How do pathogens cause disease, and how do we defend against them?
Pathogens and the global impact of infectious disease, the immune response, antibiotics and antibiotic resistance.
A focused answer to WJEC A-Level Biology Unit 2, covering pathogens and the global impact of infectious disease, the non-specific and specific immune responses, antibiotics, and the spread of antibiotic resistance.
Reviewed by: AI editorial process; not yet individually human-reviewed
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What this dot point is asking
WJEC wants you to describe types of pathogen and the global impact of infectious disease, explain the non-specific and specific immune responses (including memory and vaccination), and explain the action of antibiotics and how antibiotic resistance arises and spreads.
Pathogens and global impact
The non-specific response
The first lines of defence are non-specific and act against any pathogen. Physical and chemical barriers include the skin, mucus and stomach acid. If a pathogen gets through, phagocytosis follows: a phagocyte engulfs the pathogen into a phagosome, which fuses with a lysosome so hydrolytic enzymes digest it. The phagocyte then displays the pathogen's antigens on its surface, becoming an antigen-presenting cell that triggers the specific response.
The specific immune response
Antibodies are Y-shaped proteins with variable regions complementary to a specific antigen. They agglutinate pathogens, neutralise toxins and mark pathogens for phagocytosis. The first exposure gives a slow, weak primary response; later exposure to the same antigen gives a fast, strong secondary response driven by memory cells. Vaccination exploits this by exposing the body to a harmless antigen, priming memory cells without causing disease.
Antibiotics and resistance
Antibiotics treat bacterial infections, for example by inhibiting cell wall (peptidoglycan) synthesis so bacteria cannot withstand osmotic pressure and burst. They do not work against viruses, which have no such structures. Resistance arises when a random mutation produces a resistant allele; the antibiotic then acts as a selection pressure, so resistant bacteria survive and reproduce while others die. Overuse and unfinished courses speed this up, and resistance genes spread between bacteria horizontally on plasmids.
Examples in context
Example 1. MRSA in hospitals. Methicillin-resistant Staphylococcus aureus carries genes that change the target of beta-lactam antibiotics, so the drugs no longer bind. Strict hygiene, isolation and limiting antibiotic use reduce the selection pressure that lets MRSA spread, a real demonstration of resistance evolving under antibiotic selection.
Example 2. Smallpox eradication by vaccination. A worldwide vaccination campaign primed memory cells in enough of the population to break transmission, and smallpox was declared eradicated in 1980. It remains the clearest proof that creating immunological memory through vaccination can eliminate a pathogen entirely.
Try this
Q1. State two non-specific defences against pathogens. [1 mark]
- Cue. Physical barriers such as skin and mucus, and phagocytosis.
Q2. Explain why finishing a full course of antibiotics helps limit resistance. [2 marks]
- Cue. A full course kills all the bacteria, including less susceptible ones, so fewer survive to reproduce and pass on resistance alleles.
Q3. Explain why the secondary immune response is faster than the primary response. [2 marks]
- Cue. Memory cells from the primary response are already present; on re-exposure they divide rapidly into plasma cells, so antibodies appear much sooner.
Exam-style practice questions
Practice questions written in the style of WJEC exam questions on this dot point, with worked answer explainers. The year tag is the paper they imitate, not the source.
WJEC 20174 marksExplain how antibiotic resistance arises and spreads in a population of bacteria.Show worked answer →
A random mutation in a bacterium can produce an allele giving resistance to an antibiotic; this happens by chance, not because of the antibiotic.
When the antibiotic is present it acts as a selection pressure, killing non-resistant bacteria while resistant bacteria survive and reproduce.
Resistant bacteria pass the allele to offspring, and can also spread it horizontally on plasmids, so the proportion of resistant bacteria in the population increases over time.
Markers reward mutation, selection by the antibiotic, survival and reproduction of resistant bacteria, and spread by plasmids.
WJEC 20205 marksDescribe the difference between the primary and secondary immune responses, and explain why vaccination gives long-lasting protection.Show worked answer →
In the primary response, when an antigen is met for the first time, the few B cells with a complementary antibody must be selected and divide by clonal expansion before antibodies appear, so the response is slow (several days) and antibody levels are relatively low.
Memory cells produced in the primary response remain in the blood for years.
In the secondary response, the same antigen is recognised by these memory cells, which divide rapidly into plasma cells, so antibodies are produced much faster, in greater quantity, and for longer, often clearing the pathogen before symptoms appear.
A vaccine introduces a harmless form of the antigen, triggering a primary response and memory cell production without causing disease, so a later real infection meets a rapid secondary response.
Markers reward the slow weak primary response, memory cells, the fast strong secondary response, and how a vaccine primes memory cells safely.
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Sources & how we know this
- WJEC A-level Biology specification — WJEC (2015)