Types of Pathogen

Spec Mapping — OCR H420 Module 4.1.1 — Communicable diseases, disease prevention and the immune system, opening content statement on the classification of pathogens into bacteria, viruses, protoctista and fungi, with named examples of disease in animals and plants (refer to the official OCR H420 specification document for exact wording). This lesson establishes the pathogen taxonomy on which the rest of the module rests.

A pathogen is any microorganism that causes disease in its host. Communicable (infectious) diseases — those transmissible from one individual to another — emerge from a tractable handful of biological architectures: prokaryotic cells, acellular nucleoprotein assemblies, eukaryotic protists and eukaryotic fungi. OCR A-Level Biology A specification 4.1.1 requires you to know all four of these groups and to be able to link cellular structure to mechanism of disease and to symptom. Equally important, the lesson sets the historical and conceptual frame: the germ theory of disease consolidated by Louis Pasteur in the 1860s–1870s and Robert Koch in the 1880s replaced miasmatic and humoral models with the modern one-pathogen-one-disease paradigm. Koch's celebrated postulates (the suspect organism must be present in every case; isolable in pure culture; capable of reproducing the disease in a healthy host; and re-isolable from that host) still underpin the way clinical microbiology operates, with caveats for viruses, asymptomatic carriers and polymicrobial disease.

The intellectual heritage you should be able to name in extended answers: Antonie van Leeuwenhoek (1670s — first observation of "animalcules" through a hand-ground microscope); Edward Jenner (1796 — first vaccination, against smallpox, exploiting the cross-protective immunity conferred by the related cowpox virus); Ignaz Semmelweis (1847 — empirical demonstration that handwashing reduces puerperal fever in maternity wards, rejected in his lifetime); Joseph Lister (1860s — surgical antisepsis with carbolic acid); Louis Pasteur (germ theory; attenuated rabies vaccine, 1885); Robert Koch (1880s — pure-culture technique on solid media, postulates, isolation of Bacillus anthracis and Mycobacterium tuberculosis); Dmitri Ivanovsky (1892 — tobacco mosaic disease persists after passage through bacterial filters, the first hint of viruses); Wendell Stanley (1935 — crystallisation of TMV, establishing its molecular nature).

Key Definitions:

• Pathogen — a microorganism that causes disease in its host.
• Communicable disease — a disease that can be transmitted from one organism to another, by direct or indirect routes.
• Host — an organism that harbours and supports a pathogen, either symptomatically or as an asymptomatic carrier.
• Virulence — the quantitative degree of pathogenicity; the capacity of a pathogen to cause severe disease, often measured as LD₅₀ (the dose lethal to half of a test population).
• Obligate intracellular parasite — a pathogen that can only replicate inside a host cell; all viruses qualify, as do some bacteria such as Chlamydia and Rickettsia.

---

The Four Groups of Pathogen — Architecture Compared

flowchart TD
    A[Pathogens] --> B[Bacteria]
    A --> C[Viruses]
    A --> D[Protoctista]
    A --> E[Fungi]
    B --> B1[Prokaryotic, 0.5-5 um]
    B --> B2[Peptidoglycan wall]
    B --> B3[Binary fission]
    C --> C1[Acellular, 20-300 nm]
    C --> C2[Nucleic acid + capsid]
    C --> C3[Obligate intracellular]
    D --> D1[Eukaryotic, 1-200 um]
    D --> D2[Nucleus + organelles]
    D --> D3[Often intracellular]
    E --> E1[Eukaryotic, um to m]
    E --> E2[Chitin wall]
    E --> E3[Hyphae or yeast]

A visual comparison of the four architectures highlights the contrasts in scale and cellular complexity.

