Biology • Year 12 • Module 7 • Lesson 9
Physical and Chemical Responses in Animals
Apply the inflammatory cascade, fever physiology, and physical barrier mechanisms to real data, experimental scenarios, and a case study involving an Australian bushfire worker.
1. Interpret experimental data — temperature, phagocytosis, and bacterial replication
The table below is drawn from an in vitro study investigating the effect of temperature on the activity of the innate immune system. Neutrophils were isolated from human blood and challenged with a Staphylococcus aureus culture at each experimental temperature. Bacterial replication rate was measured in the same culture conditions without neutrophils. 9 marks
| Temperature (°C) | Neutrophil phagocytosis rate (bacteria/neutrophil/hr) | Bacterial replication rate (doublings/hr) |
|---|---|---|
| 36.0 (sub-normal) | 4.1 | 2.8 |
| 37.0 (normal body temp) | 5.2 | 2.9 |
| 38.0 (mild fever) | 6.8 | 2.7 |
| 38.5 (moderate fever) | 7.4 | 2.4 |
| 39.5 (high fever) | 7.1 | 2.1 |
| 40.5 (very high fever) | 5.3 | 1.8 |
| 41.5 (dangerous fever) | 2.9 | 1.5 |
Adapted from the lesson's Activity 02 dataset, modelled after published in vitro fever studies.
1.1 Describe the trend in neutrophil phagocytosis rate as temperature increases from 37.0°C to 38.5°C, and then from 38.5°C to 41.5°C. Use data from the table in your answer. 2 marks
1.2 Using the data, explain the adaptive value of a moderate fever (38.0–38.5°C) from the perspective of the host. Refer to both columns in your answer. 3 marks
1.3 At 41.5°C, neutrophil phagocytosis has dropped to 2.9 bacteria/neutrophil/hr — below the 37.0°C baseline — while bacterial replication is at its lowest (1.5 doublings/hr). Using lesson content, suggest a biological explanation for why high fever is still considered dangerous to the host even if it further suppresses bacterial replication. 2 marks
1.4 A doctor advises patients to take antipyretics (e.g. paracetamol) for any fever above 37.5°C. Evaluate this recommendation using the data in the table. 2 marks
2. Interpret graph — capillary permeability during inflammation
The graph below shows the relative change in capillary permeability (arbitrary units) in rat subcutaneous tissue over the first 6 hours following injection of a bacterial endotoxin (lipopolysaccharide, LPS), compared to a saline control. Antihistamine was administered to a third group immediately prior to LPS injection. 7 marks
Figure 2.1. Relative capillary permeability in rat subcutaneous tissue following LPS injection. Adapted from in vitro inflammation research models (illustrative data).
2.1 At what time point does peak capillary permeability occur in the LPS-only group, and what is the approximate permeability value? 1 mark
2.2 Compare the LPS-only and LPS + antihistamine curves. What does this comparison suggest about histamine's specific role in the permeability response? 2 marks
2.3 The LPS + antihistamine group still shows an elevated permeability compared to the saline control throughout the experiment. Using lesson content, identify one other chemical mediator (not histamine) that could account for this residual increase and explain its role. 2 marks
2.4 Using the lesson's explanation of swelling, explain why the elevated capillary permeability shown in the LPS-only group (hours 1–3) is beneficial to the host, not merely a harmful side effect of infection. 2 marks
3. Case study — a volunteer bushfire worker with a hand injury
During the 2019–20 Black Summer bushfire season in NSW, a volunteer firefighter sustained a deep laceration to the palm of her hand from a wire fence. She treated the wound in the field with basic first aid but did not seek medical attention for two days. When examined at a rural clinic, the wound showed marked redness extending 3 cm from the cut, oedema, warmth to touch, and a pus-filled pocket. She reported a body temperature of 38.3°C. The attending nurse practitioner debated whether to prescribe antibiotics immediately or to monitor, noting the temperature was within the moderate fever range. 7 marks
3.1 For each of the four cardinal signs visible at the wound site (redness, oedema, warmth, and pus), identify the specific cellular mechanism responsible and state its defensive purpose. 4 marks (1 per sign)
3.2 The patient's temperature of 38.3°C is within the moderate fever range. Using lesson content, argue for and against immediate antipyretic treatment in this case, referencing the data from Section 1 of this worksheet where relevant. 3 marks
Q1.1 — Trend in neutrophil phagocytosis rate (2 marks)
From 37.0°C to 38.5°C, neutrophil phagocytosis rate increases steadily from 5.2 to 7.4 bacteria/neutrophil/hr [1]. From 38.5°C to 41.5°C, the rate declines sharply, falling from 7.4 to 2.9 bacteria/neutrophil/hr — below the normal-temperature baseline [1].
Q1.2 — Adaptive value of moderate fever (3 marks)
At 38.0–38.5°C, neutrophil phagocytosis rate reaches its peak (6.8–7.4 bacteria/neutrophil/hr), representing a 31–42% increase over the 37.0°C rate [1]. Simultaneously, bacterial replication rate begins to decline (from 2.9 to 2.4 doublings/hr), reducing pathogen proliferation [1]. Together, these two changes — more rapid neutrophil activity and slower bacterial replication — shift the balance in favour of the host, meaning fewer bacteria survive each hour. A moderate fever therefore simultaneously enhances the host's offensive capacity and reduces the pathogen's reproductive rate, demonstrating its adaptive value [1].
