Communicable Diseases, Disease Prevention And The Immune System¶

Part of Module 4: Biodiversity, evolution and disease.

This topic connects pathogens, host defences, medical intervention and evolution. The key pattern is that organisms are under constant biological threat, so both plants and animals have evolved defence systems, and humans intervene through vaccination and medicines — with benefits and risks. Understanding how pathogens cause disease, how the body responds, and why medicines can fail is central to this module.

Learning Objectives¶

Pathogens And Transmission¶

Communicable diseases are diseases that can be passed from one organism to another. They are caused by microorganisms known as pathogens. There are four types of pathogen: bacteria, which produce toxins that damage body cells; viruses, which use host cells to replicate before bursting out and destroying them; protoctists (also called protists), which take over cells and break them open; and fungi, which digest living cells and may also produce toxins.

Named examples anchor each category. Tuberculosis (TB) and bacterial meningitis are bacterial diseases: TB damages the lungs and suppresses the immune system; bacterial meningitis damages the membranes of the brain and can cause blood poisoning. HIV/AIDS and influenza are viral diseases: HIV gradually destroys the immune system, while influenza kills ciliated epithelial cells in the gas exchange system. Malaria is caused by a protoctist and damages red blood cells, the liver, and the brain. Athlete's foot and ringworm are fungal diseases causing skin and surface tissue damage.

Transmission can be direct or indirect. Direct transmission includes skin-to-skin contact, kissing, sexual intercourse, and airborne droplets from coughing or sneezing. Indirect transmission involves contaminated food or water, vectors (for example, the Anopheles mosquito transmits malaria), and contaminated objects where pathogens persist briefly outside the host. The risk of communicable disease is increased by overcrowded living conditions (which increase direct contact), warm climates that allow vectors such as mosquitoes to breed, and social factors including limited health education and inadequate healthcare systems.

Plant Diseases And Defences¶

Plants can contract communicable diseases through direct contact with infected plants or through indirect transmission via soil contamination, wind-carried spores, water surfaces, animals such as insects and birds, and human handling, farming tools, and clothing.

Key plant diseases include Tobacco Mosaic Virus (TMV), a viral disease causing a mosaic pattern on leaves that disrupts photosynthesis; black sigatoka, a fungal disease of banana plants; and ring rot, a bacterial disease causing decay in potato and tomato crops. The risk of plant disease is increased by overcrowding (which favours direct contact), crop variety susceptibility, poor mineral nutrition (which reduces resistance), and climate change (which increases rainfall and wind spread of pathogens).

Plants have evolved both physical and chemical defences. Physical defences include the waxy cuticle covering leaves and stems, which forms a barrier against pathogen entry; cellulose cell walls that must be breached before infection can proceed; and callose production. Callose is a polysaccharide deposited between the cell wall and the cell-surface membrane when a plant is attacked, making it harder for pathogens to enter cells. Chemical defences include insect repellents that reduce the number of insects feeding on plants, insecticides that kill insects outright, antibacterial substances including plant-produced antibiotics, and toxins — some plants produce chemicals that break down into cyanide when cells are attacked.

Non-Specific Animal Defences¶

The body has two broad categories of defence mechanism. Non-specific defences act quickly and respond in the same way to all pathogens. Specific defences are slower but produce a response tailored to each individual pathogen and create immunological memory.

The first line of non-specific defence consists of physical and chemical barriers. The skin acts as a physical barrier and also produces sebum, an oily antimicrobial substance that lowers surface pH to inhibit pathogen growth. Mucous membranes line the ears, nose, throat, and digestive tract; they secrete mucus to trap pathogens and contain lysozymes to destroy them. Expulsive reflexes — coughing, sneezing, vomiting, and diarrhoea — physically expel pathogens from the gas exchange system and gut. Blood clotting rapidly seals any wounds that provide a potential pathogen entry point: a clot dries to form a scab, epidermal cells underneath divide to regenerate the skin, damaged blood vessels regrow, and collagen fibres restore tissue strength.

Inflammation is also a non-specific response. It is triggered by damaged tissues releasing chemicals that act on nearby blood vessels in two ways: blood vessels dilate, increasing blood flow to the area, raising local temperature and inhibiting pathogen reproduction; and blood vessel walls become more permeable so they leak tissue fluid, causing swelling that isolates pathogens in the damaged tissue.

Antigens And The Distinction Between Self And Non-Self¶

Antigens are unique molecules, usually proteins, found on cell surfaces. The immune system uses antigens to distinguish between the body's own cells (self) and foreign cells (non-self). Pathogens carry foreign antigens that trigger an immune response. Abnormal body cells such as cancerous or virally infected cells display altered antigens that also provoke a response. Toxins are themselves antigenic molecules. Cells from other individuals of the same species may carry different antigens, which explains why transplanted organs can be rejected.