Feature	Bacteria	Viruses	Protoctista	Fungi
Cell type	Prokaryotic	Acellular	Eukaryotic	Eukaryotic
Genetic material	Circular dsDNA + plasmids	DNA or RNA, ss/ds	Linear DNA in nucleus	Linear DNA in nucleus
Cell wall	Peptidoglycan	None	Usually absent	Chitin
Reproduction	Binary fission (every 20 min)	Replication inside host cell	Schizogony, binary fission, sexual	Spores, budding, hyphal extension
Size	0.5–5 µm	20–300 nm	1–200 µm	µm (yeasts) to m (mycelia)
Example disease	TB, cholera, ring rot	HIV, influenza, TMV	Malaria, late blight	Ringworm, athlete's foot, black sigatoka

1. Bacteria — Prokaryotic Cells

Bacteria are prokaryotic: single cells lacking a membrane-bound nucleus and organelles, with their genome packaged as a single circular DNA chromosome in a region called the nucleoid, supplemented by smaller circular plasmids carrying accessory genes (often antibiotic-resistance or virulence determinants). Their cytoplasm contains 70S ribosomes (slightly smaller than the 80S ribosomes of eukaryotic cytosol). A defining structural feature is the peptidoglycan cell wall — a mesh of N-acetylglucosamine and N-acetylmuramic acid sugars cross-linked by short peptide chains. This wall is the target of penicillins and the substrate of lysozyme, both of which we shall meet repeatedly in this module.

Christian Gram (1884) discovered that bacteria can be split into two classes by their differential retention of crystal violet dye:

Gram-positive bacteria have a thick (20–80 nm) peptidoglycan wall that retains the dye after a brief alcohol wash, staining purple. Gram-negative bacteria have a thin peptidoglycan layer sandwiched between two membranes; the outer membrane is rich in lipopolysaccharide (LPS), a potent endotoxin that triggers fever and septic shock when bacteria lyse. The classification matters clinically — most β-lactam antibiotics work better on gram-positives, whereas the LPS outer membrane of gram-negatives offers an extra permeability barrier.

Bacteria can also be classified by shape — cocci (spheres, e.g. Staphylococcus), bacilli (rods, e.g. E. coli, M. tuberculosis), spirilla (rigid helices), spirochaetes (flexible helices, e.g. Treponema pallidum of syphilis), vibrio (commas, e.g. V. cholerae) — and by oxygen requirement (aerobe, facultative anaerobe, obligate anaerobe). Reproduction is by binary fission, in which the chromosome replicates and the cell elongates and divides; under ideal conditions E. coli doubles every 20 minutes, which explains both the explosive course of bacterial infections and the rapid emergence of antibiotic-resistant lineages.

Bacteria damage hosts in two main ways:

1. Toxin production. Exotoxins are proteins secreted into the surroundings (cholera toxin, diphtheria toxin, tetanus toxin); they typically have very high specific activity, with a few molecules sufficient to kill a cell. Endotoxins are structural — LPS released when gram-negative cells lyse — and act systemically through the innate immune system, producing fever, hypotension and disseminated intravascular coagulation in septic shock.
2. Tissue invasion. Some bacteria (such as Mycobacterium tuberculosis) survive inside host cells, replicate, and trigger granuloma formation that destroys host tissue. Others (such as Streptococcus pyogenes) secrete enzymes — hyaluronidases, streptolysins — that degrade host extracellular matrix and lyse blood cells, enabling deep tissue invasion.

2. Viruses — Acellular Obligate Intracellular Parasites

Viruses sit at the boundary of life. Outside a host cell, a virus particle (virion) is a metabolically inert assembly of:

• A nucleic acid core — DNA or RNA, single- or double-stranded; segmented (influenza) or unsegmented (HIV).
• A protein coat (capsid) built from identical subunits (capsomeres) arranged with helical or icosahedral symmetry — economy through self-assembly from a small genome.
• Often an outer lipid envelope acquired by budding from a host membrane, studded with virally-encoded glycoprotein spikes that mediate attachment (HIV gp120; influenza HA; SARS-CoV-2 spike).

Viruses are obligate intracellular parasites: they carry no ribosomes, no metabolism and no ATP generation of their own, and can only replicate by hijacking the synthetic machinery of a host cell. The standard replication cycle has six stages — attachment, entry, uncoating, replication and gene expression, assembly, release — though enveloped viruses bud rather than lyse. Particularly important for OCR is the retrovirus strategy of HIV: an RNA genome is copied to dsDNA by viral reverse transcriptase (an RNA-dependent DNA polymerase that violates the classical DNA→RNA→protein flow) and integrated into the host chromosome by integrase, producing a permanent provirus that the immune system cannot eliminate.

