Microbial Diseases and Host–Pathogen Interaction: Infection, Pathogenicity and Immunity

This is the first chapter of Section XL3.7 of XL3 Microbiology, one of the five optional sections of the Life Sciences (XL) paper. It answers the syllabus heading "Microbial Diseases and Host Pathogen Interaction": normal microbiota; classification of infectious diseases; reservoirs of infection; nosocomial, opportunistic and emerging infections; mechanisms of microbial pathogenicity; nonspecific defence of the host; antigens and antibodies; humoral and cell-mediated immunity; vaccines; passive immunization; immune deficiency; and human diseases caused by viruses, bacteria and pathogenic fungi with their standard causal organisms. The chapter teaches the vocabulary of infection and epidemiology, how pathogens attach, invade and injure, how innate and adaptive immunity answer them, and how vaccination exploits that answer. Its numericals are epidemiological: attack rate, the herd-immunity threshold 1 − 1/R₀, vaccination coverage corrected for vaccine efficacy, and the effective reproduction number.

1. Normal microbiota, infection, and the classification of infectious disease

The normal microbiota (normal flora) is the community of microorganisms that routinely lives on the skin, in the mouth, gut, upper respiratory tract and genitourinary tract of a healthy body; internal organs, blood and the lower airways are normally sterile. Most are commensals (benefit without harming) and many are mutualists: gut anaerobes such as Bacteroides ferment fibre and synthesise vitamin K and some B vitamins, and the resident flora resists colonisation by pathogens (microbial antagonism, or competitive exclusion). An infection is the growth of a microbe in or on the host; disease is the measurable impairment of function that may follow. Pathogenicity is the capacity to cause disease and virulence its degree. A primary pathogen causes disease in a healthy host; an opportunistic pathogen causes disease only when defences are breached or the microbe reaches an abnormal site.

Four ways infectious diseases are classified
BasisCategoriesExample
Occurrence in a populationSporadic, endemic, epidemic, pandemicA constant background of typhoid is endemic; a sudden rise is an epidemic
Duration and onsetAcute, chronic, subacute, latentInfluenza is acute; tuberculosis is chronic; herpes is latent
Extent in the bodyLocal, focal, systemic (generalised)A boil is local; measles is systemic
TransmissibilityCommunicable/contagious vs non-communicableCholera is communicable; tetanus is not spread person to person
ℹ️ Reservoirs of infection
A reservoir is where the pathogen is maintained between hosts. Human reservoirs include symptomatic cases and carriers (infected but well, e.g. a Salmonella Typhi carrier). Animal reservoirs give rise to zoonoses (rabies, plague, brucellosis). Non-living/environmental reservoirs are soil and water (Clostridium tetani spores in soil; Vibrio cholerae in water). Controlling the reservoir is often the most effective break in the chain of transmission.

2. Nosocomial, opportunistic and emerging infections

A nosocomial (healthcare-associated) infection is one acquired in a hospital or healthcare setting, neither present nor incubating at admission. Three factors converge there: a population of compromised hosts, invasive procedures that breach barriers (catheters, intravenous lines, ventilators, surgery), and a resident flora of hardy, often drug-resistant organisms. The commonest are catheter-associated urinary tract infection, surgical-site infection, ventilator-associated pneumonia and bloodstream infection. Typical agents are opportunists: Escherichia coli, Staphylococcus aureus (including MRSA), Pseudomonas aeruginosa, Klebsiella pneumoniae, Enterococcus species and Clostridioides difficile (after antibiotics wipe out the protective gut flora).

Opportunistic infections also dominate in people with HIV/AIDS, cancer chemotherapy or transplant immunosuppression: Candida albicans, Pneumocystis jirovecii pneumonia, Cryptococcus neoformans and Aspergillus fumigatus. Emerging infectious diseases are those newly recognised or rapidly increasing in incidence or geographic range — SARS-CoV-2 (COVID-19), HIV, Ebola virus, Zika virus — while re-emerging diseases return after decline, often as drug-resistant forms such as multidrug-resistant tuberculosis. Drivers include new or mutated pathogens, ecological and climate change, human encroachment on wildlife, global travel and trade, and the misuse of antimicrobials.

