Communicable diseases, disease prevention and the immune system (4.1.1)
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Bacteria are prokaryotes, meaning their cells lack a nucleus and other membrane-bound organelles. They can cause disease by directly damaging cells or by releasing toxins that harm the organism.
Bacteria reproduce rapidly by binary fission, allowing infections to spread quickly.
Examples of bacterial diseases include:
- Tuberculosis (TB) in animals.
- Ringrot in plants such as tomatoes and potatoes.
Viruses are very small, non-living infectious agents. They infect and take over the host’s cells to produce more viruses, often causing cell damage when new viruses are released.
They have a simple structure consisting of either DNA or RNA enclosed in a protein coat.
Examples of viral diseases include:
- HIV which leads to AIDS in humans.
- Influenza (flu) in animals.
- Tobacco mosaic virus (TMV) in plants.
Protoctista (protists) are eukaryotic, mostly single-celled organisms. They are often transmitted by a vector (e.g. mosquito).
Examples of diseases caused by protoctista include:
- Malaria in humans
- Late blight in tomatoes and potatoes.
Fungi are eukaryotic organisms that can grow on the skin of animals or within plant tissues. They can be unicellular or multicellular. Many fungi reproduce by producing spores which are dispersed to infect new hosts.
Examples of fungal diseases include:
- Athlete’s foot in humans
- Black sigatoka in bananas.
Direct transmission occurs when a pathogen passes directly from one host to another, with no intermediary involved (e.g., physical contact or droplets).
Indirect transmission occurs when a pathogen is passed from one host to another via an intermediary such as a vector, contaminated food or water, or contaminated surfaces.
Vectors are living organisms that transmit communicable pathogens between hosts.
In animals, a vector is a living organism that carries and transmits disease-causing pathogens between hosts, such as mosquitoes transmitting malaria.
In plants, vectors are often insects (such as aphids or whiteflies) that transmit pathogens between individuals.
Spores are the infectious reproductive structures of many fungi. When spores land on a suitable host, they germinate and the fungal hyphae grow, initiating infection.
Fungal spores can be dispersed by wind, water, or by animals and other organisms carrying them to new hosts.
The rate at which communicable diseases are spread can be affected by living conditions.
High population density, poor ventilation, and poor sanitation can increase the rate of direct and indirect transmission.
While living in warmer climates can increase the survival and reproduction of vectors, and may also increase the rate at which pathogens develop or replicate.
Plants produce antimicrobial chemicals that inhibit pathogen growth or damage pathogens helping prevent the spread of infection.
These chemicals include phenols, alkaloids, and terpenoids many of which have antipathogenic properties. Some plant chemicals can break down pathogen cell walls or interfere with pathogen metabolism. Many of these defensive chemicals are produced in greater quantities when the plant becomes infected.
Plants have physical adaptations to reduce the entry and spread of pathogens. These include:
- Waxy cuticle: reduces the build-up of surface water, making it more difficult for pathogens to infect the plant.
- Cell walls: a physical barrier against pathogen entry and contains compounds that contribute to defence.
- Tylose formation: outgrowths from surrounding cells plug xylem vessels, reducing water movement and helping prevent the spread of pathogens through the xylem.
- Callose deposition: callose is deposited between the cell wall and cell membrane and around the sieve plates of the phloem, blocking pathogen movement and sealing damaged tissues.
In animals, the skin acts as a physical barrier covering the entire body and helping to prevent pathogen entry.
The outer layer consists of dead cells that are continually shed. This layer is waterproof, making it hard for pathogens to penetrate into an organism’s body.
Skin also produces antimicrobial secretions (e.g., sweat, sebum) that kill or inhibit microbes on the skin’s surface.
Animals have a number of non-specific defences that help prevent infection:
- Inflammation: increases blood flow and capillary permeability allowing immune cells and antimicrobial substances to reach infected tissue.
- Wound repair: restores damaged tissue to prevent pathogen entry.
- Expulsive reflexes: such as coughing or sneezing, physically remove pathogens from the body.
- Mucous membranes: trap pathogens in mucus and remove them using cilia.
Blood clotting is a non-specific defence that reduces the entry of pathogens into the body. Blood clots stop blood loss, prevent infection and allow skin to repair.
This process is complex and involves calcium along with many different clotting factors, many of which are released by platelets and damaged tissue. An enzyme cascade is activated and fibrin is formed at the site of damage, making a network and trapping platelets, to form a clot.
Phagocytes are a type of white blood cell that play a key role in the non-specific immune response by engulfing and destroying pathogens.
Neutrophils are the most abundant type of phagocyte. They rapidly respond to infections and die after engulfing pathogens.