Viruses cause disease by lysing infected cells (poliovirus, common cold rhinoviruses), by latent integration with periodic reactivation (herpesviruses, HIV), by transforming cells into cancers (human papillomavirus and cervical cancer; Epstein–Barr virus and Burkitt's lymphoma), and by provoking damaging immune responses (the cytokine storm of severe influenza or COVID-19, and most of the lung pathology of TB-coinfection HIV cases).

Exam Tip: Never describe a virus as "living" or "dying". Viruses are not classified as living organisms because they cannot independently metabolise, grow or reproduce. In exam answers use "viral particles", "virions" and "replicate" rather than "live", "die" or "grow".

3. Protoctista — Eukaryotic, Often Intracellular Parasites

Protoctista (protists) are eukaryotic microbes — a polyphyletic ragbag of organisms united by being neither animal, plant nor fungus. They have a true nucleus and full eukaryotic organelles (mitochondria, in many cases plastids, often flagella or cilia). The pathogenic protoctista typically invade host cells: in malaria, Plasmodium falciparum sporozoites injected by the Anopheles mosquito vector enter hepatocytes, multiply asexually (schizogony), and emerge as merozoites that infect erythrocytes, where they consume haemoglobin and lyse the red blood cells in synchronised waves that produce the classic 48-hour or 72-hour cyclical fever. Other examples include Trypanosoma brucei (African sleeping sickness, transmitted by tsetse flies), Leishmania (sandflies), and the oomycete Phytophthora infestans (potato late blight) — although oomycetes are now recognised as more closely related to brown algae than to fungi.

4. Fungi — Eukaryotic with Chitin Walls

Fungi are eukaryotic, with a chitin cell wall (the same nitrogenous polysaccharide that armours arthropod exoskeletons). They occur as unicellular yeasts (Saccharomyces cerevisiae, Candida albicans) and as multicellular moulds built from threadlike hyphae that branch and intersect to form a mycelium. Fungi are heterotrophic saprotrophs or parasites that secrete extracellular hydrolytic enzymes (cellulases, ligninases, keratinases, proteases) and absorb the digested products — a strategy ideal for digesting tough plant cell walls or skin keratin.

In plants, pathogenic fungi often colonise vascular tissue (Dutch elm disease, Fusarium wilts) or photosynthetic mesophyll (black sigatoka), digesting cell walls and producing toxins. In animals, fungi typically cause superficial dermatophyte infections (ringworm, athlete's foot) that disfigure but rarely kill the immunocompetent host; in the immunocompromised (HIV, chemotherapy patients), opportunistic fungi such as Pneumocystis jirovecii, Aspergillus and disseminated Candida can be lethal. Fungal spores — extraordinarily resistant to desiccation and UV — are the principal means of transmission, particularly in crop disease.

---

How Pathogens Cause Disease — A Unified Framework

At the cellular level pathogens damage hosts by a small set of mechanisms that recur across all four taxonomic groups:

1. Direct damage to host macromolecules. Toxins inactivate critical host proteins (diphtheria toxin ADP-ribosylates elongation factor EF-2, halting protein synthesis); some viruses lyse cells through their replication cycle; fungal hyphae mechanically penetrate plant cells.
2. Competition for resources. Parasitic pathogens consume glucose, amino acids and iron needed by the host; the host's iron-sequestering protein transferrin is one front in this nutritional immunity.
3. Blockage of transport. Fungal hyphae and bacterial exopolysaccharides block plant xylem (ring rot, Fusarium wilt); Plasmodium-infected red cells adhere to capillary endothelium, blocking cerebral microcirculation (cerebral malaria).
4. Subversion of immunity. HIV destroys T helper cells; M. tuberculosis survives inside the very macrophages that engulf it; Plasmodium changes its surface antigens between schizogony cycles.
5. Damaging immune responses. Bacterial endotoxin triggers septic shock; the cytokine storm of severe influenza kills more by host response than by direct viral cytopathy.

