The four groups of pathogen

You are expected to name specific diseases and their causative organisms — vague answers score nothing.

• Bacteria — tuberculosis (Mycobacterium tuberculosis), bacterial meningitis, ring rot in potatoes.
• Viruses — HIV/AIDS, influenza, and tobacco mosaic virus in plants.
• Fungi — black sigatoka (bananas), ringworm and athlete’s foot in animals.
• Protoctista — malaria, caused by Plasmodium and transmitted by the Anopheles mosquito, which acts as a vector (not a pathogen).

Transmission may be direct (contact, droplet, body fluids) or indirect (vectors, contaminated food or water, fomites). Factors increasing transmission include overcrowding, poor sanitation, poor nutrition (weakening the immune system), climate change extending vector range, and social or cultural factors.

Plant defences you must know: physical — waxy cuticle, bark, and callose, a polysaccharide deposited in the sieve plates and between cell walls to block the pathogen’s spread. Chemical — alkaloids (bitter, toxic to herbivores), terpenoids (antibacterial and antifungal) and phenols. Plants also produce hydrolytic enzymes and undergo necrosis, deliberately killing cells around the infection to isolate it.

Non-specific and specific immunity

Primary (non-specific) defences: the skin as a physical barrier (with sebum), mucous membranes that trap pathogens, lysozyme in tears and saliva, stomach hydrochloric acid, and blood clotting to seal wounds. Inflammation — mast cells release histamine, causing vasodilation and increased permeability, so more blood and white cells reach the site.

Phagocytosis: the phagocyte (neutrophil or macrophage) is attracted by chemicals, binds to the pathogen’s antigens, engulfs it into a phagosome, which fuses with a lysosome; hydrolytic enzymes digest it. The macrophage then displays the antigen on its surface — becoming an antigen-presenting cell, which activates the specific response.

Specific immunity — clonal selection and expansion:

• T lymphocytes — T helper cells bind the presented antigen and release cytokines, which stimulate phagocytes, T killer cells and B cells. T killer (cytotoxic) cells destroy infected cells using perforin. T memory cells persist. T regulator cells shut the response down afterwards and help prevent autoimmunity.
• B lymphocytes — a B cell with a complementary antibody binds the antigen and is activated by a T helper cell. It divides into plasma cells (secreting thousands of antibodies per second) and B memory cells.

Antibody structure: four polypeptides — two heavy, two light — held by disulfide bridges, with two variable regions forming antigen-binding sites, and a hinge region allowing flexibility. Antibodies cause agglutination, neutralise toxins, and act as opsonins that make pathogens easier to engulf. Autoimmune disease (rheumatoid arthritis, lupus, type 1 diabetes) is the failure of self-recognition.

Why the second infection is harmless

Resistance, and the arms race

Antibiotics target structures found in bacteria but not in human cells — the peptidoglycan (murein) cell wall, and the 70S ribosome (ours are 80S). This is why antibiotics are useless against viruses, which have neither.

How resistance evolves — get the order right:

• A random mutation occurs in a bacterium, giving resistance (e.g. producing β-lactamase, or altering the target protein). The antibiotic does not cause the mutation.
• The antibiotic is the selection pressure. Non-resistant bacteria are killed; the resistant one survives and reproduces.
• The resistance allele is passed on — vertically by binary fission, and horizontally between bacteria on plasmids (conjugation), which is why resistance spreads so alarmingly fast, even between species.
• Over time the frequency of the resistance allele in the population increases. MRSA and C. difficile are the results.

Reducing the problem: prescribe antibiotics only when necessary and never for viral infections; complete the full course (so that partially resistant bacteria are not left alive); rotate antibiotics; and improve hygiene and isolation in hospitals. Alternatives under investigation include bacteriophages and antimicrobial peptides.

Vaccination, herd immunity and antibodies as tools

A vaccine introduces antigen (a dead or attenuated pathogen, or an isolated antigen) so that the primary response occurs safely and memory cells are made. On real infection, the secondary response produces antibody faster, in greater concentration and for longer, destroying the pathogen before symptoms develop.

• Active immunity — your own immune system makes the antibodies. Natural (after infection) or artificial (vaccination). Slow to develop, but long-lasting, because memory cells are produced.
• Passive immunity — antibodies are given to you. Natural (across the placenta and in breast milk) or artificial (an antivenom or an antitoxin injection). Immediate, but short-lived, because no memory cells are made and the antibodies are broken down.
• Herd immunity — if a high enough proportion of the population is vaccinated, the pathogen cannot find enough susceptible hosts to spread. Transmission chains break, and even the unvaccinated (the very young, the immunocompromised) are protected.

Why some vaccines fail: antigenic variability. Influenza and HIV mutate rapidly, so their surface antigens change; memory cells from a previous strain no longer recognise them, and the flu vaccine must be reformulated each year. Monoclonal antibodies — identical antibodies from a single clone of B cells — are used in targeted cancer therapy, in pregnancy tests, and in the ELISA test, where an enzyme-linked antibody produces a colour change if the antigen is present.

