Investigate and assess the effectiveness of pharmaceuticals as treatment strategies for the control of infectious disease, including: antivirals and antibiotics, the development of antibiotic resistance, and the role of immunisation including the impact of vaccination programs in conferring herd immunity

What this dot point is asking

NESA wants you to evaluate pharmaceutical strategies for controlling infectious disease, including antibiotics, antivirals and vaccines, and to explain antibiotic resistance and herd immunity. This is one of the largest dot points in Module 7 and appears in extended responses worth 6 to 9 marks.

The answer

Pharmaceutical control of infectious disease has three main tools: antibiotics (against bacteria), antivirals (against viruses) and vaccines (preventive). Each has strengths and limitations, and each is shaped by the evolutionary biology of the pathogen.

Antibiotics

Antibiotics target structures or processes unique to bacteria, sparing host cells.

Mechanisms of action.

• Cell wall synthesis inhibitors (penicillin, amoxicillin, cephalosporins) prevent peptidoglycan cross-linking, lysing actively growing bacteria.
• Protein synthesis inhibitors (tetracycline, erythromycin) bind the bacterial 70S ribosome.
• DNA replication inhibitors (fluoroquinolones such as ciprofloxacin) target bacterial DNA gyrase.
• Folate synthesis inhibitors (sulphonamides, trimethoprim) block bacterial vitamin synthesis.

Limitations. Antibiotics do not work against viruses, fungi, protozoa or prions. Many cause side effects by killing beneficial gut bacteria.

Antivirals

Antivirals target viral-specific enzymes and life-cycle steps.

Mechanisms of action.

• Reverse transcriptase inhibitors (zidovudine, tenofovir) block HIV's conversion of RNA to DNA.
• Protease inhibitors (lopinavir, paxlovid) block the cleavage of viral polyproteins.
• Neuraminidase inhibitors (oseltamivir) prevent influenza release from infected cells.
• Polymerase inhibitors (remdesivir, sofosbuvir) block viral RNA replication.

Limitations. Antivirals are typically pathogen-specific (an HIV antiviral does not work on influenza). Resistance can develop, especially in RNA viruses with high mutation rates.

Antibiotic resistance

Origin. Random mutations in bacterial DNA occasionally produce a resistance gene (e.g. beta-lactamase that degrades penicillin). In an antibiotic-free environment, resistance confers no advantage. Once antibiotics are applied, natural selection favours resistant individuals: susceptible bacteria die, resistant bacteria reproduce.

Spread. Bacteria reproduce rapidly (every 20 minutes in good conditions) and share genes by horizontal gene transfer.

• Conjugation. Plasmids carrying resistance genes are transferred between cells via a pilus.
• Transformation. Bacteria take up free DNA from the environment.
• Transduction. Bacteriophages carry resistance genes between bacterial hosts.

Consequences. Resistant infections cost lives and treatment dollars. Methicillin-resistant Staphylococcus aureus (MRSA), multi-drug resistant tuberculosis (MDR-TB) and carbapenem-resistant Enterobacteriaceae are major threats. The WHO ranks antibiotic resistance among the top ten threats to global health.

Strategies to slow resistance.

1. Prescribe only when bacterial infection is confirmed.
2. Complete the prescribed course.
3. Reduce agricultural antibiotic use (banned in EU food animals as growth promoters since 2006).
4. Invest in new antibiotic discovery (a class gap of 1987 to 2015 in approval of truly novel classes).
5. Improve hospital infection control (handwashing, isolation of resistant cases).
6. Surveillance programs such as Australia's AURA.

Immunisation and vaccination

Vaccines provide active artificial immunity by exposing the immune system to a pathogen antigen without causing disease, generating memory B and T cells.

Vaccine types.

• Live attenuated (MMR, oral polio, BCG, varicella). Weakened pathogen replicates briefly. Strong immunity. Not suitable for severely immunocompromised people.
• Inactivated (influenza, hepatitis A, rabies). Killed pathogen. Safer but often needs boosters.
• Subunit / toxoid (tetanus, diphtheria, hepatitis B, HPV). Specific antigen or inactivated toxin.
• mRNA (COVID-19 vaccines, in development for flu and HIV). mRNA encoding a pathogen antigen is delivered in a lipid nanoparticle. The host's cells produce the antigen and trigger immunity.
• Viral vector (some COVID-19 and Ebola vaccines). A harmless virus delivers the pathogen antigen gene.

Herd immunity

When a high enough proportion of a population is immune, transmission chains break and even unvaccinated individuals are protected.

Threshold. The proportion of the population that must be immune is approximately 1 - 1/R0.

• Measles (R0 = 12 to 18): 92 to 95 per cent.
• COVID-19 ancestral strain (R0 = 2 to 3): 50 to 67 per cent. Higher for Delta and Omicron variants.
• Polio (R0 = 5 to 7): 80 to 86 per cent.

Benefits.

• Protects those who cannot be vaccinated (newborns, immunocompromised, severely allergic).
• Enables eradication (smallpox 1980; polio close).
• Reduces selection pressure for new variants.

Risks of falling below the threshold. Vaccine hesitancy or supply gaps can drop coverage below the herd immunity threshold. Measles outbreaks resurged in 2019 in parts of Europe, North America and the Pacific where coverage had fallen.

Worked example

A new strain of influenza emerges with an R0 of 4.

Herd immunity threshold. 1 - 1/4 = 75 per cent of the population must be immune.

Vaccine efficacy adjustment. If the vaccine is 80 per cent effective, the proportion vaccinated must be at least 75 / 80 = 94 per cent for coverage alone to reach the threshold.

Implication. Public health planners aim for very high coverage, supplement with antivirals (oseltamivir) for high-risk individuals, and combine with hygiene and case isolation. This is the standard pandemic preparedness model.

Common traps

Saying antibiotics work on viruses. They do not. This kills marks every year.

Saying resistance "happens because bacteria want to survive." Resistance is the result of random mutation and natural selection. Avoid intentional language.

Confusing herd immunity threshold with vaccine coverage. Vaccines are rarely 100 per cent effective, so coverage must exceed the herd immunity threshold to achieve it.

Treating vaccines as treatment. Vaccines are preventive, given before exposure (with some exceptions like post-exposure rabies vaccine).

Ignoring evaluation. When asked to "evaluate," weigh effectiveness against limitations and give an overall judgement supported by evidence.

In one sentence

Pharmaceutical control of infectious disease uses antibiotics that target bacterial-specific structures, antivirals that block viral enzymes and vaccines that pre-arm the adaptive immune system with memory cells, but the long-term effectiveness of antibiotics is undermined by the evolution of resistance, while vaccines can achieve herd immunity when coverage exceeds 1 - 1/R0.