Investigate the transmission of a disease during an epidemic, including: adaptations of pathogens that facilitate their entry into and transmission between hosts

What this dot point is asking

NESA wants you to identify the structural, biochemical and behavioural adaptations that pathogens use to enter hosts and pass between them. Strong answers cite named adaptations with their specific function and link them to transmission mode.

The answer

Pathogens have evolved specific adaptations that solve three problems: getting into a new host, evading the host's defences, and getting back out to a new host. These adaptations are usually shaped by the transmission mode.

Adaptations for entry into the host

Surface attachment proteins

Many pathogens carry surface molecules that bind to specific host cell receptors. Influenza haemagglutinin binds to sialic acid on respiratory cells. HIV gp120 binds to CD4 receptors on T helper cells. Plasmodium sporozoites bind to hepatocyte surface proteins.

Enzymes that breach tissue barriers

Streptococcus pyogenes produces hyaluronidase and streptokinase, which break down connective tissue and clot proteins, allowing the bacterium to spread through skin and soft tissue. Some fungi secrete keratinases to digest skin.

Specialised entry structures

Bacteriophages and many bacterial pathogens use pili and fimbriae to attach to host cells before invasion. Salmonella uses a type III secretion system, a needle-like structure, to inject proteins that force gut cells to engulf the bacterium.

Spore and cyst stages

Bacillus anthracis forms endospores that resist heat, drying and chemical insult, allowing the pathogen to remain infectious in soil for decades. Giardia lamblia forms tough cysts that survive in water until ingested.

Adaptations for evading the host's defences

Antigenic variation

Influenza and HIV mutate rapidly (antigenic drift) so that antibodies raised against earlier strains do not recognise new ones. Trypanosoma brucei changes its surface glycoprotein coat repeatedly, evading antibody recognition.

Capsules and biofilms

Streptococcus pneumoniae has a polysaccharide capsule that prevents phagocytosis. Pseudomonas aeruginosa forms biofilms that block antibiotics and immune cells.

Intracellular hiding

Viruses replicate inside host cells, hidden from antibodies. Mycobacterium tuberculosis survives inside macrophages, the very cells meant to destroy it.

Adaptations for transmission between hosts

Inducing symptoms that spread the pathogen

Vibrio cholerae triggers severe watery diarrhoea, flooding water supplies with new bacteria. Influenza triggers coughing and sneezing, aerosolising the virus. Rabies virus alters host behaviour to encourage biting.

Vector-specific adaptations

Plasmodium has separate stages for the mosquito and human host, with surface proteins matching each. The parasite manipulates mosquito feeding behaviour to favour transmission.

Environmental durability

Norovirus is non-enveloped and resists drying, surviving on surfaces for weeks. Prions resist boiling, UV and standard disinfection, allowing transmission via contaminated surgical instruments.

High shedding rate

Measles virus produces enormous numbers of virions in the airway, and an infected person typically infects 12 to 18 susceptibles in a fully susceptible population.

Examples in context

Example 1. Influenza antigenic drift and the annual vaccine reformulation. Influenza A virus carries two surface glycoproteins, haemagglutinin (HA) and neuraminidase (NA), which are the major targets of host antibodies. The viral RNA polymerase lacks proofreading, so mutations accumulate continuously in HA and NA (antigenic drift). The Australian Influenza Vaccine Committee reviews global surveillance data from WHO sentinel labs in February each year to decide which HA and NA variants to include in the southern hemisphere vaccine, ready for May rollout. Periodically, two influenza strains reassort their RNA segments inside a co-infected pig or bird host (antigenic shift), producing a novel strain such as the 2009 H1N1 pandemic strain that swept Sydney. Both adaptations help influenza evade adaptive immunity.

Example 2. Bacillus anthracis spores and biosecurity at NSW abattoirs. Bacillus anthracis, the cause of anthrax in cattle, produces highly durable endospores when nutrients become scarce. The spores have a thick keratin-like coat that resists boiling, desiccation, UV radiation and many disinfectants for decades. In NSW, sporadic anthrax outbreaks occur in livestock when cattle graze over old burial sites of previously infected animals, sometimes more than 50 years later. NSW DPI biosecurity protocols require carcasses of anthrax-suspected animals to be incinerated and buried at least 2 metres deep, and abattoir surfaces are disinfected with sporicidal agents (formaldehyde or peracetic acid) because routine disinfectants cannot inactivate the spores.

Try this

Q1. Identify three adaptations that allow Mycobacterium tuberculosis to persist in human lungs for decades. [3 marks]

• Cue. Waxy mycolic acid cell wall resists phagocytic digestion, intracellular survival inside macrophages, granuloma formation enclosing dormant bacteria, slow growth rate.

Q2. A laboratory finds that 95 percent of Helicobacter pylori bacteria survive at pH 2 in human stomach acid, compared with only 2 percent of Escherichia coli. Identify the adaptation responsible and explain its mechanism. [3 marks]

• Cue. H. pylori produces urease, which converts urea into ammonia and neutralises stomach acid in a microenvironment surrounding the bacterium.

Q3. Compare adaptations for transmission in (a) Plasmodium falciparum (malaria) and (b) Vibrio cholerae (cholera). State one adaptation that facilitates onward transmission for each, and explain how host symptoms support spread. [2+2+3 marks]

• Cue. (a) Plasmodium develops gametocytes that infect feeding Anopheles mosquitoes; host fever does not directly aid transmission. (b) Cholera toxin causes massive watery diarrhoea contaminating water supplies. (c) Symptoms are sometimes pathogen adaptations to enhance spread.