Exam Tip: When asked "how does the pathogen cause symptoms?" always link mechanism (toxin / intracellular replication / blockage / immune subversion) to tissue damaged (gut epithelium / alveolar macrophages / red blood cells) to observable symptom (diarrhoea / chronic cough / cyclical fever). Three-step chains pick up the marks.

---

Synoptic Links

Synoptic Links — Connects to:

• ocr-alevel-biology-cell-structure — bacteria are the prototypical prokaryotes; the prokaryote/eukaryote comparison there is now operationalised through pathogen examples.
• ocr-alevel-biology-nucleic-acids-enzymes — DNA versus RNA viruses, retroviral reverse transcriptase, and the molecular basis of vaccination all draw on the central dogma covered in Module 2.1.3.
• ocr-alevel-biology-biological-molecules — peptidoglycan structure, chitin and capsid quaternary protein architecture are direct applications of macromolecule chemistry.

Practical Activity Group anchor

Practical Activity Group anchor: PAG 7 — Microbiological techniques. OCR PAG 7 requires aseptic technique, the cultivation of bacteria on agar plates, and the antibiotic disc-diffusion (Kirby–Bauer) assay. This first lesson provides the taxonomic context: when you set up a serial-dilution viable count for E. coli, you are working with a gram-negative facultative anaerobe of the Enterobacteriaceae, and the assumptions of your protocol (incubation at 25–30 °C in a school lab, not 37 °C; no presumptive identification of pathogenic strains) follow from its classification.

Specimen question modelled on the OCR H420 paper format

Question (9 marks): Compare bacteria and viruses as pathogens. Your answer should refer to cell structure, replication, mechanism of damage, and the consequences for treatment.

AO breakdown

Mark	AO	Awarded for
1	AO1	Bacteria are prokaryotic cells with peptidoglycan walls and 70S ribosomes
2	AO1	Viruses are acellular, comprising nucleic acid + capsid (± envelope)
3	AO1	Bacteria reproduce by binary fission; viruses can only replicate inside host cells
4	AO2	Bacteria damage by toxins or tissue invasion (named example)
5	AO2	Viruses damage by hijacking host machinery and lysing cells (named example)
6	AO2	Antibiotics target bacterial-specific structures (cell wall, 70S ribosome, DNA gyrase)
7	AO2	Antivirals must target viral enzymes or block entry, because viruses use host machinery
8	AO3	Evaluative: explain why antibiotics do not work on viruses, with reference to the lack of bacterial-style targets
9	AO3	Evaluative: synoptic comment — e.g. retroviral integration makes complete cure of HIV impossible with current drugs

AO split: AO1 = 3, AO2 = 4, AO3 = 2.

Grade C model answer (~190 words)

Bacteria are single prokaryotic cells with a peptidoglycan cell wall and 70S ribosomes, and reproduce by binary fission. Viruses are not cells; they are particles made of a nucleic acid (DNA or RNA) inside a protein capsid, sometimes with an envelope. Viruses can only replicate inside a host cell because they have no ribosomes or metabolism of their own.

Bacteria cause disease in two main ways. They can produce toxins, for example Vibrio cholerae produces a toxin that causes intestinal cells to lose chloride ions and water, giving severe diarrhoea. They can also invade tissues, for example Mycobacterium tuberculosis survives inside macrophages and damages the lungs.

Viruses cause disease by hijacking host cells to make more viruses, then lysing the cell. For example, influenza damages the ciliated epithelium of the airways, leaving the lungs open to secondary bacterial infection.

Antibiotics like penicillin target the bacterial peptidoglycan cell wall, so they work on bacteria but not on viruses, because viruses do not have a cell wall. Antiviral drugs work in different ways, for example by blocking enzymes like reverse transcriptase in HIV.

Examiner commentary: M1 (prokaryotic + peptidoglycan), M1 (acellular nucleic-acid–capsid), M1 (binary fission vs obligate intracellular), M1 (bacterial toxin example), M1 (viral lysis example), M1 (antibiotics target peptidoglycan). Around 6/9 — secures all AO1 and most AO2 but fails to develop AO3 evaluative depth. The candidate has not explained why antibiotics fundamentally cannot work on viruses (the AO3 point) and offers no synoptic comment.