Active or passive?

Sampling and Simpson’s index of diversity

Biodiversity can be considered at three levels: habitat diversity, species diversity (richness and evenness) and genetic diversity within a species.

Sampling must be random (generate coordinates with random numbers) to avoid bias, and the sample must be large enough for chance to average out. Use quadrats (frame, point or gridded) for plants and sessile animals — recording density, frequency or percentage cover; use transects (line or belt) where there is an environmental gradient; use pitfall traps, sweep nets, pooters and mark-release-recapture for motile animals. Opportunistic (non-random) sampling is quicker but biased and less representative.

D ranges from 0 to 1. A value near 1 means high diversity: many species, evenly represented. A community with high diversity is more stable, because it has more feeding relationships and is less vulnerable to the loss of any one species.

Species richness alone is not enough: a wood with 100 oaks and one elm is far less diverse than one with 50 of each, yet both have a richness of 2. Simpson’s index captures evenness as well as richness, which is exactly why it is used.

Your turn — Simpson’s index

Your turn — genetic biodiversity

Why diversity matters

Maintaining biodiversity

Biodiversity is threatened by habitat loss and fragmentation, over-exploitation, pollution, invasive species, agriculture (monoculture, hedgerow removal, pesticides) and climate change.

• In situ conservation — protecting a species in its natural habitat: nature reserves, national parks, marine conservation zones, controlled grazing, coppicing, and legal protection. Advantages: the whole ecosystem and its interactions are conserved, and the species continues to evolve in its own environment. It is also usually cheaper. Disadvantage: the original threat may still be present.
• Ex situ conservation — removing the organism to a safe place: botanic gardens, seed banks (seeds are dried and frozen, storing enormous genetic diversity very cheaply) and captive breeding in zoos, with the aim of reintroduction. Disadvantages: small populations risk inbreeding and loss of genetic diversity, animals may not survive reintroduction, and it is expensive.

International agreements: CITES regulates and restricts international trade in endangered species and their products. The Rio Convention on Biological Diversity committed nations to develop national strategies for sustainable use. In the UK, Countryside Stewardship schemes pay farmers to manage land for biodiversity — restoring hedgerows, leaving field margins and buffer zones.

In situ or ex situ?

Taxonomy, phylogeny and the three domains

The taxonomic hierarchy — each group nested entirely within the one above:

The binomial name is Genus species — universal, so scientists worldwide refer unambiguously to the same organism. A species is a group of organisms that can breed to produce fertile offspring.

• The three domains (Woese) — Bacteria, Archaea and Eukarya. Archaea and bacteria are both prokaryotes but differ fundamentally in their ribosomal RNA, in their cell wall chemistry (archaea have no peptidoglycan) and in their membrane lipids. This reclassification came directly from molecular evidence and could not have been made from appearance.
• The five kingdoms — Prokaryotae, Protoctista, Fungi, Plantae, Animalia.
• Phylogeny classifies by evolutionary relationship and common ancestry. Evidence: DNA base sequences, amino acid sequences of common proteins (e.g. cytochrome c), and immunological comparison of proteins.

Convergent evolution is the trap: unrelated species facing the same selection pressure evolve similar features (the streamlined shape of sharks and dolphins; the wings of birds and bats). Similar appearance therefore does not prove close relationship — only molecular evidence can settle it.

Variation, natural selection and the evidence

Variation may be interspecific (between species) or intraspecific (within one). Its causes are genetic (mutation, meiosis, random fertilisation), environmental, or — usually — a combination. Continuous variation (height, mass) is polygenic and gives a normal distribution; discontinuous variation (blood group) is controlled by one or few genes and gives discrete categories.

Natural selection, in the order the examiner wants:

• Random mutation creates a new allele — variation exists before the selection pressure appears.
• A selection pressure (predation, disease, competition, climate) acts.
• Individuals with the advantageous allele are more likely to survive and reproduce — differential reproductive success.
• They pass the allele to their offspring, so the frequency of the allele in the population increases over generations. That is evolution.

Evidence: the fossil record (organisms appear in rocks in an order consistent with complexity and with molecular phylogeny); comparative anatomy — homologous structures such as the pentadactyl limb, adapted to different functions from a common ancestral plan (divergent evolution); comparative biochemistry — highly conserved molecules such as cytochrome c and ribosomal RNA, whose degree of difference reflects the time since divergence.

Examples with real data: antibiotic resistance in bacteria; the peppered moth; insecticide resistance; and the flightless cormorant. All show the same logic: pre-existing variation + selection pressure = change in allele frequency.

Getting the logic right

Name that pathogen group

Tap a disease, then tap the group of organism that causes it.

Cell and role

Tap an item on the left, then its partner on the right.

The big ideas to take away

That is the whole of OCR Module 4 — Biodiversity, evolution and disease. Press Finish to see your score.