Antibiotics vs antivirals; resistance (overview) - Biology IGCSE Study Notes

Antibiotics are medicines that kill or inhibit the growth of bacteria by targeting bacterial-specific structures or processes. They are ineffective against viruses because viruses lack cellular structures like cell walls or ribosomes. Common examples include penicillin (disrupts cell wall synthesis) and tetracycline (inhibits protein synthesis).

Antivirals are medicines that specifically target viruses by interfering with viral replication inside host cells. They work by blocking viral enzymes or preventing viral entry/exit from cells. Examples include aciclovir (treats herpes) and oseltamivir (treats influenza). Antivirals are generally harder to develop than antibiotics because viruses reproduce inside living cells, making it difficult to target the virus without harming host cells.

Antibiotic resistance occurs when bacteria evolve to survive exposure to antibiotics through natural selection. Resistant bacteria possess genes (often on plasmids) that allow them to: neutralize antibiotics, pump them out, or alter target sites. This process follows these stages:

1. Random mutation creates antibiotic-resistant bacteria in a population
2. When antibiotics are used, non-resistant bacteria die
3. Resistant bacteria survive and reproduce, passing resistance genes to offspring
4. The resistant strain becomes dominant in the population

Key contributing factors to resistance include: incomplete antibiotic courses (allowing resistant bacteria to survive), overuse in agriculture, inappropriate prescribing for viral infections, and horizontal gene transfer between bacteria. This represents a major public health crisis, making previously treatable infections potentially fatal.

Cambridge Key Term: Antibiotic resistance is an evolutionary process driven by natural selection, not bacteria "getting used to" antibiotics.

The Lock-and-Key Analogy: Think of antibiotics as specially shaped keys designed to unlock and destroy bacterial "locks" (cell walls, ribosomes). These keys don't fit viral locks because viruses have completely different structures—they're like trying to use a house key on a car ignition.

Real-World Case: MRSA (Methicillin-Resistant Staphylococcus aureus) In the 1940s, penicillin revolutionized medicine. However, by the 1960s, S. aureus bacteria had evolved resistance through a gene producing penicillinase enzyme that breaks down penicillin. Hospitals switched to methicillin, but by 1961, MRSA emerged. Today, MRSA causes thousands of deaths annually in healthcare settings, demonstrating evolution in action.

Agricultural Impact: Approximately 70% of antibiotics globally are used in livestock farming to promote growth and prevent disease in crowded conditions. Resistant bacteria like E. coli develop in animal intestines, transfer to humans through food, environment, or direct contact, creating "superbugs" resistant to multiple antibiotics.

The Antiviral Challenge: Developing antivirals for COVID-19 took years because viruses hijack your cells' machinery. An antiviral must distinguish between viral enzymes and your own enzymes—like trying to disable a burglar hiding inside your house without damaging the house itself. This explains why antivirals are more specific and fewer in number than antibiotics.

Memory Aid - RAPID: Resistance arises through Random mutation, Antibiotic exposure, Population selection, Inheritance of resistance genes, Dominance of resistant strains.

The tuberculosis crisis in developing countries illustrates consequences of incomplete treatment—when patients don't finish their 6-9 month antibiotic course, partially resistant bacteria survive, multiply, and create treatment-resistant TB strains.