⚠️ Nosocomial need not mean virulent
The organisms behind hospital infections are usually low-virulence opportunists that a healthy immune system clears easily. They cause disease because the host is compromised and a barrier has been bypassed — not because the microbe is intrinsically a fierce pathogen. Reading a resistant hospital isolate as inherently more virulent is a common error; resistance is about surviving the drug, not about causing worse disease.

3. Mechanisms of microbial pathogenicity

Causing disease is a sequence: entry through a portal (respiratory, gastrointestinal, genitourinary, skin break, or parenteral), adhesion, invasion or toxin delivery, evasion of defences, and injury. Adhesion uses adhesins on pili/fimbriae, flagella or the glycocalyx that bind specific host receptors; without attachment, flow and ciliary clearance sweep the microbe away. Invasion is helped by enzymes: hyaluronidase and collagenase break down connective tissue, coagulase clots plasma to shield staphylococci, and kinases (streptokinase) dissolve clots to spread. Defences are evaded by antiphagocytic capsules (Streptococcus pneumoniae, Klebsiella), IgA proteases, intracellular survival (Mycobacterium tuberculosis blocks phagosome–lysosome fusion) and antigenic variation.

Exotoxins versus endotoxin
FeatureExotoxinsEndotoxin
Chemical natureSecreted proteinsLipid A of LPS in the outer membrane
SourceGram-positive and Gram-negativeGram-negative only
ReleasedSecreted by living cellsOn lysis of the cell
Potency and specificityVery potent, specific action (A-B toxins, superantigens)Weaker, general: fever, inflammation, septic shock
Heat and toxoidHeat-labile; can be made into toxoid vaccinesHeat-stable; no toxoid
🎯 ID₅₀ and LD₅₀ measure virulence
Virulence is quantified by dose. The ID₅₀ is the infectious dose that infects 50% of a test group, and the LD₅₀ the lethal dose that kills 50%. A lower ID₅₀ or LD₅₀ means a more virulent organism, because fewer organisms (or less toxin) are needed. Shigella, with an ID₅₀ of only tens of cells, is far more infectious than Vibrio cholerae, which needs millions.

4. Nonspecific (innate) defence of the host

Innate defence is present from birth, acts within minutes to hours, and does not improve with repeated exposure. The first line is barriers: intact skin, mucous membranes with mucus and cilia, the flushing of tears, saliva and urine, stomach acid, lysozyme (cleaves peptidoglycan), antimicrobial peptides and the normal flora. The second line is cellular and chemical: phagocytes (neutrophils first, then macrophages) that engulf and digest microbes, natural killer (NK) cells that kill virus-infected and tumour cells, the inflammatory response (redness, heat, swelling, pain, bringing cells and plasma to the site), fever (a raised set-point that slows many pathogens), and interferons (host proteins that make neighbouring cells resist viral replication).

The complement system is about 30 serum proteins activated in a cascade by three routes — the classical pathway (triggered by antibody bound to antigen), the lectin pathway (mannose-binding lectin on microbial sugars) and the alternative pathway (spontaneous, on microbial surfaces). All three converge on C3. The effects are threefold: opsonisation (C3b coats microbes for phagocytosis), inflammation (anaphylatoxins C3a and C5a recruit cells), and cytolysis by the membrane attack complex (MAC, C5b–C9) that punches pores in the target membrane. Complement bridges innate and adaptive immunity because its classical pathway is launched by antibody.

5. Antigens, antibodies, and humoral and cell-mediated immunity

An antigen is any molecule the adaptive system recognises; an immunogen provokes a response. The specific part bound is the epitope (antigenic determinant). A hapten is too small to be immunogenic alone but becomes so when coupled to a carrier protein. An antibody (immunoglobulin) is a Y-shaped glycoprotein of two identical heavy and two identical light chains joined by disulfide bonds. Each arm ends in a variable region forming the antigen-binding site (two Fab arms, so a single IgG monomer is bivalent); the stem is the constant Fc region that determines class and binds complement and phagocyte receptors.

