Defence against disease
IB Biology SLΒ· Topic 6.3 Defence against infectious diseaseΒ· 12 min read
1. Non-Specific Primary Defencesβ β ββββ± 3 min
The human bodyβs first line of defence blocks all pathogen entry non-selectively, with no prior exposure required to activate a response. The outer layer of skin is a tough, dry, keratinised barrier that is almost impenetrable to microbes when intact. Mucous membranes lining the respiratory, digestive and urinary tracts secrete sticky mucus that traps pathogens, which are then removed by cilia or expelled via coughing/sneezing.
Non-specific immunity
An immune response that acts against all pathogens in the same way, with no targeted recognition of unique pathogen markers.
Explain why lysozyme in tears and saliva is classified as a non-specific defence.
- 1
Step 1: Recall the mechanism of lysozyme action
- 2
Lysozyme is an enzyme that breaks down the peptidoglycan in bacterial cell walls, killing any bacterial cell it encounters.
- 3
Step 2: Link to non-specific definition
- 4
It does not target any single bacterial species, and acts against all susceptible bacteria equally, with no antigen-specific recognition.
- 5
Step 3: Final conclusion
- 6
This generalised, non-targeted action confirms it is a non-specific defence.
Test your understanding of primary defences:
Which of the following is an example of a chemical non-specific defence?
Intact skin
Stomach hydrochloric acid
Cilia in the trachea
Mucus
Reveal answer
Stomach hydrochloric acid βStomach acid kills most ingested pathogens, acting as a chemical barrier, while the other options are physical barriers.
2. The Blood Clotting Cascadeβ β β βββ± 3 min
When a blood vessel is damaged, the clotting cascade activates to seal the wound and prevent blood loss as well as pathogen entry into the bloodstream. Damaged tissue and platelets release clotting factors that trigger the conversion of prothrombin to thrombin. Thrombin then catalyses the conversion of soluble fibrinogen in blood plasma to insoluble fibrin threads, which form a mesh across the wound site to trap platelets and red blood cells, forming a solid clot.
Place the following steps of blood clotting in the correct order: fibrin mesh formation, platelet activation, prothrombin conversion to thrombin, fibrinogen conversion to fibrin.
- 1
Step 1: Start with the initial wound response
- 2
Damage to the blood vessel wall first triggers circulating platelets to activate and aggregate at the wound site.
- 3
Step 2: Activate the clotting factor cascade
- 4
Released clotting factors then catalyse the conversion of prothrombin to active thrombin enzyme.
- 5
Step 3: Generate the clot structural protein
- 6
Thrombin then converts soluble fibrinogen to insoluble fibrin threads.
- 7
Step 4: Form the final clot structure
- 8
Fibrin threads cross-link to form a mesh that traps blood cells to seal the wound.
Exam tip:
IB exam mark schemes almost always require you to name fibrin as the structural component of the clot, not just reference platelets.
3. Phagocyte Actionβ β β βββ± 2.5 min
If pathogens breach the primary barriers and enter the bloodstream, the second non-specific line of defence activates. Phagocytes are large white blood cells that squeeze through capillary walls to migrate to sites of infection. They recognise and bind to pathogen surface markers, then engulf the pathogen inside a membrane-bound vesicle, where digestive lysosome enzymes break the pathogen down into harmless fragments.
Phagocytosis
The process by which a cell engulfs a foreign particle or pathogen, enclosing it in an internal vesicle for digestion.
Explain why phagocyte action is still classified as non-specific immunity.
- 1
Step 1: Identify the recognition mechanism
- 2
Phagocytes bind to broad, conserved molecular patterns found on the surface of almost all pathogens, not unique antigens specific to one species.
- 3
Step 2: No targeted adaptation occurs
- 4
Phagocytes do not generate custom receptors for individual pathogens, and their response strength does not increase with repeat exposure to the same pathogen.
- 5
Step 3: Final classification
- 6
This generalised response means phagocytosis remains part of the non-specific immune system.
4. Specific Immunity and Antibodiesβ β β β ββ± 3 min
The specific immune response relies on B and T lymphocytes, which generate unique antigen receptors. When a B lymphocyte binds to its matching specific antigen, it is activated and divides to produce large numbers of plasma cells, which secrete mass quantities of antibodies that bind to the target antigen to neutralise the pathogen or mark it for destruction by phagocytes.
Describe two ways antibodies reduce pathogen harm in the body.
