the major groups of pathogens (bacteria, viruses, protozoa, fungi, prions) and the management of disease, including vaccination (active and passive, herd immunity), antibiotics, antivirals, and the emergence of antibiotic resistance

What this dot point is asking

VCAA wants the major groups of pathogens, their structure and how they cause disease, and the principles of disease management including vaccination, antibiotics, antivirals, and the emergence of antibiotic resistance.

The answer

A pathogen is any organism or agent that causes disease in a host. Pathogens are diverse, ranging from non-living protein particles to complex single-celled animals. Effective treatment depends on the type of pathogen.

Major groups of pathogens

Bacteria

Single-celled prokaryotes with a cell wall (containing peptidoglycan), a circular chromosome and 70S ribosomes. They reproduce asexually by binary fission, often every 20 to 30 minutes in ideal conditions. Bacteria cause disease by releasing toxins (cholera, tetanus, diphtheria) or by damaging host tissues directly (tuberculosis, strep throat).

Viruses

Acellular particles consisting of genetic material (DNA or RNA, single or double stranded) inside a protein capsid, sometimes surrounded by a lipid envelope taken from the host membrane. Viruses are obligate intracellular parasites: they cannot reproduce without a host cell. They attach to specific receptors on host cells, inject or release their genome, hijack the cell's ribosomes and machinery to make new virions, and exit by lysis or budding. Examples include influenza, SARS-CoV-2, HIV, measles and HPV.

Protozoa

Single-celled eukaryotes with a nucleus and membrane-bound organelles. They cause diseases mostly in tropical regions: Plasmodium (malaria, transmitted by mosquitoes), Giardia (intestinal infection), Trypanosoma (sleeping sickness). Many have complex life cycles involving multiple hosts.

Fungi

Eukaryotes with a chitinous cell wall, mostly multicellular (hyphae forming a mycelium) but some single-celled (yeasts). Fungal pathogens include Candida (thrush), Tinea (ringworm, athlete's foot) and Aspergillus (lung infections in immunocompromised people). Fungi are harder to treat than bacteria because their cells are biochemically similar to ours.

Prions

Misfolded versions of normal cellular proteins (not organisms at all). Prions cause normal proteins to misfold into the same abnormal shape, forming aggregates that destroy brain tissue. Diseases include Creutzfeldt-Jakob disease, mad cow disease (bovine spongiform encephalopathy) and scrapie in sheep. Prions contain no nucleic acid, are not destroyed by standard sterilisation, and have no cure.

Vaccination

A vaccine trains the adaptive immune system without causing disease. Vaccine types include:

• Live attenuated (weakened pathogen, for example MMR, BCG).
• Inactivated (killed pathogen, for example polio Salk vaccine).
• Subunit, recombinant or conjugate (protein fragments, for example HPV, hepatitis B).
• Toxoid (inactivated toxin, for example tetanus, diphtheria).
• mRNA or viral vector (instructions to make a viral antigen, for example several COVID-19 vaccines).

How vaccines work. The vaccine presents antigens to the immune system. Helper T cells, B cells and cytotoxic T cells with matching receptors activate and proliferate. Plasma cells secrete antibodies and memory B and T cells persist for years. On real exposure, the secondary response clears the pathogen quickly.

Active vs passive immunity.

• Active immunity. The body makes its own antibodies and memory cells. Produced by infection or vaccination. Long-lasting (often lifelong).
• Passive immunity. Pre-made antibodies are transferred from another individual. Examples: maternal IgG crossing the placenta, IgA in breast milk, antivenom injections, monoclonal antibody therapies. Immediate but short-lived (weeks to months), because no memory cells form.

Herd immunity

When a high proportion of a population is immune, the pathogen has too few susceptible hosts to spread. Transmission chains break and outbreaks die out. Unvaccinated people (infants, immunocompromised patients, vaccine non-responders) are indirectly protected.

The threshold depends on the basic reproduction number (R0):

• Measles (R0 around 12 to 18): about 95 per cent immunity required.
• Polio (R0 around 5 to 7): about 80 to 86 per cent.
• COVID-19 (R0 varies by strain): about 60 to 90 per cent for early strains.

Below the threshold, outbreaks recur. Vaccine refusal in pockets of a population can break herd immunity locally even when overall coverage is high.

Antibiotics

Antibiotics are drugs that kill or stop the growth of bacteria. They target bacterial structures absent from human cells:

• Penicillins and cephalosporins. Disrupt the bacterial cell wall (no human equivalent).
• Tetracyclines and macrolides. Bind 70S bacterial ribosomes (humans have 80S).
• Fluoroquinolones. Inhibit bacterial DNA gyrase.
• Sulfonamides. Block bacterial folate synthesis.