Phagocytosis¶

Phagocytosis is a non-specific cellular defence. Phagocytes are white blood cells found in blood and body tissues that engulf and destroy pathogens. There are two main types. Neutrophils rapidly engulf and destroy pathogens at the site of infection. Macrophages engulf pathogens and, after digestion, present the pathogen's antigens on their cell surface, becoming antigen-presenting cells (APCs) that activate the specific immune response.

The process of phagocytosis follows a defined sequence. First, the pathogen releases chemicals that attract the phagocyte by chemotaxis. The phagocyte recognises the pathogen's antigens as non-self and binds to it. The phagocyte engulfs the pathogen, enclosing it in a membrane-bound vesicle called a phagosome. A lysosome containing hydrolytic enzymes called lysozymes then fuses with the phagosome to form a phagolysosome. The lysozymes digest and destroy the pathogen. The phagocyte then presents the pathogen's antigens on its surface and is now called an antigen-presenting cell.

Two classes of molecule assist phagocytosis. Cytokines are chemicals released by phagocytes that have engulfed a pathogen; they act as cell-signalling molecules to attract additional phagocytes to the infection site and also trigger an increase in body temperature, which inhibits pathogen reproduction and accelerates the specific immune response. Opsonins are molecules (including antibodies) that bind to pathogens and make them easily recognisable by phagocytes, whose surface receptors bind opsonins and thereby improve pathogen capture.

The Specific Immune Response: Cellular Component¶

The specific immune response depends on lymphocytes, which are white blood cells produced in the bone marrow. T lymphocytes (T cells) mature in the thymus gland and are responsible for the cellular response, which targets antigens displayed on body cells. B lymphocytes (B cells) mature in the bone marrow and are responsible for the humoral response, producing antibodies found in body fluids.

There are four functionally distinct types of T cell. T helper cells have surface receptors that bind to complementary antigens on antigen-presenting cells. Upon binding, they produce interleukins, a type of cytokine, which stimulate B cells and phagocytes. T helper cells can also develop into memory cells or T killer cells. T killer cells produce a protein called perforin that makes holes in the membrane of target cells, causing them to become freely permeable and die; this allows T killer cells to destroy both infected body cells and abnormal cells. T regulator cells suppress the immune response once pathogens have been destroyed, preventing the immune system from attacking the body's own cells. T memory cells persist long-term and provide a rapid response if the same pathogen is encountered again.

The stages of the cellular response are as follows. Macrophages engulf pathogens and present their antigens on the cell surface, becoming antigen-presenting cells. T helper cells with complementary receptors bind to these displayed antigens and are activated. The activated T helper cell divides by mitosis to form genetically identical clones. These cloned T cells then differentiate: some become memory cells circulating in the body for long-term immunity; some become T killer cells; and others produce interleukins that stimulate phagocytosis and B cell division.

The Specific Immune Response: Humoral Component¶

The humoral response is so named because it involves antibodies found in body fluids (historically called "humors"). It is driven by B lymphocytes and results in the production of specific antibodies.

B cells carry antibodies on their surface that act as receptors; when a complementary antigen binds to a B cell, the B cell engulfs the antigen and presents it on its surface, becoming an antigen-presenting cell in its own right. The crucial next step is clonal selection: an activated T helper cell binds to the antigen-presenting B cell, causing the B cell to become activated. Clonal expansion follows — the activated B cell divides rapidly by mitosis to produce many genetically identical clones. These clones differentiate into two cell types: plasma cells, which have a short lifespan of only a few days but produce and secrete large quantities of specific antibody; and memory B cells, which have a much longer lifespan, circulate through blood and tissue fluid, and can rapidly divide into plasma cells if the same pathogen is encountered later.

Primary And Secondary Immune Responses¶

The primary immune response is the body's first encounter with a particular pathogen. It is slow, with a long lag phase before antibody concentration rises; this is because there are very few B cells specific to the pathogen's antigens, and it takes time for these to divide and produce plasma cells. The individual experiences symptoms during this period.

The secondary immune response is triggered by re-exposure to the same pathogen. It is much faster and produces a higher concentration of antibodies. Memory B cells recognise the pathogen's antigens and quickly divide into plasma cells. Memory T cells are also activated, differentiating into T killer cells. Pathogens are destroyed before symptoms appear. This contrast between primary and secondary responses is the immunological basis for vaccination.

Autoimmune Diseases¶

Sometimes the immune system fails to recognise self antigens and attacks the body's own cells. This is known as an autoimmune disease. Examples include Type 1 diabetes, where the immune system attacks the insulin-secreting cells of the pancreas; lupus, where connective tissue cells are attacked; and rheumatoid arthritis, where cells in the joints are attacked, causing inflammation and pain.

