance and Research Network monitors resistance in clinically important pathogens. The National Centre for Disease Control also coordinates an AMR surveillance network and containment activities.

Under the Drugs and Cosmetics Rules, Schedule H1 imposes additional controls on listed medicines, including specified antibiotics and anti-tuberculosis drugs. Retail supply requires a registered medical practitioner’s prescription, and specified sale records must be maintained for three years. Red-line marking on designated prescription medicines supports awareness against unsupervised use. In 2019, India prohibited colistin and its formulations for food-producing animals, poultry, aquaculture and animal-feed supplements, reflecting concern over resistance to an important last-resort antibiotic.

6. Global frameworks and examination distinctions

WHO’s AWaRe classification supports antibiotic stewardship. Access antibiotics generally have lower resistance potential and are recommended for many common infections. Watch antibiotics have higher resistance potential and require closer monitoring. Reserve antibiotics are intended for selected infections involving highly resistant bacteria when suitable alternatives are unavailable. These are stewardship categories, not a ranking of simple potency.

The World Health Assembly adopted the Global Action Plan on Antimicrobial Resistance in 2015. WHO’s Global Antimicrobial Resistance and Use Surveillance System, GLASS, supports comparable surveillance. WHO, FAO, UNEP and the World Organisation for Animal Health cooperate through the One Health Quadripartite. Effective policy must balance restricting unnecessary use with ensuring timely access to quality-assured treatment.

• Vaccines prevent specific infections; antibiotics treat susceptible bacterial infections.
• Antiseptics act on living tissues; disinfectants are generally used on inanimate surfaces.
• Resistance and tolerance are not identical: tolerance involves surviving exposure without necessarily increasing the concentration needed to inhibit growth.

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