The five immunoglobulin classes
ClassFormRole to remember
IgGMonomer; most abundant in serumSecondary response, crosses the placenta, opsonises, neutralises, fixes complement
IgMPentamerFirst made in a primary response; strongest complement activator
IgADimer in secretionsMucosal and secretory defence; in milk, saliva, tears
IgEMonomerBinds mast cells; allergy and anti-parasite response
IgDMonomerB-cell surface receptor; little in serum

Adaptive immunity has two arms. Humoral immunity is mediated by antibodies made by plasma cells (differentiated B cells) and defends mainly against extracellular microbes and toxins by neutralisation, opsonisation and complement fixation. Cell-mediated immunity is run by T cells, which recognise antigen only when displayed on MHC molecules: CD4⁺ helper T cells read peptide on MHC class II of antigen-presenting cells and secrete cytokines that direct both arms; CD8⁺ cytotoxic T cells read peptide on MHC class I of any infected cell and kill it, clearing intracellular pathogens such as viruses. Both arms follow clonal selection: a first exposure gives a slow primary response dominated by IgM; surviving memory cells give a faster, larger, IgG-rich secondary response — the basis of immunological memory and of vaccination.

6. Vaccines, passive immunization, and immune deficiency

Active immunization exposes the immune system to antigen so the host makes its own response and memory; it is slow to protect but long-lasting. Live attenuated vaccines use a weakened microbe (BCG, oral polio/Sabin, MMR) and give strong, lasting immunity but must not be given to the severely immunodeficient. Inactivated/killed vaccines (injected polio/Salk, rabies) are safer but weaker and often need boosters. Subunit, toxoid and conjugate vaccines use parts: tetanus and diphtheria toxoids (inactivated exotoxin), hepatitis B surface antigen, and polysaccharide–protein conjugates (Hib, pneumococcal). A pure polysaccharide is a T-independent antigen, so infants answer it weakly, mostly with IgM and little memory; coupling it to a protein lets helper T cells join, giving a T-dependent response with class switching and memory. Newer platforms include mRNA and viral-vector vaccines.

🧠 Active vs passive immunization
Passive immunization transfers ready-made antibodies rather than antigen, so protection is immediate but short-lived and leaves no memory: maternal IgG across the placenta and IgA in milk, tetanus and diphtheria antitoxin, rabies and hepatitis B immunoglobulin, snake antivenom, and therapeutic monoclonal antibodies. Rule of thumb: give the antigen (vaccine) before exposure for lasting protection; give the antibody (serum) after a dangerous exposure when there is no time to wait for an active response.

Immune deficiency is a failure of host defence. Primary (congenital) deficiencies are inherited: severe combined immunodeficiency (SCID) loses both T and B function, X-linked (Bruton) agammaglobulinaemia (defective Bruton's tyrosine kinase) loses B cells and antibody, and DiGeorge syndrome loses the thymus and hence T cells. Secondary (acquired) deficiencies are far commoner and arise from HIV/AIDS (progressive loss of CD4⁺ T cells, which disables both arms and opens the door to opportunistic infections), malnutrition, cancer, and immunosuppressive or cytotoxic drugs. The pattern of infections points to the arm that has failed: recurrent pyogenic bacterial infections suggest an antibody defect, while severe viral, fungal and intracellular infections suggest a T-cell defect.

7. Human diseases caused by viruses, bacteria and pathogenic fungi

GATE expects the standard causal organism for each disease. Group them by agent and learn the one organism each disease is attributed to; the trap is swapping a bacterial for a viral cause, or naming the wrong genus.

