Defence against disease

Defence against disease is a comprehensive topic that encompasses the body's various mechanisms to protect itself from harmful organisms and substances, known as pathogens, which cause infectious diseases. The immune system is the internal defence system of the body.

1. Definition of Disease and Pathogens A disease is an illness or disorder of the body or mind that leads to poor health and is associated with a set of signs and symptoms. Infectious diseases are caused by pathogens, which are organisms that cause disease, such as bacteria, viruses, fungi, or protoctists. Pathogens are biological agents that cause disease and have proteins as part of their structure that are different from those of the human host, acting as antigens. Non-infectious diseases, like lung cancer or sickle cell anaemia, are not caused by pathogens and cannot be passed from person to person.

2. External Defence System (Barriers to Infection) The body has several mechanisms to prevent pathogens from entering:

• Skin: Acts as a physical barrier. If damaged, blood clots to prevent pathogens from entering, though some may get in before the clot forms.

• Mucus: Internal surfaces like the trachea, bronchi, and gut are lined by moist epithelial tissue, protected by mucus. Mucus traps bacteria and microorganisms, while cilia beat to move mucus away from the lungs and towards the mouth.

• Digestive Enzymes/Strong Acid: Digestive enzymes or strong acid (e.g., in the stomach) can kill many ingested bacteria.

• Gut and Skin Flora: Billions of harmless microorganisms (flora) naturally cover the intestines and skin, competing with pathogens for nutrients and space, thereby limiting their numbers.

• Lysozyme: An antibacterial enzyme found in tears and saliva.

3. Internal Defence System (Immune Response) If pathogens successfully enter the body, white blood cells recognize them as foreign and destroy them. This system involves non-specific and specific responses.

3.1 Non-Specific Immune Response (Innate Immunity) This response is immediate and happens in the same way for all microorganisms, regardless of their specific antigens.

• Phagocytosis: Phagocytes (e.g., macrophages and neutrophils) are types of white blood cells found in blood and tissues. They recognize foreign antigens on a pathogen. The phagocyte's cytoplasm engulfs the pathogen into a phagocytic vacuole. Lysosomes then fuse with the vacuole, and lysozymes (hydrolytic enzymes) break down the pathogen. Neutrophils are short-lived and form pus at infection sites, while macrophages are principal 'rubbish-collecting cells' throughout the body.

• Inflammation: Occurs at the site of infection, causing redness, warmth, swelling, and pain. It involves increased blood flow and accumulation of white blood cells and plasma.

• Interferons: Cells infected with viruses produce proteins called interferons. These bind to healthy neighboring cells, triggering the synthesis of antiviral proteins which prevent viral replication and activate cells involved in the specific immune response.

3.2 Specific Immune Response (Adaptive Immunity) This response is triggered by and directed towards specific pathogens and provides long-term immunity.

• Antigens: Molecules, usually proteins, found on the surface of cells (including pathogens). Foreign antigens can generate an immune response. The immune system distinguishes between "self" antigens (normally found in the body) and "non-self" (foreign) antigens.

• Lymphocytes: Key cells of the specific immune system, including B-lymphocytes and T-lymphocytes, which originate from stem cells in the bone marrow.

  • B-lymphocytes (B-cells): Mature in the bone marrow. Each B-cell can make one type of antibody molecule. When activated by a foreign antigen (often with help from T-helper cells), B-cells undergo clonal selection (binding to specific antigen) and clonal expansion (rapid division by mitosis) to form a clone of plasma cells and memory cells.

  • Plasma cells: Short-lived cells that secrete large quantities of specific antibodies.

  • T-lymphocytes (T-cells): Mature in the thymus gland. They have specific T-cell receptors that bind to antigens presented on the surface of host cells (e.g., by macrophages, known as antigen-presenting cells). T-cells differentiate into helper T-cells and cytotoxic T-cells (killer T-cells). Helper T-cells stimulate B-cells, cytotoxic T-cells, and phagocytes. Cytotoxic T-cells search for and kill infected cells or abnormal body cells.

• Antibodies: Proteins (immunoglobulins) produced by B-cells in response to antigens. They have a Y-shape with four polypeptide chains held by disulfide bridges. The variable regions at the tips of the "Y" arms have unique tertiary structures that form highly specific binding sites for antigens.

  • Functions of Antibodies:

    • Agglutination: Clumping together of pathogens, making them easier for phagocytes to engulf.

