Immunity and pathogen evolution (6.12, 6.13, 6.14, 6.15)

During the primary immune response, plasma cells are produced from activated B cells.

They make and release antibodies specific to the antigen which help destroy the pathogen.

This response is slow, so symptoms may appear before the pathogen is removed. Memory cells are also made during this time.

There are two types of immunity:

• Active immunity: the body’s own immune system makes antibodies and memory cells following exposure to an antigen (e.g., vaccinations or after infection).
• Passive immunity: ready-made antibodies are transferred to an individual, so no memory cells are made (e.g., breast milk being ingested by infants or antibody injection such as antivenom).

Natural active immunity occurs when a person becomes infected by a pathogen. The immune system responds by producing antibodies and memory cells. This provides long-term immunity because the immune system ‘remembers’ the pathogen.

Natural passive immunity is passed from mother to baby. Antibodies cross the placenta or are found in breast milk, providing short-term protection (no memory cells are made).

Artificial immunity is immunity gained through human intervention. It involves exposure to antigens or antibodies in a controlled way.

Artificial active immunity is gained through vaccination. A harmless form of the antigen (e.g., dead or weakened pathogen) is introduced stimulating the immune system to produce memory cells and antibodies, giving long-term immunity.

Artificial passive immunity involves injection of antibodies from another person or animal. Gives immediate but short-term protection (e.g., antivenom, rabies treatment) as no memory cells are made.

There is an evolutionary arms race between pathogens and their hosts, in which both are constantly evolving to outcompete one another.

Hosts evolve more effective defence mechanisms, while pathogens evolve ways to evade the immune system, such as antigenic variation or antibiotic resistance. This results in natural selection acting on both the host and the pathogen.

Pathogens have evolved several mechanisms to evade a host’s immune system, supporting the theory of an evolutionary race between pathogens and hosts:

• Antigenic variation: pathogens (e.g., influenza) change their surface antigens, making it harder for the immune system to recognise and destroy them.
• Hiding inside host cells: viruses and some bacteria (e.g., TB) live inside host cells, where they are shielded from antibodies and other immune defences.
• Inhibiting the immune response: some pathogens (e.g., HIV) release molecules that suppress or block immune cell function.

Bacteriostatic antibiotics inhibit the growth and reproduction of bacteria but do not kill them directly. This gives the immune system time to eliminate the infection.

Bactericidal antibiotics kill bacteria directly, for example, by disrupting cell wall synthesis or damaging the cell membrane.

The choice of antibiotic will depend on the type of infection and the patient’s immune status.

Antibiotics are drugs that kill bacteria or inhibit their growth by targeting structures or processes unique to bacterial cells, helping to treat bacterial infections.

Since the discovery of penicillin by Alexander Fleming in 1928, antibiotics have dramatically reduced deaths from bacterial infections, particularly those resulting from infected wounds and surgical procedures.

Understanding the causes of hospital-acquired infections has led to introduction of strict codes of practice to reduce their spread.

Antibiotics are prescribed only when necessary and patients are encouraged to complete the full-course to reduce the selection of antibiotic-resistant bacteria.

Infected patients may be isolated and all staff must follow strict hand washing and cleaning protocols to reduce the spread of infection.