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.

Worked example

A child has a runny nose, sore throat and mild fever. The doctor diagnoses a common cold, caused by a rhinovirus. Prescribing an antibiotic would not help (the pathogen is viral) and would contribute to resistance in the child's bacterial microbiota. Instead, the doctor recommends rest, fluids and paracetamol. A few days later the child develops a bacterial ear infection on top of the cold. Now an antibiotic (amoxicillin) is appropriate, targeting Streptococcus pneumoniae. The doctor stresses completing the full course to prevent partially resistant bacteria from surviving.

Common traps

Confusing viruses and bacteria. Bacteria are cells; viruses are not. Antibiotics work on bacteria, antivirals on viruses.

Saying vaccines "cause" the disease. Most vaccines cannot cause disease. Live attenuated vaccines very rarely cause mild forms in immunocompromised people.

Calling passive immunity "long-lasting". Passive immunity lasts only as long as the transferred antibodies (weeks to months). No memory forms.

Saying bacteria become resistant "because they are exposed". Exposure does not create resistance. Resistance arises by random mutation or horizontal gene transfer; exposure selects for already-resistant individuals.

Forgetting that prions are not organisms. Prions are misfolded proteins with no nucleic acid. They are not killed by antibiotics, antivirals or normal sterilisation.

In one sentence

Pathogens span bacteria (prokaryotic cells, treated with antibiotics that target cell walls or 70S ribosomes), viruses (acellular particles needing host cells, treated with antivirals targeting replication steps), protozoa, fungi and prions (misfolded proteins with no nucleic acid); vaccines train the adaptive immune system to produce active, long-lasting immunity and herd protection, while antibiotic resistance evolves by natural selection when antibiotic use selects for rare resistant variants and horizontal gene transfer spreads resistance genes between bacteria.