Antibody Structure And Function¶

Antibodies are Y-shaped glycoproteins made from four polypeptide chains: two identical heavy chains and two identical light chains, held together by disulphide bridges. Each antibody has three structural regions. The constant region is the same for all antibodies and binds to receptors on cells such as B cells. The variable region differs between antibodies because its shape is complementary to a specific antigen; this is the part that binds to antigens. The hinge region provides flexibility so the antibody can simultaneously bind to multiple antigens.

When an antibody's variable region binds to a complementary antigen, an antigen-antibody complex is formed. Antibodies carry out three distinct functions to assist destruction of pathogens. Agglutination: antibodies act as agglutinins, crosslinking pathogens and causing them to clump together, making it easier for phagocytes to locate and engulf many pathogens at once. Antibodies also act as opsonins at this stage, coating pathogens and making them more recognisable to phagocytes. Neutralisation of toxins: antibodies bind to toxins produced by pathogens, inactivating them and preventing them from damaging body cells. Prevention of cell binding: antibodies block the surface receptors pathogens use to attach to and invade host cells, stopping infection from spreading.

Immunity Types¶

Immunity can be characterised along two dimensions: whether it involves the body's own immune response (active) or ready-made antibodies from an external source (passive), and whether it arose naturally or through medical intervention (artificial).

Active immunity develops when the immune system makes its own antibodies following antigen exposure. It takes time to establish but provides long-term protection because memory cells are produced. Passive immunity occurs when an individual receives antibodies made by a different organism; it provides immediate protection but is short-term because the antibodies are gradually broken down and no memory cells are formed.

The four combinations are: natural active immunity, acquired by recovering from an infection; natural passive immunity, acquired by a foetus or infant receiving maternal antibodies through the placenta or breast milk; artificial active immunity, produced by vaccination; and artificial passive immunity, produced by injection of antibodies harvested from another organism, used for immediate short-term protection (for example, following snake bite).

Vaccination And Herd Immunity¶

Vaccination involves introducing a pathogen's antigens into the body, usually by injection, to stimulate a primary immune response and the production of memory cells — conferring artificial active immunity without the risk of disease. Vaccines may contain dead or inactivated pathogens, attenuated (weakened) pathogen strains, a harmless version of a toxin, isolated antigens, or genetically engineered antigens.

When many individuals in a population are vaccinated, protection extends even to those who are not vaccinated. This is herd immunity. It works because vaccinated individuals cannot transmit the pathogen, reducing the overall chance that non-vaccinated individuals encounter it. Herd immunity is important because some individuals cannot be vaccinated — babies, elderly people, and those with compromised immune systems. Mass vaccination can prevent epidemics and pandemics.

Several factors determine the success of a vaccination programme: vaccines must be available in sufficient quantities and at affordable cost; side effects should be minimal to maintain public acceptance; infrastructure for production, cold-chain storage, and distribution must exist; trained healthcare workers are needed for administration; and a sufficiently large proportion of the population must be vaccinated to achieve herd immunity.

Why Some Diseases Cannot Be Eliminated By Vaccination¶

Several obstacles can prevent a disease from being fully eliminated even with a vaccination programme in place. Individuals with weak immune systems may not mount an adequate immune response to the vaccine. Some individuals contract the disease in the window between vaccination and the development of full immunity. Pathogen mutation and antigenic variability — where pathogens change their surface antigens — can render existing vaccines ineffective; the immune system can no longer recognise the pathogen's new antigens, and memory cells from prior vaccination will not respond. This is particularly problematic with influenza, which requires annual vaccine reformulation. Some pathogens exist as many variants (as with the common cold), making universal vaccines impractical. Certain pathogens evade the immune system by hiding inside host cells or in difficult-to-reach compartments. Personal, religious, ethical, or medical objections and vaccine misinformation can also reduce vaccination uptake.

Antibiotics And Antibiotic Resistance¶

Antibiotics are drugs that kill bacteria or inhibit their growth. They act by targeting bacterial-specific structures and processes: preventing cell wall synthesis, disrupting protein activity in the cell membrane, inhibiting enzyme action, or preventing DNA and protein synthesis. Because human cells use different ribosomes and enzymes from bacteria, antibiotics selectively harm bacteria without damaging human cells.

Antibiotics are completely ineffective against viruses. Viruses lack independent cell structures, relying on host cell machinery to replicate. Antibiotics cannot reach them inside host cells and have no bacterial targets to disrupt.