Grade B model answer (~260 words)

Bacteria are prokaryotic cells: single cells with a circular chromosome in a nucleoid, no membrane-bound organelles, 70S ribosomes and a peptidoglycan cell wall (gram-positive: thick wall, retains crystal violet; gram-negative: thin wall with outer LPS membrane). They reproduce by binary fission, doubling every 20 minutes under ideal conditions.

Viruses are acellular obligate intracellular parasites composed of a nucleic acid (DNA or RNA, single- or double-stranded) inside a protein capsid; many are also enveloped (e.g. HIV, influenza). They lack ribosomes, ATP synthesis and metabolism, so they must enter a host cell to replicate, hijacking the host's ribosomes and nucleotide pool.

Bacterial damage happens through exotoxins (cholera toxin causes secretory diarrhoea), endotoxin (LPS of gram-negatives causes septic shock), or invasion (M. tuberculosis forms granulomas in the lungs).

Viral damage happens through cell lysis (poliovirus killing motor neurones), integration (HIV inserting its DNA into T-helper cells), or immune-mediated injury (cytokine storms in severe COVID-19).

For treatment, antibiotics like β-lactams (penicillin) inhibit peptidoglycan cross-linking, aminoglycosides target the 30S ribosomal subunit, and fluoroquinolones inhibit DNA gyrase. All of these targets are bacterial-specific. Viruses lack peptidoglycan walls, lack 70S ribosomes and lack DNA gyrase — so antibiotics simply do nothing. Antivirals must instead target viral enzymes (reverse transcriptase inhibitors against HIV, neuraminidase inhibitors against influenza) or block entry, which is much harder pharmacologically.

Examiner commentary: Excellent AO1 (M1 prokaryote+wall, M1 acellular, M1 fission vs intracellular), strong AO2 (M1 bacterial damage, M1 viral damage, M1 antibiotic targets, M1 antivirals), one AO3 mark (M1 explanation of why antibiotics fail on viruses). Around 8/9 — falls short only on the second AO3 evaluative move (e.g. retroviral integration making HIV uncurable).

Grade A* model answer (~350 words)

Bacteria and viruses are pathogens of fundamentally different biological category. Bacteria are prokaryotic cells: nucleoid-organised circular dsDNA chromosome supplemented by plasmids; 70S ribosomes; cytoplasm without organelles; cell membrane surrounded by a peptidoglycan wall (thick in gram-positives, thin and overlaid by an LPS outer membrane in gram-negatives). They reproduce autonomously by binary fission, doubling every ~20 minutes under permissive conditions, which is the basis for exponential growth in unrestricted culture and the rapid selection of resistant clones. Viruses are not cells at all: a virion is an assembly of nucleic acid (DNA or RNA, single- or double-stranded, segmented or not) packaged in a self-assembled protein capsid, often acquired with an envelope from a host membrane on egress. Lacking ribosomes, ATP synthesis and metabolism, viruses are obligate intracellular parasites and replicate only by hijacking host cell biosynthesis.

Mechanistically, bacteria damage through exotoxins (e.g. V. cholerae choleragen, locking adenylate cyclase to drive Cl⁻ efflux and osmotic diarrhoea; Clostridium tetani tetanospasmin, blocking glycine release at inhibitory interneurones), through endotoxin (LPS, triggering TLR4-driven cytokine storms in gram-negative sepsis), or through invasion (intracellular survival of M. tuberculosis inside macrophages, producing fibrotic granulomas). Viruses damage by lysis (poliovirus killing anterior horn motor neurones), latent integration (HIV provirus permanently incorporated into host CD4⁺ T-cell genomes by integrase, making sterilising cure with current antiretrovirals impossible), or immunopathology (severe influenza driven by cytokine storm).

The pharmacological consequence is decisive. Antibiotics target bacterial-specific structures (β-lactams: peptidoglycan cross-linking; aminoglycosides: 30S ribosome; fluoroquinolones: DNA gyrase). Viruses possess none of these targets — antibiotics are biochemically inert against viral infection, and prescribing them for viral disease drives resistance without therapeutic benefit. Antivirals must instead target viral enzymes (reverse transcriptase, neuraminidase, protease, polymerase) or block entry — a smaller chemical-space and a much harder problem because the virus exploits host machinery the host cannot tolerate inhibiting.