Macrophages are larger, longer-lived phagocytes that develop from monocytes (a type of white blood cell). Macrophages act as antigen-presenting cells (APCs) to activate specific immune responses.
Phagocytosis is the process by which phagocytes (e.g., neutrophils, macrophages) engulf and destroy pathogens.
Phagocytosis involves the following steps:
- Chemotaxis – phagocytes use chemical signals to move toward pathogens.
- Recognition and attachment – receptors on the phagocyte membrane bind to antigens on the pathogen surface.
- Engulfment – the pathogen is enclosed in a phagosome (a membrane-bound vesicle).
- Digestion – lysosomes fuse with the phagosome to form a phagolysosome, releasing enzymes to break down the pathogen.
- Antigen presentation – macrophages display the pathogen’s antigens on their surface membrane to activate the immune response.
It is possible to identify different types of white blood cells based on their structure when stained in a blood smear:
B lymphocytes are a type of lymphocyte that mature in the bone marrow and play a key role in the specific (humoral) immune response. They are responsible for targeting pathogens in body fluids such as blood and lymph.
When a B cell detects a specific antigen, it becomes activated and divides to form plasma cells (B effector cells), which produce antibodies that bind to and neutralise the pathogen.
Some B cells become memory cells, which remain in the body and provide long-term immunity by responding quickly if the same antigen is encountered again.
There are several types of T lymphocytes:
- T helper cells (Th): release cytokines to activate B cells, phagocytes, and other T cells such as cytotoxic T cells.
- T killer (cytotoxic) cells (Tc): destroy infected or abnormal cells by releasing substances that cause cell lysis.
In order for an immune response to work effectively, it is important that cells and their actions are coordinated.
Cytokines (hormone-like chemicals) are released and are responsible for this communication.
Clonal selection occurs when an antigen binds to a B cell with a complementary receptor on its cell surface.
The B cell presents the antigen on its surface, where it is recognised by a helper T cell with a complementary receptor. The helper T cell activates the selected B cell, ensuring that only the B cell specific to that antigen responds.
During clonal expansion, activated helper T cells divide by mitosis to produce many identical helper T cells (clones),increasing the effectiveness of the immune response.
The cloned cells may then:
- Form memory T helper cells.
- Release interleukins that stimulate B cells to divide and differentiate.
- Release interleukins that activate phagocytes, increasing phagocytosis.
- Release interleukins that activate cytotoxic (killer) T cells.
During the primary immune response, plasma cells are produced from activated B cells.
They make and release antibodies specific to the antigen which help destroy the pathogen.
This response is slow, so symptoms may appear before the pathogen is removed. Memory cells are also made during this time.
During the secondary immune response, memory B cells quickly recognise the pathogen’s antigen.
They rapidly divide and form plasma cells. These plasma cells produce antibodies faster and in larger quantities than during the primary immune response.
The pathogen is usually destroyed before symptoms develop which is why people are often immune after the first infection or following vaccination.
An antibody is a Y-shaped globular protein made of four polypeptide chains (two heavy and two light), held by disulfide bonds.
The variable region at the tips form two antigen-binding sites; they have a specific tertiary structure that is complementary to a specific antigen, meaning specific binding will occur at these sites.
The constant region is the same in all antibodies of that class and interacts with other components of the immune system, helping to recruit immune cells.
The hinge region provides flexibility, allowing the antibody to bind to antigens at different angles.
Antibodies bind to antigens on pathogens (or to toxins). The binding is specific, like a lock and key and forms an antigen–antibody complex.
Once the antigen-antibody complex is formed then there are several different ways in which the antibody itself or the immune system will destroy the pathogen.
Opsonins are molecules that tag pathogens for destruction. They bind to antigens on the pathogen’s surface, making the pathogens easier for phagocytes to recognise and engulf.
This enhances the process of phagocytosis.
The role of agglutins is to clump pathogens together. They bind to antigens on the surface of multiple pathogens, forming antigen–antibody complexes.
The clumped pathogens are more easily recognised and engulfed by phagocytes.
Anti-toxins are antibodies that neutralise toxins produced by pathogens. They bind specifically to toxins, preventing them from damaging host cells.
Anti-toxins form harmless toxin–antibody complexes that are then removed by phagocytes.
There are two types of immunity:
- Active immunity: the body’s own immune system makes antibodies and memory cells following exposure to an antigen (e.g., vaccinations or after infection).
- Passive immunity: ready-made antibodies are transferred to an individual, so no memory cells are made (e.g., breast milk being ingested by infants or antibody injection such as antivenom).
Natural active immunity occurs when a person becomes infected by a pathogen. The immune system responds by producing antibodies and memory cells. This provides long-term immunity because the immune system ‘remembers’ the pathogen.