- 1
Step 1: Neutralisation mechanism
- 2
Antibodies can bind directly to the surface of viruses or bacterial toxins, blocking them from attaching to and entering host cells.
- 3
Step 2: Opsonisation mechanism
- 4
Antibodies bound to pathogen surfaces act as markers that phagocytes recognise, making phagocytosis far more efficient at clearing the pathogen.
5. Antibiotics and Antibiotic Resistanceβ β β βββ± 2.5 min
Antibiotics target structures and metabolic pathways unique to prokaryotic bacterial cells, including 70S ribosomes, peptidoglycan cell walls and prokaryote-specific enzyme pathways. These structures are not present in human eukaryotic cells or in viruses, so antibiotics cannot kill viruses. Random pre-existing mutations in bacterial genomes can confer resistance to antibiotics, and exposure to antibiotics creates a selection pressure that makes these resistant bacteria far more likely to survive and reproduce.
Agent Type | Target Structure | Effective Against |
|---|---|---|
Penicillin | Bacterial cell wall synthesis | Bacteria only |
Tetracycline | Bacterial 70S ribosomes | Bacteria only |
Antiviral drugs | Viral replication enzymes | Viruses only |
Explain why overprescription of antibiotics for viral colds contributes to antibiotic resistance.
- 1
Step 1: Antibiotics do not affect viruses
- 2
The antibiotic will not treat the viral infection at all, but will still be present in the patientβs system.
- 3
Step 2: Selection pressure on commensal bacteria
- 4
The antibiotic will kill non-resistant commensal bacteria living in the patientβs body, leaving any rare resistant bacterial mutants unharmed.
- 5
Step 3: Resistant bacteria multiply
- 6
The resistant bacteria have no competition for resources, and replicate to form a large resistant population that can spread to other people.
6. Common Pitfalls
Wrong move:
Stating that antibiotics kill viruses
Why:
Antibiotics target prokaryote-specific structures that viruses do not possess, so they have no effect on viral pathogens
Correct move:
Explicitly note that antibiotics are only effective against bacterial infections, not viral illness
Wrong move:
Classifying skin as a specific immune defence
Why:
Skin acts against all pathogens equally with no antigen-specific recognition, so it cannot be part of specific immunity
Correct move:
Categorise skin as a non-specific primary physical barrier defence
Wrong move:
Claiming phagocytes produce antibodies
Why:
Phagocytes only engulf and digest pathogens; antibody production is exclusive to activated plasma B lymphocytes
Correct move:
Clearly separate phagocyte pathogen clearance from B lymphocyte antibody secretion
Wrong move:
Omitting fibrin as the core structural component of blood clots
Why:
Platelets alone cannot form a stable clot; the insoluble fibrin mesh is required to trap cells and seal the wound
Correct move:
Name the full sequence of prothrombin β thrombin β fibrinogen β fibrin when describing clotting
Wrong move:
Claiming bacteria develop resistance mutations in response to antibiotic exposure
Why:
Resistance mutations arise randomly before antibiotic exposure, not as a deliberate adaptive response to the drug
Correct move:
Explain that pre-existing resistant mutants are selected for by antibiotic presence, leading to a resistant population
7. Quick Reference Cheatsheet
Defence Category | Key Components | Specificity Level |
|---|---|---|
Primary non-specific | Skin, mucous membranes, lysozyme, stomach acid | None |
Clotting cascade | Platelets, thrombin, fibrin | None |
Secondary non-specific | Phagocytes | Low |
Specific immunity | B lymphocytes, antibodies | High |
Antibiotics | Bacterial cell wall/ribosome inhibitors | Target prokaryotes only |
When this came up on past exams
AI-estimated based on syllabus patterns β cross-check with official past papers for accuracy. Use only as revision-focus signals.
- 2023 Β· Paper 2
Antibody production explanation
- 2022 Β· Paper 1
Blood clotting multiple choice
- 2021 Β· Paper 2
Antibiotic resistance extended response
What's Next
Mastering defence against disease builds the core immunology foundation you will use for higher-level IB Biology content and real-world public health applications including vaccine development and pandemic response. This sub-topic directly links to the next unit section on infectious disease epidemiology, where you will explore how pathogens spread through populations and the public health measures used to limit outbreaks. You will also connect these concepts to the evolution unit, as antibiotic resistance is one of the most widely examined examples of natural selection acting on populations over very short time scales. Before moving on, confirm you can distinguish specific and non-specific defences, and outline the full blood clotting cascade to avoid losing easy marks in Paper 2 structured questions.