Examiner commentary: Full 9/9. M1 prokaryote + peptidoglycan, M1 acellular nucleic-acid + capsid, M1 fission vs obligate intracellular (AO1 trio); M1 bacterial damage with named toxin mechanism, M1 viral damage with named example, M1 antibiotic targets with three examples, M1 antiviral strategy (AO2 quartet); M1 AO3 explaining why antibiotics fail on viruses (bacterial-specific targets absent), M1 AO3 retroviral integration / sterilising cure synoptic remark.

---

A-Level-depth misconceptions

The errors that distinguish A from A*:

1. Treating "all bacteria are pathogenic". The vast majority of bacterial species are harmless or beneficial; the gut microbiome carries ~10¹³ commensal bacteria that aid digestion and exclude pathogens.
2. Confusing virus and bacterium. Viruses have no cytoplasm, no ribosomes, no metabolism; calling them "tiny cells" loses the central point.
3. Mistaking the oomycete Phytophthora for a true fungus. OCR accepts either "fungus-like protoctist" or "oomycete", but molecularly oomycetes are stramenopiles closer to brown algae.
4. Stating that antibiotics kill viruses. They do not — and prescribing them for viral disease drives bacterial resistance through bystander selection on the microbiome.
5. Conflating pathogen with parasite. All pathogens are parasitic in a broad sense, but A-Level OCR uses "pathogen" specifically for disease-causing microbes; helminths are studied separately.

Common errors and mark-loss patterns

• A typical pitfall is writing "bacteria are small viruses" — they are different classes of entity entirely. Examiners expect a structural distinction (cellular vs acellular) first.
• Candidates often miss that plasmids carry the genes for antibiotic resistance — when describing horizontal gene transfer, naming the plasmid scoops an extra mark.
• A common pitfall is omitting the host range of vectors — Anopheles mosquitoes are essential for malaria transmission, Aedes for dengue/Zika, Culex for West Nile; mark schemes reward naming the vector.
• Candidates frequently lose marks by stating "viruses are alive" — examiners want the textbook position that viruses are non-living because they lack metabolism and independent reproduction.

Going further

• Madigan et al., Brock Biology of Microorganisms — the canonical undergraduate microbiology text; chapters 2–4 develop the bacterial-cell topology and gram-stain biochemistry far beyond A-Level depth.
• Flint et al., Principles of Virology — the structural and replication-strategy classification of viruses (Baltimore classification) extends the OCR DNA/RNA-virus split into seven mechanistically distinct categories.
• Oxbridge-style prompt: "Are viruses alive? Make the case both ways." A strong answer accepts that viruses fail the metabolism/growth/independent-reproduction criteria but argues that they undergo evolution by natural selection and exhibit heritable variation — properties usually associated with life.
• Undergraduate analogue: the Cambridge IB Microbiology paper revisits this taxonomy in its first lecture, then immediately splits into prokaryote diversity (Bergey's manual), virus structure (Baltimore), and eukaryotic-microbe diversity (the multikingdom protistan tree).

Quick Recap

• Four pathogen groups: bacteria (prokaryotic, peptidoglycan wall, binary fission), viruses (acellular, nucleic acid + capsid, obligate intracellular), protoctista (eukaryotic, often intracellular parasites) and fungi (eukaryotic, chitin walls, hyphae or yeasts).
• Bacteria damage by toxins (exo- and endotoxins) or tissue invasion; viruses by lysis, integration or immunopathology; protoctista by intracellular invasion and red-cell lysis; fungi by tissue digestion and toxin secretion.
• Gram-positive vs gram-negative is a structural distinction with major clinical implications for antibiotic choice.
• Antibiotics target bacterial-specific structures (peptidoglycan, 70S ribosome, DNA gyrase) and cannot work on viruses.
• The intellectual heritage runs from van Leeuwenhoek (1670s) through Jenner (1796), Pasteur and Koch (1860s–1880s) to Stanley's crystallisation of TMV (1935).

---

Reference: OCR A-Level Biology A (H420) specification 4.1.1 (refer to the official OCR H420 specification document for exact wording).