    • Neutralizing Toxins: Binding to and preventing toxins from affecting human cells.

    • Preventing Pathogen Binding: Blocking cell surface receptors pathogens need to bind to host cells.

    • Lysis: Some antibodies can create holes in bacterial cell walls, causing them to burst due to osmosis.

• Primary vs. Secondary Immune Response:

  • Primary Response: The body's initial response to an antigen, leading to the production of plasma cells and memory cells. It takes time to develop, during which symptoms may occur.

  • Secondary Response: A faster, stronger, and longer-lasting response upon re-exposure to the same antigen, due to the activation of memory cells. This often prevents the person from getting ill.

4. Types of Immunity Immunity can be categorized based on how it's acquired:

• Active Immunity: When the immune system makes its own antibodies after being stimulated by an antigen.

  • Natural Active Immunity: Acquired after catching a disease.

  • Artificial Active Immunity: Acquired after vaccination.

• Passive Immunity: When a person receives antibodies made by another organism (or in vitro); the immune system does not produce its own antibodies.

  • Natural Passive Immunity: Antibodies received from the mother across the placenta or in breast milk (colostrum). This provides immediate but short-term protection as no memory cells are produced.

  • Artificial Passive Immunity: Antibodies are injected (e.g., antitoxins for tetanus or rabies). This also provides immediate but temporary protection.

5. Vaccination Vaccination involves introducing antigens (often harmless forms of pathogens, dead or attenuated, or toxins) into the body to stimulate an immune response and produce memory cells, leading to immunity without causing disease.

• Herd Immunity: When a large proportion of the population is vaccinated, it reduces the occurrence of the disease, indirectly protecting unvaccinated individuals who are susceptible.

• Ethical Issues: Concerns include animal testing of vaccines, risks of side effects in human trials, and perceived unfairness if unvaccinated individuals benefit from herd immunity.

• Challenges: Antigenic variation (pathogens changing their surface antigens) makes vaccine development difficult (e.g., HIV, influenza, malaria) because memory cells from a previous infection won't recognize the new antigens, requiring a new primary response. Some vaccines are ineffective against certain pathogens (e.g., malaria, cholera) due to the pathogen's life cycle or habitat.

6. Pathogen Evasion Mechanisms Pathogens have evolved ways to evade the immune system.

• Antigenic Variation: Pathogens like HIV and influenza can change their surface antigens due to genetic changes. This means memory cells from previous infections don't recognize the new strains, requiring a new primary immune response.

• Antigenic Concealment: Some pathogens hide inside host cells (e.g., Plasmodium in liver and red blood cells, Mycobacterium tuberculosis inside phagocytes) to avoid antibodies in the plasma or suppress the immune system. HIV specifically kills the helper T-cells it infects, reducing overall immune cells.

7. Antibiotics Antibiotics are medicinal drugs specifically designed to kill or inhibit the growth of bacteria. They are a type of antimicrobial substance.

• Mechanism: They act on structures or metabolic pathways unique to bacteria, such as cell wall synthesis (e.g., penicillin prevents peptidoglycan cross-links) or protein synthesis (e.g., tetracycline binds to bacterial ribosomes). Some are bactericidal (kill bacteria), others are bacteriostatic (prevent growth).

• Ineffectiveness Against Viruses: Antibiotics are completely ineffective against viruses because viruses are non-cellular, lack their own cell structures (like cell walls), and hijack host cell machinery (enzymes, ribosomes) for replication. Antibiotics target bacterial processes that differ from human ones, and thus cannot target human host cell processes exploited by viruses.

• Antibiotic Resistance: Bacteria can evolve resistance to antibiotics through random mutations, which gives resistant bacteria a selective advantage, leading to natural selection. Resistance can spread via binary fission (vertical transmission) and horizontal gene transfer (e.g., plasmids via conjugation). This creates "superbugs" like MRSA and Clostridium difficile.

• Reducing Resistance: Measures include prescribing antibiotics only when necessary, completing the full course, using narrow-spectrum drugs, reducing agricultural use, improving hygiene, and monitoring resistance.

• Testing Effectiveness: Investigated using bacterial cultures on agar plates with antibiotic discs, observing inhibition zones. Larger zones indicate greater effectiveness. The Minimum Inhibitory Concentration (MIC) can also be determined.