Antibiotics — FAQ

For Cambridge 9700 Biology, key mechanisms of antibiotic action include inhibiting bacterial cell wall synthesis (e.g., penicillin), disrupting protein synthesis by binding to 70S ribosomes (e.g., streptomycin, tetracycline), interfering with nucleic acid synthesis, and disrupting cell membrane function. These methods exploit differences between bacterial (prokaryotic) and host (eukaryotic) cells, a principle known as selective toxicity.

Antibiotic resistance develops primarily through random genetic mutations. When an antibiotic is used, it creates a selective pressure, killing susceptible bacteria but allowing resistant mutants to survive and reproduce. This increases the frequency of resistance in the population. Resistance genes can also spread rapidly between bacteria via horizontal gene transfer (conjugation, transformation, and transduction), often on plasmids.

Antibiotic resistance is a critical global health concern because it makes bacterial infections harder to treat, leading to prolonged illnesses, higher mortality rates, and increased healthcare costs. It also threatens the safety of modern medical procedures like surgery, chemotherapy, and organ transplants. 'Superbugs' like MRSA highlight the challenge, as they are resistant to multiple antibiotics.

Bactericidal antibiotics kill bacteria directly (e.g., penicillin, which causes cell lysis). Bacteriostatic antibiotics inhibit the growth and reproduction of bacteria without killing them (e.g., tetracycline, which stops protein synthesis). This gives the host's immune system time to clear the infection. Both are important in medicine.