Diseases and their standard causal organisms
Agent typeDiseaseCausal organism
VirusAIDS; rabies; dengueHIV; Rabies virus; Dengue virus
VirusMeasles; poliomyelitis; hepatitis BMeasles virus; Poliovirus; Hepatitis B virus
BacteriumTuberculosis; cholera; typhoidMycobacterium tuberculosis; Vibrio cholerae; Salmonella Typhi
BacteriumDiphtheria; tetanus; plagueCorynebacterium diphtheriae; Clostridium tetani; Yersinia pestis
BacteriumPeptic ulcer; leprosyHelicobacter pylori; Mycobacterium leprae
FungusCandidiasis; cryptococcal meningitisCandida albicans; Cryptococcus neoformans
FungusAspergillosis; ringworm (dermatophytosis)Aspergillus fumigatus; Trichophyton / Microsporum / Epidermophyton
📖 Koch's postulates, in one line
To prove a microbe causes a disease, the classical test is Koch's postulates: the organism is found in every case, isolated in pure culture, reproduces the disease when introduced into a healthy host, and is re-isolated from that host. They anchor the whole idea of a specific causal organism — and their limits (unculturable pathogens, asymptomatic carriers, agents like HIV that cannot ethically be tested in humans) are exactly why molecular criteria now supplement them.

Key takeaways

  • The normal microbiota protects by competitive exclusion and nutrition; disease needs a pathogen, a susceptible host and a route, and infection is classified by occurrence (sporadic/endemic/epidemic/pandemic), duration, extent and transmissibility.
  • Nosocomial, opportunistic and emerging infections share a theme: low-virulence organisms exploit compromised hosts, breached barriers, drug resistance, or new ecological opportunity.
  • Pathogenicity is adhesion, invasion, evasion and injury; exotoxins are potent specific proteins (toxoid-able) while endotoxin is the heat-stable lipid A of Gram-negative LPS causing fever and shock. Lower ID₅₀/LD₅₀ means higher virulence.
  • Innate defence (barriers, phagocytes, NK cells, inflammation, fever, interferons, complement) is fast and fixed; complement acts by opsonisation (C3b), inflammation (C3a/C5a) and the MAC (C5b–C9).
  • Humoral immunity (B cells, antibodies) clears extracellular microbes; cell-mediated immunity (CD4⁺ helper on MHC II, CD8⁺ cytotoxic on MHC I) clears intracellular ones. IgM leads the primary response; IgG, from memory cells, leads the faster secondary one.
  • Active immunization (vaccines) builds lasting memory; passive immunization (preformed antibodies) protects at once but briefly. Learn the one standard causal organism per disease across viruses, bacteria and pathogenic fungi.

Practice questions (18)

Attempt each one before opening the answer. Every explanation names the tempting wrong option as well as the right one, because that is where marks are lost.

  1. Which organism is the standard causal agent of cholera?

    1. Salmonella Typhi, a Gram-negative bacterium causing an enteric fever with bacteraemia
    2. Shigella dysenteriae, a Gram-negative bacterium causing bloody dysentery
    3. Rotavirus, an RNA virus that is the leading cause of infantile diarrhoea
    4. Vibrio cholerae, a curved Gram-negative bacterium transmitted by contaminated water
    Show answer

    Answer: D — *Vibrio cholerae*, a curved Gram-negative bacterium transmitted by contaminated water

    Cholera is caused by Vibrio cholerae, whose enterotoxin drives the watery diarrhoea. Salmonella Typhi causes typhoid, a different enteric fever, and is the tempting swap because both are water-borne Gram-negative gut pathogens; but typhoid is systemic with fever, not the profuse rice-water stool of cholera.

  2. A Gram-negative septic patient develops fever and shock only after antibiotics lyse large numbers of the bacteria. Which bacterial component best explains this?

    1. A secreted A-B exotoxin that acts enzymatically on one specific host target inside the cell
    2. Endotoxin (lipid A of LPS), released on cell lysis and causing fever and septic shock
    3. A polysaccharide capsule that blocks phagocytosis of the intact, living bacterial cell
    4. Hyaluronidase that spreads the organism through connective tissue
    Show answer

    Answer: B — Endotoxin (lipid A of LPS), released on cell lysis and causing fever and septic shock

    Lipid A of lipopolysaccharide is endotoxin; it sits in the Gram-negative outer membrane and is released when the cell lyses, triggering fever, inflammation and septic shock. An exotoxin is the tempting choice, but exotoxins are secreted by living cells and act specifically, whereas the release here is tied to lysis and the effects are the general ones of endotoxin.