Natural passive immunity is passed from mother to baby. Antibodies cross the placenta or are found in breast milk, providing short-term protection (no memory cells are made).
Artificial immunity is immunity gained through human intervention. It involves exposure to antigens or antibodies in a controlled way.
Artificial active immunity is gained through vaccination. A harmless form of the antigen (e.g., dead or weakened pathogen) is introduced stimulating the immune system to produce memory cells and antibodies, giving long-term immunity.
Artificial passive immunity involves injection of antibodies from another person or animal. Gives immediate but short-term protection (e.g., antivenom, rabies treatment) as no memory cells are made.
An autoimmune disease occurs when the immune system attacks the body’s own cells, mistaking them for pathogens. This can occur when self-reactive lymphocytes are not destroyed or inactivated during immune system development.
Examples of autoimmune diseases include:
- Type 1 diabetes: immune system destroys insulin-producing beta cells in the pancreas.
- Rheumatoid arthritis: attacks joint linings, causing inflammation.
- Lupus (SLE): attacks various tissues (skin, kidneys, joints).
Autoimmune diseases can cause inflammation, tissue damage, and impaired organ function.
Although there is no cure for most autoimmune diseases, they can be treated with immunosuppressant drugs, which reduce the activity of the immune system, help relieve symptoms and limit further tissue damage.
A vaccine contains antigens from a pathogen (e.g., a dead, weakened or part of a pathogen), stimulating the immune system without causing disease.
The antigens in the vaccine are recognised by the immune system. Antigen-presenting cells process the antigens and present them to T helper cells which activate B cells. The activated B cells undergo mitosis and differentiate to form:
- Plasma cells: produce antibodies (short term).
- Memory cells: remain in the body (long term).
This results in active immunity, because the body’s own immune system makes the antibodies and memory cells.
Pathogens may mutate or new diseases may emerge, producing new antigens that existing vaccines do not recognise effectively. This means new vaccines must be developed.
To reduce the risk of an epidemic (rapid spread of disease through a population), health authorities may stockpile vaccines and prioritise vaccination of high-risk groups.
Global travel can increase the spread of infectious diseases between countries, while unequal access to vaccines can make vaccination programmes less effective in some parts of the world.
Ring vaccination is used when a new case of an infectious disease is identified. People who have been in contact with the infected individual, and those in close contact with them, are vaccinated to form a protective “ring” around the case, helping to prevent further spread of the disease.
Ring vaccination is commonly used to control outbreaks of diseases such as Ebola and may also be used to control the spread of livestock diseases.
Herd immunity occurs when a large proportion of a population is immune to a specific infectious disease, making it more difficult for the disease to spread.
Pathogens spread through contact between infected and susceptible individuals but if most people are immune (through vaccination), the pathogen has fewer people to infect. As a result, unvaccinated or vulnerable individuals are indirectly protected because they are less likely to come into contact with an infected person.
Many antibiotics are produced by microorganisms. For example, penicillin was the first widely used antibiotic, discovered from the fungus Penicillium notatum.
Plants also produce a wide range of chemical compounds that can be used as medicines. For example, aspirin was originally derived from compounds found in willow bark.
Biodiversity increases the chance of discovering new medicinal compounds. Many species of plants, fungi, and microorganisms have not yet been studied and may produce chemicals that could be developed into medicines.
If a species becomes extinct, any potentially useful medicinal compounds it contains may be lost forever. Therefore, conserving biodiversity and ecosystems (e.g., rainforests and oceans) helps protect these valuable biological resources for future medical research.
Personalised medicine tailors treatments to an individual’s DNA (genome). This approach is known as pharmacogenomics. By considering a person’s genetic makeup, doctors can choose the most effective drug and dose while reducing the risk of side effects.
Synthetic biology involves designing and producing new biological products using genetic engineering. Scientists can modify microorganisms to produce complex medicines (e.g., human insulin) or create entirely new biological molecules that may be used as medicines.
Antibiotics are drugs that kill bacteria or inhibit their growth by targeting structures or processes unique to bacterial cells, helping to treat bacterial infections.
Since the discovery of penicillin by Alexander Fleming in 1928, antibiotics have dramatically reduced deaths from bacterial infections, particularly those resulting from infected wounds and surgical procedures.
Some bacteria have evolved to survive antibiotics; this is called antibiotic resistance.
Resistant bacteria, such as MRSA arise through random mutations or by acquiring resistance genes from other bacteria. The overuse and incorrect use of antibiotics creates a selection pressure that allows resistant bacteria to survive, reproduce and become more common.
Superbugs are bacteria that are resistant to multiple antibiotics. They are hard to treat and can cause life-threatening infections.