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.

Worked example

Compare two adaptations of HIV that facilitate persistence in human hosts.

1. gp120 binding to CD4. HIV's gp120 surface protein binds the CD4 receptor on T helper cells, then engages co-receptors (CCR5 or CXCR4) to fuse with the membrane. This adaptation specifically targets the cells coordinating the adaptive immune response.

2. Reverse transcription and integration. HIV reverse transcribes its RNA into DNA, which integrates into the host genome as a provirus. This adaptation hides the viral genome inside host chromosomes, where antibodies cannot reach it, allowing lifelong infection.

Common traps

Treating "adaptation" as anything the pathogen does. Markers want specific structural or biochemical features, not vague behaviours.

Forgetting evasion adaptations. Entry and exit get most attention, but immune evasion (capsules, antigenic variation, intracellular hiding) is often the highest-marks part of the question.

Generic surface proteins. "It has proteins on its surface" earns no marks. Name the protein (haemagglutinin, gp120, pili) and the receptor it binds.

Confusing adaptation with disease symptoms. Symptoms are sometimes adaptations (diarrhoea spreads cholera). But fever, fatigue and pain are usually host responses, not pathogen adaptations.

In one sentence

Pathogen adaptations including surface attachment proteins, tissue-degrading enzymes, antigenic variation, capsules, durable spore stages and behaviour-altering symptoms allow successful entry into hosts, evasion of immune responses, and onward transmission to new hosts.