Antibiotics are ineffective against viruses because viruses have no cell wall, no ribosomes, and no metabolism of their own. Antibiotics for a viral infection (cold, flu) do nothing useful and contribute to resistance.

Antivirals

Antiviral drugs target steps in the viral replication cycle:

• Attachment or entry inhibitors (maraviroc against HIV).
• Reverse transcriptase inhibitors (zidovudine, AZT).
• Protease inhibitors (used for HIV and hepatitis C).
• Neuraminidase inhibitors (oseltamivir / Tamiflu against influenza).
• Nucleoside analogues (acyclovir against herpes simplex).

Antivirals are usually specific to one virus or family of viruses. They reduce viral load and shorten illness but rarely "cure" in the way antibiotics can.

Antibiotic resistance

Antibiotic resistance is a textbook example of natural selection:

1. Variation. A bacterial population contains rare individuals with mutations or plasmid-borne genes that happen to confer resistance.
2. Selection pressure. The antibiotic is administered. Susceptible bacteria are killed.
3. Differential reproductive success. Resistant bacteria survive and reproduce, doubling every 20 to 30 minutes.
4. Change in allele frequency. After a short time, the population is mostly resistant.

Mechanisms of resistance. Bacteria can:

• Inactivate the drug (beta-lactamases break down penicillin).
• Alter the drug target so it no longer binds.
• Reduce uptake of the drug.
• Use efflux pumps to expel the drug.

Horizontal gene transfer (via plasmids passing between bacteria) spreads resistance much faster than mutation alone, and across species. Multi-drug resistant strains (MRSA, multi-drug resistant TB) are now common in hospitals.

Drivers of resistance.

• Over-prescription of antibiotics (including for viral infections).
• Incomplete courses (allowing partially resistant bacteria to survive).
• Routine use in agriculture and livestock.
• Poor infection control.

Slowing resistance. Prescribe antibiotics only when needed, complete the full course, use narrow-spectrum drugs where possible, develop new antibiotics, vaccinate to reduce infections, and improve hygiene and infection control.

Examples in context

Example 1. Vancomycin-resistant enterococci at Austin Health. Austin Health Heidelberg's antimicrobial stewardship team tracks vancomycin-resistant enterococci (VRE) in their wards. Enterococci acquired the vanA gene complex by horizontal transfer, allowing them to remodel cell-wall precursors so vancomycin no longer binds. In hospital wards using vancomycin heavily, VRE outcompetes susceptible strains within months. Mitigation: restrict vancomycin to confirmed cases; isolate colonised patients; use newer agents (linezolid, daptomycin) sparingly to avoid driving further resistance. The case illustrates antibiotic resistance arising via mutation and horizontal gene transfer, accelerated by selection pressure from antibiotic use - one reason the WHO declared antimicrobial resistance a top ten global health threat.

Example 2. COVID-19 mRNA vaccines and the Victorian Department of Health. The Victorian Department of Health rolled out Pfizer (Comirnaty) and Moderna (Spikevax) mRNA vaccines from 2021. Both contain mRNA encoding the SARS-CoV-2 spike protein in lipid nanoparticles. Active immunisation: host cells translate spike protein, immune system mounts B-cell (antibody) and T-cell responses against it, including memory cells. Two doses produce neutralising antibodies in over 95 percent of recipients. Boosters maintain titres as variants emerge. Passive immunisation, by contrast, transfers preformed antibodies (e.g. monoclonal antibodies for high-risk patients) - faster but short-lived. Herd-immunity threshold for the Delta variant was estimated at 80 to 90 percent vaccine coverage.

Try this

Q1. Identify the five major groups of pathogens and give one Australian disease example for each. [5 marks]

• Cue. Bacteria (golden staph wound infection); viruses (influenza); protozoa (Cryptosporidium in unfiltered water); fungi (tinea); prions (variant CJD, very rare in Australia).

Q2. A new strain of Streptococcus is resistant to penicillin. (a) Identify two mechanisms by which resistance can arise. (b) Predict the effect of restricting penicillin use on resistance allele frequency over 12 months. [3 marks]

• Cue. (a) Spontaneous mutation (e.g. in penicillin-binding protein); horizontal gene transfer (plasmid carrying beta-lactamase). (b) Without selection pressure, resistant strains lose competitive advantage; resistant frequency may slowly decline if they carry a fitness cost.

Q3. Refer to vaccination. (a) Distinguish active from passive immunisation. (b) Explain how an mRNA vaccine generates antibodies without containing the pathogen. (c) Calculate the herd-immunity threshold for a disease with R0 = 10. [2+2+2 marks]

• Cue. (a) Active: host produces immune response and memory. Passive: preformed antibodies, short-lived, no memory. (b) Host cells translate spike mRNA; B and T cells respond to translated spike protein. (c) 1 - 1/10 = 90 percent of population must be immune.