C3.2_Defence against disease

C3.2 Defence against disease

Interaction and interdependence—Organisms

• How do body systems recognize pathogens and fight infections?
• What factors influence the incidence of disease in populations?

C3.2.1 Pathogens as the cause of infectious diseases

Pathogen: disease causing organism

C3.2.1 Pathogens as the cause of infectious diseases

Halloween Bonus Question: Discuss what type of pathogen could be the cause of a Zombi outbreak

C3.2.1 Pathogens as the cause of infectious diseases

NOS: Careful observation can lead to important progress.

Careful observations during 19th-century epidemics of childbed fever (due to an infection after childbirth) in Vienna

Careful observations during the cholera epidemics in London led to breakthroughs in the control of infectious disease.

C3.2.4 Differences between the innate immune system and the adaptive immune system

Immune defences

Adaptive immune responses are specific to particular pathogens and become more effective upon re-exposure (has memory)

Innate immune responses are broad-acting (no differentiation between types of pathogens) and do not change during an organism’s life (do not generate memory)

C3.2.4 Differences between the innate immune system and the adaptive immune system

Innate (IR) and adaptive (AR)responses are connected by the lymphatic system:

• Phagocytes (IR) travel to the site of an infection within the bloodstream and then engulf the resident pathogens
• They travel into the lymphatic system and are filtered at the lymph nodes
• At the lymph nodes, the phagocytes present pathogenic fragments (antigens) to the lymphocytes, resulting in the production of specific antibodies (AR)

The IR is needed to activate the AR, while specific antibodies (AR) heighten the efficacy of the phagocytes (AR)

The lymphatic system

C3.2.2 Skin and mucous membranes as a primary defence

Surface barriers (first line of defence):Prevent entry of pathogens into the body. Include:

• Physical Barriers

• Chemical barriers

• Microbiological barriers

C3.2.2 Skin and mucous membranes as a primary defence

Surface barriers (first line of defence):Prevent entry of pathogens into the body. Include:

• Physical Barriers:
• Skin: epithelial cells tight junctions and layer of dead cells that impede crossing of pathogens
• Mucose membranes: cover cavities, contain mucus, may be ciliated to remove pathogens
• Chemical barriers:

• Microbiological barriers:

C3.2.2 Skin and mucous membranes as a primary defence

Surface barriers (first line of defence):Prevent entry of pathogens into the body. Include:

• Physical Barriers:

• Chemical barriers:
• Sebaceous glands: secrete chemicals that inhibit microbial growth on the surface of the skin
• Tears and saliva contain lysozyme (enzyme) which can destroy cell walls
• Sticky mucins (in mucus) help to clear pathogens
• The stomach and genitourinary tracts produce acids that create a hostile pH to pathogens
• Microbiological barriers:

C3.2.2 Skin and mucous membranes as a primary defence

Surface barriers (first line of defence):Prevent entry of pathogens into the body. Include:

• Physical Barriers:

• Chemical barriers:

• Microbiological barriers: microbiota that line specific cavities, preventing colonisation by pathogens (e.g. digestive tract, vulva and vagina...)

C3.2.3 Sealing of cuts in skin by blood clotting

C3.2.3 Sealing of cuts in skin by blood clotting

The coagulation cascade

C3.2.5 Infection control by phagocytes

The innate immune system (sedond line of defence)The main components are the phagocytic leukocytes

C3.2.5 Infection control by phagocytes

The innate immune system (sedond line of defence)The main components are the phagocytic leukocytes

1. Damaged tissues release chemicals (e.g. histamine)
2. Phagocytes circulate in the blood and move into the tissue (extravasation) in response to the chemicals (chemotaxis)
3. Phagocytes membrane receptors recognize pathogens
4. Phagocytes form pseudopods that surround the pathogens and engulfe them through endocytosis
5. The vesicle fuses to a lysosome forming a phagolysosome
6. The pathogen is digested by enzymes within the lysosome

https://www.tempobioscience.com/the-many-faces-of-phagocytes/

C3.2.5 Infection control by phagocytes

The innate immune system (sedond line of defence)The main components are the phagocytic leukocytes

7. Pathogen fragments (antigens) may be presented on the surface of the phagocyte.8. These antigen-presenting cells will drain into the lymphatic system and stimulate the production of specific antibodies by lymphocytes (AR).

https://www.sciencedirect.com/topics/immunology-and-microbiology/antigen-presenting-cell

https://www.monash.edu/student-academic-success/biology/initial-responses-of-immune-systems/key-leukocytes-of-the-innate-immune-system

C3.2.7 Antigens as recognition molecules that trigger antibody production

The immune system reacts to the presence of foreign materials

• The innate immune response responds to broad categories of pathogen by detecting pathogen-associated molecular patterns (PAMPs)
• Phagocytes engulf them and break them down within their lysosomes
• The adaptive immune response responds to highly specific molecular markers on the outer surface of the pathogen: antigens
• Antigens trigger the production of antibodies by B-lymphocytes
• E.g., the glycoproteins on the surface of red blood cells (ABO blood groups)

