Antibiotics, resistance and infection controlEdexcel A-Level Biology A: Revision notes

Hosts evolve defences such as phagocytosis, antibodies and memory cells. These act as selection pressures on pathogens. Pathogens with mutations that help them evade the defences survive, reproduce and pass on the advantageous alleles, so the host is then selected for new defences. This continuing cycle is the theory of an evolutionary race (arms race).

Evasion mechanisms support the theory:

• Antigenic variation - mutation of genes for surface antigens (e.g. influenza haemagglutinin, HIV envelope proteins) means memory cells and antibodies from earlier infections are no longer complementary, so there is no rapid secondary response.
• Surviving inside phagocytes - Mycobacterium tuberculosis stops the phagosome fusing with lysosomes, so it is protected and reproduces inside macrophages.
• Hiding inside host cells - viruses and Plasmodium spend part of their cycle inside cells where antibodies cannot reach them.

Bacteriostatic antibiotics (e.g. tetracyclines) stop bacteria reproducing but do not kill them. The population stops growing and the immune system destroys the remaining bacteria, so they work well in healthy patients. If the antibiotic is removed, growth restarts.

Bactericidal antibiotics (e.g. penicillin) kill bacteria directly, so the number of living cells falls. They are preferred in severe infections and for patients with a weakened immune system, for example after chemotherapy.

In a broth culture, a bacteriostatic antibiotic holds the viable count steady, while a bactericidal one reduces it.

A lawn of a non-pathogenic bacterium is spread on sterile nutrient agar using aseptic technique: flame the loop, work near a Bunsen flame, and keep the lid on as much as possible. Sterile paper discs soaked in different antibiotics are placed on the agar with sterile forceps. A control disc soaked in sterile water is also added.

The lid is taped in two or three places (not sealed, so oxygen can enter and anaerobic pathogens do not grow) and the plate is incubated upside down at 25 °C (no higher than 30 °C) to reduce the risk of growing human pathogens. Clear zones of inhibition show where bacteria did not grow.

Measure the diameter and calculate the area as $\pi r^2$. A larger zone means the bacteria are more susceptible. For example, a zone of diameter 18 mm has area $\pi \times 9^2 = 254\ \text{mm}^2$.

Random mutation can give a bacterium an allele for resistance. When an antibiotic is used, it acts as a selection pressure: susceptible bacteria die or stop growing, while resistant ones survive, reproduce and pass on the allele by vertical transmission. Resistance genes on plasmids can also be passed to other bacteria, even of other species, by horizontal transfer.

Misuse of antibiotics makes this worse: prescribing for viral infections, using broad-spectrum antibiotics unnecessarily, and patients not completing the course, which leaves partly resistant survivors. MRSA (meticillin-resistant Staphylococcus aureus) is a well-known example.

Hospital acquired infections (e.g. MRSA, Clostridioides difficile) arise because hospitals contain many vulnerable patients, open wounds and invasive equipment, heavy antibiotic use that selects for resistance, and many opportunities for cross-infection.

Understanding these causes has led to codes of practice:

• Antibiotic prescribing: only prescribe when needed, use narrow-spectrum antibiotics where possible, test sensitivity, and make sure the full course is completed.
• Infection prevention and control: hand washing and alcohol gel between patients, bare below the elbows, screening on admission, isolating infected patients, cleaning surfaces, sterilising instruments and restricting visitors.