  3. A deficiency in the complement component C3 would most directly impair which three functions?

    1. Antibody class switching, affinity maturation of B cells and long-term plasma-cell survival
    2. Interferon signalling, NK-cell killing of infected cells and the induction of fever
    3. Opsonisation, inflammatory cell recruitment and formation of the membrane attack complex
    4. Mucociliary clearance, lysozyme activity in tears and the acidity of gastric juice
    Show answer

    Answer: C — Opsonisation, inflammatory cell recruitment and formation of the membrane attack complex

    All three complement pathways converge on C3, so losing C3 cripples opsonisation (C3b), the inflammatory anaphylatoxins (C3a/C5a) and the downstream MAC (C5b–C9). The antibody-maturation functions belong to B cells and are not complement effects, which is the plausible distractor if one confuses the two systems.

  4. Which antibody class is produced first and in greatest amount during the primary response to a new antigen?

    1. IgM, a pentamer and the strongest activator of the classical complement pathway
    2. IgG, the monomer that dominates the secondary response and crosses the placenta
    3. IgA, the secretory dimer that defends mucosal surfaces
    4. IgE, the monomer bound to mast cells in allergy and anti-parasite responses
    Show answer

    Answer: A — IgM, a pentamer and the strongest activator of the classical complement pathway

    IgM appears first in a primary response and, as a pentamer with ten binding sites, is the best complement activator. IgG is the tempting answer because it is the most abundant serum antibody overall, but that dominance is in the secondary response; early in a first exposure IgM leads.

  5. A virus mutates so that infected cells no longer display viral peptides on MHC class I. Which immune function is most directly evaded?

    1. Neutralisation of free virus particles by secreted IgG
    2. Opsonisation of the virus by complement C3b
    3. Activation of CD4⁺ helper T cells by antigen-presenting cells
    4. Killing of infected cells by CD8⁺ cytotoxic T lymphocytes
    Show answer

    Answer: D — Killing of infected cells by CD8⁺ cytotoxic T lymphocytes

    CD8⁺ cytotoxic T cells recognise peptide on MHC class I, so a cell that stops presenting on MHC I escapes their killing — though it may then become a target for NK cells, which sense missing self. Antibody neutralisation and complement act on free virus outside cells and are unaffected by intracellular MHC I loss; CD4⁺ activation uses MHC class II on antigen-presenting cells, not MHC I.

  6. A patient is bitten by a dog suspected of rabies. Alongside the vaccine, rabies immunoglobulin is given. Why the immunoglobulin?

    1. It is a live, attenuated form of the rabies virus that multiplies slowly and establishes lasting immunological memory
    2. It is a toxoid prepared from the rabies exotoxin that neutralises the toxin in the bloodstream
    3. It supplies preformed antibody at once (passive immunity) until the vaccine raises an active response
    4. It suppresses the immune system so that the vaccine is tolerated without allergic reactions
    Show answer

    Answer: C — It supplies preformed antibody at once (passive immunity) until the vaccine raises an active response

    Rabies immunoglobulin is passive immunisation: ready-made antibody giving instant but short-lived protection while the vaccine slowly builds active immunity and memory. Calling it attenuated virus confuses passive serum with an active vaccine; rabies has no exotoxin, so the toxoid idea is wrong.

  7. A disease is constantly present at a low, steady level in a region without large fluctuations. This pattern is termed:

    1. Pandemic
    2. Endemic
    3. Sporadic
    4. Epidemic
    Show answer

    Answer: B — Endemic

    A constant, predictable background level in a population is endemic. Epidemic is a sudden rise above that expected level, pandemic is an epidemic over several countries or continents, and sporadic means occasional, scattered cases with no steady presence.