Since penicillin's discovery in the mid-twentieth century, antibiotics have dramatically reduced deaths from bacterial communicable diseases. However, increased use has driven antibiotic resistance through natural selection. Some bacteria acquire random mutations conferring resistance. When antibiotics are used, susceptible bacteria die but resistant individuals survive and reproduce, passing on resistance alleles to offspring. Resistance genes often occur on plasmids and can be transferred between bacteria by conjugation, spreading resistance rapidly. This is natural selection operating in observable, medically relevant time frames.

Notable examples include methicillin-resistant Staphylococcus aureus (MRSA), which causes wound infections and resists multiple antibiotics, and Clostridium difficile, which infects the digestive system and survives in the presence of many antibiotics.

Strategies to reduce antibiotic resistance include: testing antibiotics against specific bacterial strains before prescribing; restricting antibiotic use to genuine bacterial infections; using narrow-spectrum rather than broad-spectrum antibiotics wherever possible; ensuring patients complete the full course of treatment so no bacteria survive to acquire resistance; and avoiding routine antibiotic use in farming.

Sources Of Medicine¶

Medicines come from a wide range of natural sources, including plants, animals, and microorganisms. Penicillin is an antibiotic extracted from the mould Penicillium. Aspirin is based on compounds originally derived from willow bark. Prialt is a pain-killing drug derived from the venom of a cone snail. Because scientists have not yet analysed all organisms on Earth, undiscovered species may yield treatments for currently incurable diseases — which is one of the most compelling arguments for maintaining biodiversity. Future research directions include personalised medicines tailored to an individual's genome (reducing side effects and improving efficacy) and synthetic biology, in which genetic engineering is used to develop artificial proteins, cells, or microorganisms that produce therapeutic drugs.

Key Terms¶

• Pathogen: a disease-causing microorganism or agent.
• Communicable disease: a disease that can be transmitted from one organism to another.
• Vector: an organism that transmits a pathogen from one host to another without itself being the primary host.
• Antigen: a molecule, usually a surface protein, recognised as foreign by the immune system.
• Non-specific defence: a defence mechanism that responds to any pathogen in the same way, without producing immunological memory.
• Specific defence: a defence mechanism that targets a particular pathogen's antigens and generates memory cells.
• Inflammation: a non-specific response to infection or injury involving vasodilation, increased permeability, and swelling.
• Phagocyte: a white blood cell that engulfs and digests pathogens.
• Phagocytosis: the process by which a phagocyte engulfs a pathogen into a phagosome, which then fuses with a lysosome for digestion.
• Antigen-presenting cell (APC): a phagocyte or B cell that displays pathogen antigens on its surface to activate T cells.
• Cytokine: a chemical signal released by phagocytes or T helper cells that recruits other immune cells or triggers fever.
• Opsonin: a molecule (including antibodies) that binds to pathogens and enhances recognition and phagocytosis.
• T helper cell: a T lymphocyte that, on antigen binding, produces interleukins to activate B cells, phagocytes, and T killer cells.
• T killer cell: a T lymphocyte that destroys infected or abnormal cells by secreting perforin.
• T regulator cell: a T lymphocyte that suppresses the immune response after pathogens are cleared.
• Clonal selection: activation of the specific B or T lymphocyte carrying the complementary receptor for the presented antigen.
• Clonal expansion: rapid mitotic division of the selected lymphocyte to produce a large clone of identical cells.
• Plasma cell: a short-lived B cell that secretes large quantities of specific antibody.
• Memory cell: a long-lived B or T lymphocyte that persists after infection and enables the faster, stronger secondary response.
• Antibody: a Y-shaped glycoprotein with variable regions complementary to a specific antigen, produced by plasma cells.
• Agglutination: clumping of pathogens caused by antibodies crosslinking surface antigens.
• Anti-toxin: an antibody that binds to and neutralises a pathogen-derived toxin.
• Active immunity: immunity resulting from the body's own immune response generating memory cells.
• Passive immunity: immunity from receiving ready-made antibodies from an external source; short-term, no memory cells.
• Vaccination: introduction of antigen in a safe form to stimulate a primary immune response and memory-cell formation.
• Herd immunity: population-level protection when a high proportion of individuals are immune, reducing pathogen transmission to unvaccinated individuals.
• Antigenic variability: changes in a pathogen's surface antigens through mutation, rendering existing antibodies and vaccines ineffective.
• Autoimmune disease: a condition in which the immune system attacks the body's own cells, failing to distinguish self from non-self.
• Antibiotic resistance: reduced or absent effectiveness of an antibiotic because bacteria carrying resistance alleles have been selected for by antibiotic use.
• Callose: a polysaccharide deposited by plants between the cell wall and membrane in response to pathogen attack.
• Perforin: a protein produced by T killer cells that forms pores in the target cell membrane, causing cell death.

Connected Pages¶

• 2.1.6 Cell division, cell diversity and cellular organisation
• 4.2.1 Biodiversity
• 4.2.2 Classification and evolution