C3.2.6 Lymphocytes as cells in the adaptive immune system that cooperate to produce antibodies

Adaptive immune response (third line of defence)

Every individual possesses a very large number of distinct T and B lymphocytes that each recognise and respond to a particular antigen. Some lymphocytes circulate within the bloodstream, most reside within the lymphatic system (lymph nodes) Individuals contain a large number of B-lymphocytes, each making a specific type of antibody

C3.2.8 Activation of B-lymphocytes by helper T-lymphocytes

Phagocytic leukocytes present surface antigens to the lymphocytes at the lymph nodes

C3.2.8 Activation of B-lymphocytes by helper T-lymphocytes

Clonal selection:When a helper T lymphocyte is activated, it forms a complex with the specific B lymphocyte and releases cytokines, activaing the B lymphocyteThe specific B cell divides and forms a large population of clonesThe clones differentiate into:

• Plasma cells: produce large quantities of specific antibody
• Memory cells that provide long-term immunity

C3.2.8 Activation of B-lymphocytes by helper T-lymphocytes

Opsonisation

C3.2.8 Activation of B-lymphocytes by helper T-lymphocytes

Clonal selection: Only one specific lymphocyte can be activated by a particular antigenic fragment to divide and form copies

Polyclonal activation: a pathogen may contain multiple antigen fragments and hence activate multiple specific lymphocytes

C3.2.9 Multiplication of activated B-lymphocytes to form clones of antibody-secreting plasma cells

Each specific B cell exists within the body as a relatively small population of cells and must proliferate to form sufficient quantities to fight off infections The activated B cells will divide via mitosis and then differentiate into short-lived plasma cells that produce large amounts of antibodies

C3.2.9 Multiplication of activated B-lymphocytes to form clones of antibody-secreting plasma cells

AntibodiesAn antibody (or immunoglobulin) is a protein produced by B lymphocytes (and plasma cells) that is specific to a given antigen

Variable regions differ between antibodies and bind the antigens

Constant region serves as a recognition site for non-specific phagocytes (opsonisation)

Contain 4 polypeptide chains that are joined together by disulphide bonds to form Y-shaped molecules

C3.2.9 Multiplication of activated B-lymphocytes to form clones of antibody-secreting plasma cells

AntibodiesEach type of antibody recognises a unique antigen, making antigen-antibody interactions specific Antibodies coat the pathogen, making them easier to detect, aiding the detection and removal of pathogens by phagocytes (opsonisation)

C3.2.10 Immunity as a consequence of retaining memory cells

Long-term immunityThe adaptive immune system relies on the clonal expansion of plasma cells to produce sufficiently large numbers of antibodies

• Therefore, there is a delay between the initial exposure to a pathogen and the production of large quantities of antibodies
• If pathogens can reproduce rapidly during this delay period, they can impede normal body functioning and cause disease

• Memory cells are produced to prevent this delay in subsequent exposures and hence prevent disease symptoms developing

C3.2.10 Immunity as a consequence of retaining memory cells

Summary of the immune response

https://www.youtube.com/watch?v=AucZlvEv29Y

C3.2.11 Transmission of HIV in body fluids

C3.2.11 Transmission of HIV in body fluids

How can we avoid HIV transmission?

C3.2.12 Infection of lymphocytes by HIV with AIDS as a consequence

Immunodeficiency: When the immune system’s capacity to fight infection is compromised or absent AIDS (Acquired ImmunoDeficiency Syndrome) is caused by the HIV (Human Immunodeficiency Virus)

• HIV is a retrovirus (RNA virus that is retrotranscribed into DNA in the cells)
• HIV infects and destroys T-helper lymphocytes
• Without T-helper lymphocytes, B cells cannot be activated when there's an infection
• Therefore, antibodies are not produced against pathogens

C3.2.12 Infection of lymphocytes by HIV with AIDS as a consequence

HIV life cycle and AIDS progression:

• Following infection, the virus undergoes a period of inactivity (clinical latency) during which infected helper T cells reproduce

• Eventually, the virus becomes active again and begins to spread, destroying all infected T lymphocytes in the process (lysogenic cycle)

• The immunity response is reduced
• The body becomes susceptible to opportunistic infections, eventually resulting in death if the condition is not managed

C3.2.15 Zoonoses as infectious diseases that can transfer from other species to humans

Zoonosis: Infectious disease that can be transmitted from other species to humans

• Directly from the non-human host
• By an unaffected intermediate species (vector)

Facilitates the re-emergence of an infectious disease in a population where it had previously been eliminated

Reservoirs

C3.2.15 Zoonoses as infectious diseases that can transfer from other species to humans