  8. Ringworm (dermatophytosis) of the skin is caused by which group of organisms?

    1. A ring-shaped parasitic helminth whose larvae burrow through the dermis
    2. Staphylococcus aureus colonising and inflaming the hair follicles of the skin
    3. A cutaneous strain of Mycobacterium leprae that infects peripheral skin nerves
    4. Dermatophytic fungi such as Trichophyton, Microsporum and Epidermophyton
    Show answer

    Answer: D — Dermatophytic fungi such as *Trichophyton*, *Microsporum* and *Epidermophyton*

    Despite the name, ringworm is a fungal infection by dermatophytes (Trichophyton, Microsporum, Epidermophyton) that digest keratin. The name is the trap: no worm is involved, so the helminth option is wrong, and the bacterial options do not cause the classic scaly annular lesion.

  9. A boy has had repeated pneumonias and ear infections with encapsulated bacteria since about six months of age. He clears common viral infections normally, his T-cell numbers and function are normal, serum immunoglobulins of every class are very low, and no circulating B cells are found. Which diagnosis fits best?

    1. DiGeorge syndrome, with absence of the thymus and of mature T cells
    2. Severe combined immunodeficiency, with loss of both T and B function
    3. X-linked (Bruton) agammaglobulinaemia, a block in B-cell development
    4. HIV infection, with progressive loss of CD4⁺ helper T cells
    Show answer

    Answer: C — X-linked (Bruton) agammaglobulinaemia, a block in B-cell development

    Absent B cells and antibody with intact T cells is X-linked agammaglobulinaemia, caused by defective Bruton's tyrosine kinase; infections begin near six months because maternal IgG has waned, and they are pyogenic bacterial infections, the signature of an antibody defect. SCID is the tempting choice since antibody is also low there, but SCID removes T-cell function too and brings severe viral and fungal infections, which this boy does not have; DiGeorge syndrome and HIV are primarily T-cell defects.

  10. A vaccine of purified capsular polysaccharide of Haemophilus influenzae type b protects adults but protects infants under two years poorly. Coupling the polysaccharide to a carrier protein makes it effective in infants mainly because the conjugate:

    1. is a live replicating organism that keeps supplying a larger antigen dose over several weeks
    2. recruits helper T cells through carrier peptides on MHC II, enabling class switching and memory
    3. binds MHC class I on all nucleated cells and so activates CD8⁺ cytotoxic T cells against the capsule
    4. acts purely as an adjuvant that stimulates innate cells without needing any B-cell response
    Show answer

    Answer: B — recruits helper T cells through carrier peptides on MHC II, enabling class switching and memory

    A polysaccharide is a T-independent antigen: infants respond weakly, mostly with IgM and little memory. A B cell whose receptor binds the polysaccharide internalises the whole conjugate and presents carrier peptides on MHC class II to helper T cells, turning the response T-dependent, with switching to IgG, affinity maturation and memory. The vaccine is not live, MHC class I presents endogenous peptides rather than a vaccine capsule, and protection here is antibody, so B cells are essential.

  11. Which of the following pairings of a disease with its standard causal organism are correct?

    1. Tuberculosis — Mycobacterium tuberculosis
    2. Plague — Yersinia pestis
    3. Typhoid — Shigella dysenteriae
    4. Candidiasis — Cryptococcus neoformans
    Show answer

    Answer: A — Tuberculosis — *Mycobacterium tuberculosis*; B — Plague — *Yersinia pestis*

    Tuberculosis is caused by Mycobacterium tuberculosis and plague by Yersinia pestis. Typhoid is caused by Salmonella Typhi, not Shigella, which causes bacillary dysentery; candidiasis is caused by Candida albicans, while Cryptococcus neoformans causes cryptococcal meningitis.

