Defence, immunity and vaccination explained
Infection and response • Communicable diseases
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Non-specific first-line defences
The skin forms a continuous physical barrier that prevents pathogen entry and secretes antimicrobial compounds that kill some microbes. Dead outer skin cells slough off and remove attached pathogens. Tears and saliva contain lysozymes that chemically break down bacterial cell walls and provide local immunity at eyes and mouth. Hairs and mucus in the nose trap inhaled particles and pathogens; swallowing transfers trapped material to the stomach where acid destroys many microbes. Ciliated epithelial cells in the trachea and bronchi waft mucus up the airways so trapped pathogens move to the throat and are swallowed, preventing lung infection.
Phagocytosis by white blood cells
Phagocytes act as a non-specific cellular defence that locates and engulfs invading pathogens. The phagocyte membrane surrounds the pathogen and internalises it into a vacuole. Digestive enzymes fuse with the vacuole and chemically break down the pathogen, removing the infection source. High phagocyte numbers in blood allow rapid response at infection sites and reduce pathogen numbers before specific immunity develops.
Antibodies and antitoxins from lymphocytes
Lymphocytes recognise foreign antigens on pathogens and produce highly specific antibodies that bind to those antigens. Antibodies cause pathogens to clump together, making phagocytosis more efficient. Some lymphocytes produce antitoxins that bind and neutralise toxins released by pathogens, preventing toxin-mediated damage. After a primary response, memory lymphocytes persist and enable faster, stronger secondary responses on re-exposure to the same antigen.
Role of the immune system in defence
The immune system coordinates layered defences: non-specific barriers prevent entry; innate cellular responses such as phagocytosis limit early spread; and adaptive responses produce specific antibodies and memory cells to eliminate pathogens and prevent repeat disease. This combination minimises tissue damage and clears infections while building lasting immunity to particular pathogens. Limitations include antigen variability between strains and immunosuppression, which reduce effectiveness.
How vaccination generates immunity
A vaccine contains a dead, inactive or modified form of a pathogen that retains the pathogen’s antigens. Injection of the vaccine provokes a primary immune response: phagocytes engage the antigen and lymphocytes produce antibodies and memory cells without causing the full disease. Memory lymphocytes enable a rapid, large-scale antibody response on later exposure to the live pathogen, preventing illness. Booster doses refresh memory cell numbers when required.
Herd immunity and its limits
Herd immunity occurs when a high proportion of a population is immunised so that transmission chains break and even unvaccinated individuals gain indirect protection. Herd immunity effectiveness depends on vaccination coverage, vaccine effectiveness, pathogen transmissibility and population mixing. Low uptake or waning immunity reduces herd protection and permits outbreaks. Herd immunity does not protect against pathogens with many antigenic variants unless vaccine coverage and match remain high.
Global use and evaluation of vaccination
Global vaccination programmes reduce morbidity and mortality from many infectious diseases and can aim for elimination. Programmes require high coverage, cold-chain logistics, public trust and equitable access to achieve impact. Declines in vaccine uptake correlate with disease resurgence, illustrated by rising measles cases where coverage falls. Evaluation of vaccination programmes balances high population-level benefits against rare adverse events, logistical costs and ethical debates about compulsion versus voluntary immunisation. Public health goals rely on monitoring, education and international coordination.
Key notes
Important points to keep in mind