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MI2.{4,6} | Immunity in Infection & Immunoprophylaxis — SDL Guide (Part 2)

Immunoprophylaxis: Active Immunity

Active immunisation uses vaccines to induce antigen-specific immunological memory, mimicking the effects of natural infection without causing disease.

Types of vaccines and their immunological basis:

Vaccine type	Examples (Indian UIP / National Programme)	Immune response
Live attenuated	OPV, MMR, BCG, varicella, rotavirus, yellow fever	Strong, long-lasting CMI + antibody; mimics natural infection; risk of reversion in immunocompromised
Killed/inactivated	IPV, whole-cell pertussis (DPT), hepatitis A, influenza (some)	Mainly antibody; often requires boosters; safe in immunocompromised
Toxoid	Diphtheria toxoid (DT), tetanus toxoid (TT)	Antibody against toxin; requires boosters
Subunit/conjugate	HepB surface antigen, PCV13, Hib, meningococcal conjugate, HPV (VLPs)	Antibody; conjugation converts TI to TD antigen (enables infant immunisation)
mRNA vaccines	COVID-19 (Covishoot technology)	Antibody + CMI; novel; no live pathogen

Primary vs booster doses: The primary schedule generates memory cells. Booster doses restimulate memory B and T cells → anamnestic response with rapid, high-titre IgG production. Example: TT schedule — primary series (3 doses in infancy) + boosters at 18 months, 5 years, and pregnancy.

Cold chain: Live attenuated vaccines are thermolabile and MUST be maintained at 2–8°C (or frozen for OPV). Failure of cold chain is the most common operational reason for vaccine failure in India's rural immunisation posts.

A two-panel schematic compares primary and secondary antibody responses, showing IgM and IgG titres after first antigen exposure and booster exposure with memory B-cell mediated IgG amplification. — **Panel A:** Main graph showing time on x-axis, antibody titre on y-axis, first antigen exposure, second antigen exposure / booster, IgM curve, IgG curve, lag phase, primary response, secondary response, booster effect, higher titre, faster response, longer duration.. **Panel B:** Simplified mechanism showing antigen exposure, naive B cell activation, plasma cell formation, memory B cell formation, booster exposure, rapid memory B-cell expansion, and abundant IgG production..

Immunoprophylaxis: Passive Immunity & Herd Immunity

Passive immunisation provides pre-formed antibodies for immediate but short-lived protection. No memory is generated.

Types of passive immunisation:

Type	Source	Duration	Indian examples
Natural passive	Maternal IgG crosses placenta; sIgA in breast milk	3–6 months after birth	Protects neonates from measles, tetanus
Artificial passive (homologous)	Human immunoglobulin preparations	2–3 weeks	HRIG (rabies PEP), VZIG (varicella PEP), tetanus immunoglobulin (TIG)
Artificial passive (heterologous)	Equine (horse) antisera	1–2 weeks; serum sickness risk	Anti-snakevenom serum, older ADS, ATS

Serum sickness: A systemic Type III hypersensitivity reaction to foreign (animal-derived) immunoglobulin. Occurs 7–14 days after administration. Features: fever, urticaria, arthralgia, lymphadenopathy. Mechanism: antigen–antibody complexes deposited in vessels/joints → complement activation → inflammation.

Herd (population/community) immunity: When a sufficient proportion of a population is immune to an infectious disease, transmission chains are broken even for non-immune individuals — the "herd" protects its vulnerable members.

Herd immunity threshold (HIT):
$$HIT = 1 - \frac{1}{R_0}$$
where R₀ = basic reproduction number (average secondary cases per primary case in a fully susceptible population).

Disease	R₀	HIT
Measles	12–18	92–95%
Polio	5–7	80–85%
COVID-19 (original)	2–3	50–67%
Influenza	2–3	50–67%

Measles in India: High R₀ means India needs >92% vaccination coverage to prevent outbreaks. Despite strong UIP, pockets of unvaccinated children in urban slums and remote tribal areas have sustained measles outbreaks in recent years, highlighting the gap between national coverage rates and local herd immunity thresholds.

Three-panel diagram showing how increasing immune individuals in a population reduces infection transmission and breaks chains above the herd immunity threshold. — **Panel A:** Susceptible individuals, index infected case, continuous transmission arrows, expanding infection chain. **Panel B:** Immune individuals, susceptible individuals, infected individuals, continued transmission through susceptible gaps. **Panel C:** High immune proportion, herd immunity threshold, blocked transmission arrows, protected susceptible individuals, broken transmission chains.

SELF-CHECK

A 6-month-old infant develops severe measles. The child received the first dose of measles vaccine at 9 months as per UIP schedule. The mother received one dose of measles vaccine at age 9 months 28 years ago but has no documented immunity. Why was this infant NOT protected by maternal immunity?

A. Maternal IgM (not IgG) is transferred to the foetus, which has a short half-life

B. Maternal IgG from a single childhood measles dose wanes over decades and was insufficient to transfer protective levels to the foetus

C. The infant's Fc receptor cannot bind maternal IgG before 6 months of age

D. Live measles vaccine produces CMI only, not IgG, so no maternal antibody is transferred

Reveal Answer

Answer: B. Maternal IgG from a single childhood measles dose wanes over decades and was insufficient to transfer protective levels to the foetus

Maternal IgG is actively transferred across the placenta via FcRn receptors during the third trimester. However, maternal IgG wanes over time. A mother vaccinated once 28 years ago with a single childhood dose likely has low measles IgG titres by adulthood — insufficient to confer protective levels to the foetus. Additionally, even when maternal IgG is transferred, it typically wanes in the infant by 4–6 months. This is why the first measles dose is given at 9 months in India (when maternal antibody has fallen enough to avoid vaccine interference), and why the schedule optimises protection at the age of highest risk.