Q1.3 — Why 41.5°C is dangerous despite low bacterial replication (2 marks)
At 41.5°C, neutrophil phagocytosis has collapsed to 2.9 — below the 37.0°C baseline — indicating that neutrophil enzyme function is being impaired, likely by heat-induced denaturation or disruption of membrane proteins [1]. While bacterial replication is low, so too is the immune system's ability to destroy those bacteria. Additionally, the lesson notes that temperatures above 40°C risk systemic protein denaturation, seizures, and organ damage in the host — the temperature at which host cell enzymes (not just pathogen enzymes) begin to malfunction [1].
Q1.4 — Evaluate the blanket antipyretic recommendation (2 marks)
The data show that at 37.5°C, neutrophil phagocytosis has not yet reached its peak (peak is at 38.5°C) — suppressing fever below 38°C would reduce an immune response that is still operating below its optimal temperature [1]. The data support treating fever only above approximately 39.5–40°C, where phagocytosis begins declining and the risk of host tissue damage increases. The blanket advice to suppress all fevers above 37.5°C is not supported by this dataset and would reduce immune effectiveness in the range 37.5–38.5°C where the immune system is most active [1].
Q2.1 — Peak permeability in LPS-only group (1 mark)
Peak capillary permeability in the LPS-only group occurs at approximately 2 hours post-injection, with a relative permeability value of approximately 4.8 units (or ~4.8 on the scale shown). [1]
Q2.2 — Role of histamine in permeability (2 marks)
The LPS + antihistamine group shows a substantially reduced peak permeability (~2.4 units at 2 hours) compared to the LPS-only group (~4.8 units), despite the same LPS dose [1]. This suggests that histamine is responsible for approximately half of the total permeability increase — it mediates a large early-phase rise in capillary permeability in response to LPS (which triggers mast-cell degranulation). Antihistamine blocks histamine receptors on capillary endothelial cells, reducing but not eliminating the permeability increase [1].
Q2.3 — Another mediator accounting for residual permeability (2 marks)
Prostaglandins (or complement proteins, or cytokines) could account for the residual permeability increase in the LPS + antihistamine group [1]. Prostaglandins are produced by most cell types at a damage site and act independently of histamine to enhance vasodilation and contribute to capillary permeability; they also sensitise endothelial cells to the effects of other mediators. Because antihistamine does not block prostaglandin receptors, the prostaglandin-driven component of the inflammatory response continues even when histamine is blocked [1].
Q2.4 — Why elevated permeability is beneficial (2 marks)
Increased capillary permeability allows plasma — and crucially its dissolved contents including antibodies, complement proteins, and clotting factors — to leak from blood vessels into the infected tissue [1]. By flooding the infection site with these plasma proteins, the host delivers ready-made antimicrobial resources directly to where they are needed: complement can opsonise bacteria and form membrane attack complexes, antibodies can neutralise pathogens, and clotting factors help seal the wound. This is why the lesson describes swelling not as a harmful side effect but as an active immune delivery mechanism [1].
Q3.1 — Four signs and their mechanisms (4 marks)
Redness: Vasodilation triggered by histamine from mast cells widens local blood vessels, increasing blood flow to the wound — this brings more warm, oxygenated blood near the surface, making the area appear red. Defensive purpose: rapid delivery of immune cells and mediators to the site. [1]
Oedema (swelling): Increased capillary permeability (also triggered by histamine and prostaglandins) allows plasma to leak out of blood vessels into the surrounding tissue. Defensive purpose: delivers antibodies, complement proteins, and other plasma proteins to the infection site. [1]
Warmth: Increased blood flow combined with the high metabolic activity of immune cells (neutrophils and macrophages) at the site raises local temperature above the surrounding tissue. Defensive purpose: elevated local temperature speeds up immune-cell enzyme reactions, accelerating pathogen clearance. [1]
Pus: Pus is composed of dead neutrophils (that migrated to the site via chemotaxis and were killed while destroying bacteria), destroyed bacterial material, and leaked tissue fluid. Its formation indicates that neutrophils successfully reached the wound and carried out phagocytosis. Defensive purpose: the presence of pus confirms active neutrophil attack — a pus-filled pocket draining is the immune response succeeding in containing the infection. [1]
Q3.2 — Fever 38.3°C: argument for and against antipyretic (3 marks)
Against immediate antipyretic treatment: The Q1 dataset shows that at ~38.5°C, neutrophil phagocytosis rate is at its peak (7.4 bacteria/neutrophil/hr). A temperature of 38.3°C is in this optimal range — suppressing the fever would move the patient toward 37.0°C where phagocytosis is slower (5.2 bacteria/neutrophil/hr). The lesson's callout explicitly states that a mild fever (37–38.5°C) "may be best left to run its course — it is actively helping" [1].
For monitoring rather than immediate treatment: The patient's temperature is safely below the 40°C threshold at which host enzyme denaturation and organ damage risk increases. With careful monitoring, the fever's adaptive benefit can be retained while watching for escalation [1].
Caveat / overall judgement: The decision is complicated by the two-day delay in treatment and the development of a pus pocket, which may signal a more established infection. If the fever rises above 39°C or the patient shows signs of systemic spread (expanding redness, spreading lymphangitis), antipyretics and antibiotics would be indicated. The lesson supports a nuanced, context-dependent approach rather than blanket suppression [1].