  12. Which of the following are features of the innate (nonspecific) defence rather than adaptive immunity?

    1. It is present from birth and responds within minutes to hours
    2. Lysozyme, phagocytes, fever and interferons are among its components
    3. It improves in speed and magnitude on each re-exposure through memory cells
    4. Its specificity is generated by somatic recombination of receptor genes
    Show answer

    Answer: A — It is present from birth and responds within minutes to hours; B — Lysozyme, phagocytes, fever and interferons are among its components

    Innate defence is constitutive, fast and made of fixed-specificity components like lysozyme, phagocytes, fever and interferons. Improvement with re-exposure (memory) and receptor-gene recombination are hallmarks of adaptive immunity, so those two statements describe the wrong system.

  13. Which of the following mechanisms help a pathogen evade host defences?

    1. An antiphagocytic capsule, as in Streptococcus pneumoniae
    2. Secretion of IgA protease that cleaves mucosal antibody
    3. Antigenic variation of surface proteins between generations
    4. Display of its peptides on host MHC class I to alert cytotoxic T cells
    Show answer

    Answer: A — An antiphagocytic capsule, as in *Streptococcus pneumoniae*; B — Secretion of IgA protease that cleaves mucosal antibody; C — Antigenic variation of surface proteins between generations

    Capsules block phagocytosis, IgA proteases destroy secretory antibody, and antigenic variation keeps the pathogen ahead of the antibody response — all genuine evasion strategies. Presenting peptides on MHC class I invites cytotoxic T-cell killing, which is the host's weapon, not an evasion, so pathogens suppress it rather than enhance it.

  14. Which statements about passive immunization are correct?

    1. Protection is immediate because antibody is supplied ready-made
    2. It leaves no lasting immunological memory
    3. Maternal IgG crossing the placenta is a natural example
    4. It stimulates the recipient's own B cells to proliferate and class-switch
    Show answer

    Answer: A — Protection is immediate because antibody is supplied ready-made; B — It leaves no lasting immunological memory; C — Maternal IgG crossing the placenta is a natural example

    Passive immunisation transfers preformed antibody, so it protects at once, fades as the antibody is catabolised, and creates no memory; maternal IgG across the placenta is the classic natural case. It does not drive the recipient's own B cells, because no antigen is given — that is active immunisation.

  15. At a wedding, 240 guests ate a buffet dish and 36 of them later developed food poisoning. Taking the 240 as the population at risk, the attack rate is ____ %.

    Numerical answer — type the value.

    Show answer

    Answer: 15

    Attack rate = (cases / population at risk) × 100 = (36 / 240) × 100 = 15%. It is a cumulative incidence over the outbreak period, so no time unit enters.

  16. For a disease with basic reproduction number R₀ = 16, the herd-immunity threshold given by 1 − 1/R₀ is ____ % (to two decimal places).

    Numerical answer — type the value.

    Show answer

    Answer: 93.75

    Herd-immunity threshold = 1 − 1/R₀ = 1 − 1/16 = 1 − 0.0625 = 0.9375 = 93.75%. Once this fraction is immune, each case infects on average fewer than one susceptible, so the chain dies out.

  17. A vaccine is only 90% effective (efficacy E = 0.90). For a disease with R₀ = 5, the fraction that must be vaccinated to reach herd immunity is Vc = (1 − 1/R₀)/E. Give Vc as a percentage to two decimal places. Vc = ____ %.

    Numerical answer — type the value.

    Show answer

    Answer: 88.89

    The herd-immunity threshold is 1 − 1/5 = 0.80. Because the vaccine protects only 90% of recipients, the coverage must be scaled up: Vc = 0.80 / 0.90 = 0.8889 = 88.89%. An imperfect vaccine always needs coverage above the bare threshold.

  18. In a population with R₀ = 5 for a pathogen, a fraction p = 0.6 is already immune. The effective reproduction number Re = R₀(1 − p) equals ____.

    Numerical answer — type the value.

    Show answer

    Answer: 2

    Re = R₀(1 − p) = 5 × (1 − 0.6) = 5 × 0.4 = 2. Because Re > 1 the infection can still spread; immunising more of the population until Re drops below 1 stops the outbreak.