Zoonosis: The frequency of of outbreaks of zoonotic diseases are increasing due to:

• Agricultural practices: increase human exposure to animals
• Human induced climate change: alters the breeding cycles and geographic distribution of vectors (rodents, mosquitoes)
• Urbanisation and deforestation is forcing native wildlife into closer proximity to humans

C3.2.15 Zoonoses as infectious diseases that can transfer from other species to humans

Examples: investigate about the following zoonotic diseases:

• Name of the pathogen
• Symptoms

Complete the task on Managebac

• Animals they spread from
• Mode of transmission

COVID-19

Japanese encephalitis

Tuberculosis

Rabies

C3.2.16 Vaccines and immunization

Vaccine A substance that provides long-term immunity to a particular pathogen by stimulating an immune response without causing the disease.

C3.2.16 Vaccines and immunization

Types of vaccines:A) Traditional (antigens)

• attenuated (weakened) or inactivated viruses
• weakened toxins (produced by bacterial pathogens)
• subunits – this could be the antigen or part of the pathogen carrying the antigen

B) Nucleic acid:

• DNA or RNA that code for a specific antigen
• The body produces the antigenic fragments

C3.2.17 Herd immunity and the prevention of epidemics

Outbreak:Sudden rise in the occurrence of an infectious disease

• Epidemic: occurs within a community or geographic region
• Pandemic: intercontinental or global spread

Herd Immunity: If a sufficient percentage of a population is immune to a disease, transmission is greatly impeded. Important for vulnerable populations that cannot be vaccinated (elderly, extremely young and immune compromised)

C3.2.17 Herd immunity and the prevention of epidemics

What proportion of population must be vaccinated to acquire herd immunity? Depends on a number of factors:

• How the disease spreads:
• mode of transmission
• period of infectivity
• Population density
• Social behaviour patterns

Measles: 95% Polyomielitis: 80% COVID-19: 80-90%

C3.2.17 Herd immunity and the prevention of epidemics

NOS: Scientists publish their research so that other scientists can evaluate it. The media often report on the research while evaluation is still happening, and consumers need to be aware of this. Vaccines are tested rigorously and the risks of side effects are minimal but not nul. The distinction between pragmatic truths and certainty is poorly understood.

What happened with AstraZeneca COVID vaccine?

C3.2.18 Evaluation of data related to the COVID-19 pandemic

To manage the COVID-19 pandemic, epidemiologists needed to consider various factors in order to determine appropriate social strategies for limiting the spread:

• The level of virulence and the rate of spread of the different strains of coronavirus
• The efficacy of the vaccines
• The level of compliance with vaccine mandates in distinct social communities (e.g. native speakers vs foreign languages)
• The rates of mortality and numbers of reported cases in different countries and states (to determine the efficacy of different health responses)

Two calculations that epidemiologists use to help analyse and interpret data related to the pandemic are percentage difference and percentage change

C3.2.18 Evaluation of data related to the COVID-19 pandemic

AoS: Calculate percentage difference and percentage change.

Evaluate the COVID pandemic data (Managebac)

C3.2.13 Antibiotics as chemicals that block processes occurring in bacteria but not in eukaryotic cells

Antibiotics Compounds that kill or inhibit the growth of bacteria by targeting prokaryotic metabolism Because eukaryotic cells do not possess these features, antibiotics will target the bacteria and not the infected host Antibiotics may either kill the invading bacteria (bactericidal) or suppress its potential to reproduce (bacteriostatic)

Viruses do not possess a metabolism so they cannot be treated with antibiotics

• Must be treated with specific antiviral agents that target features specific to viruses (e.g. viral enzymes or components of the capsid)

C3.2.14 Evolution of resistance to several antibiotics in strains of pathogenic bacteria

Antibiotic resistance

Resistance genes may confer resistance by encoding traits that:degrade the antibiotic, block its entry, increase its removal or alter the target

C3.2.14 Evolution of resistance to several antibiotics in strains of pathogenic bacteria

Antibiotic resistance

The prevalance of resistant bacterial strains is increasing rapidly due to:

• Over-prescription of antibiotics
• Antibiotic misuse (e.g. given to treat a viral infection)
• Antibiotics that are freely available without a prescription
• Antibiotics included in livestock feed

E.g., Golden Staph (MRSA – Methicillin Resistant Staphylococcus aureus)

C3.2.14 Evolution of resistance to several antibiotics in strains of pathogenic bacteria

NOS: The development of new techniques can lead to new avenues of research; for example, the recent technique of searching chemical libraries is yielding new antibiotics.

Find out more about screening chemical libraries to find new antibiotics here:

https://www.genengnews.com/resources/natural-products-inform-library-design/

https://pmc.ncbi.nlm.nih.gov/articles/PMC4765079/

https://pmc.ncbi.nlm.nih.gov/articles/PMC10963893/

https://www.nature.com/articles/s43588-024-00591-x