Viral and Bacterial Infections
- A pathogen is any organism that causes disease (some bacteria, some fungi, all viruses)
- The Human Immunodeficiency Virus (HIV) infects and destroys T helper cells, leading to Acquired Immune Deficiency Syndrome (AIDS) as the immune systems fails due to a lack of t helper cells.
- AIDS sufferers develop diseases and infections that wouldn't cause serious problems in a normal person- called opportunistic infections
- There is normally 8-10 years between HIV and AIDS. The symptoms of AIDS then progress from minor infections of mucous membranes and respiratory system, to serious infections like TB and chronic diarrhoea, to v serious infections such as toxoplasmosis (brain) which kill
- Mycobacterium tuberculosis infects phagocytes in the lungs, and causes tuberculosis. TB is not developed straight away, alveolar cells surround the infected phagocytes in tubercules. Anaerobic conditions cause the bacteria to become dormant, leading to no symptoms
- Later on, the bacteria activate and overcome the immune system to cause TB. People with weakened immune systems (eg AIDS) are more likely to reactivate.
- Time between infection and development of TB varies. TB symptoms- 1.fever, weakness and coughing 2. lung damage and respiratory failure 3. spread to other organs, which fail
- Bacteria- single celled prokaryotes, have plasma membrane, cytoplasm and ribosomes
- Viruses- nuclei acids surrounded by protein, have none of the above
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Infection and The Non-Specific Immune Response
- Pathogens enter the body through cuts, contaminated food/drink, inhalation and mucosal surfaces
- Barriers against infection include stomach acid, skin (physical barrier), gut and skin flora (compete with pathogens for food and space) and lysozyme enzymes (mucosal surfaces and tears)
- Foreign antigens trigger an immune response- non-specific then specific
- Non-specific immune response
- 1. Inflammation- IS cells respond to damage to mast cells by releasing histamines, which cause blood vessels to vasodilate, causing local heat and redness. The increased blood flow caused by dilation brings IS cells to site of infection, and increased permeability forces them into the site of infection. WBC and antibodies disable and destroy pathogens
- 2. Interferons- Interferons are released by cells infected with viruses to inhibit viral replication within cells. It binds to receptors on surface membrane of infected cells, stimulating a pathway which makes a cell resistant to viral infection by preventing viruses from reproducing
- 3. Phagocytosis- A phagocyte moves to the bacterium, engulfs it and forms a vacuole around it. A lysosome fuses with the vacuole and releases enzymes to break down the pathogen. The phagocyte presents the antigen on its surface membrane to activate other immune cells
- 4. Fever- Immune system works better, but pathogens are unable to function effectively
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The Specific Immune Response
- Phagocytes activate T cells, a type of WBC covered with receptors to bind to antigens presented on the major histocompatibility complexes (MHCs) of phagocytes. Each T cell has a different shaped receptor, so will bind to a different antigen. This activates the T cell to divide and differentiate into different types of T cell
- - T helper cells help to produce antibodies and activate B cells
- -T killer cells- attach to antigens and produce chemicals to destroy the pathogen
- T helper cells activate b cells- B cells are WBC which are covered in antibody proteins. Antibodies bind to antigens to form an antigen-antibody complex. Each B cell has a specific antibody which will only pair with the complementary antigen
- T helper cells bind to the B cells which have become antigen presenting cells (APCs) and release cytokines to activate the B cell. It divides by mitosis into plasma cells (B effectors) and B memory cells
- Plasma cells make antibodies- Plasma cells secrete antigen specific antibodies into the blood, which will bind to antigens on pathogens to form many antigen-antibody complexes
- Antibodies clear infection by agglutinating pathogens (pathogens clump together as antibodies have two binding sites- easier to phagocytose), neutralising toxins (antibodies bind to toxins to prevent them from infecting human cells) and preventing the pathogen from binding to human cells (when in an a-a complex, receptors needed for pathogens to bind to host cells are blocked)
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Developing Immunity 1
- Primary response- when a pathogen enters the body for the first time, and antigens activate the immune system. It is slow as there aren't many B cells to make the specific antibody, but eventually enough will be produced (but symptoms show)
- After exposure, T and B cells produce memory cells which remain in the body. Memory T cells recognise the specific antigen and memory B cells record the antibodies needed. If re-infected, the immune system produces a faster secondary immune response, and kill the pathogen before symptoms show
- Active immunity- when immune system makes own antibodies; natural (become immune after catching a disease) or artificial (immune after given a vaccine)
- Passive immunity- from being given antibodies from another organism (own body doesn't produce them); natural (babies get antibodies through placenta and breast milk) or artificial (become immune after injected with antibodies)
- Vaccination helps avoid getting ill while B cells divide to build up numbers to fight pathogen. Vaccines contain antigens to cause the body to produce memory B and T cells. You become immune without having symptoms. Normally contain many different antigens to protect against different strains of pathogen
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Developing Immunity 2
- Over time, the immune system has improved, and pathogens have evolved to evade the host immune systems. This struggle is an evolutionary race
- HIV evasion mechanisms
- HIV kills the immune system cells it infects-reduces chances of detection.
- High mutation rate in antigen protein genes to form new strains of the virus- this is antigenic variation.
- HIV disrupts antigen presentation in infected cells- prevent immune system from recognising and killing infected cells
- Mycobacterium Tuberculosis evasion mechanisms
- When engulfed by phagocytes, they produce substances which prevent lysosomes fusing with the vacuole- bacteria aren't broken down
- Disrupts antigen presentation in infected cells- prevent immune system from recognising and killing infected phagocytes
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- Bacteriocidal antibiotics kill bacteria, bacteriostatic antibiotics prevent bacteria from growing.
- They work by interfering with metabolic reactions. Some inhibit enzymes needed to make bonds in bacterial cells walls, so prevent the bacteria from growing properly, or cause death as the wall can burst due to water leaving by osmosis
- Some inhibit protein production by binding to ribosomes. No enzymes can be made, which carry out metabolic processes needed for growth and development
- Hospital acquired infections (HAIs) are infections caught while a patient is hospital. Are transmitted through poor hygiene- staff and visitors not washing hands, coughs and sneezes not being contained, and equipment and surfaces not being disinfected
- Ill patients are more likely to catch infections as they have weakened immune systems
- Codes of practice to prevent and control HAIs- hand washing encouraged, equipment and surfaces disinfected, and people with HAIs are moved into isolation
- Some HAIs are caused by antibiotic resistant bacteria (eg MRSA), which are v difficult to treat.
- They are more common in hospitals as more antibiotics are used, so bacteria are more likely to have evolved resistance
- Codes of practice- antibiotics not for viral/minor infections or to prevent infection, no use of narrow-spectrum antibiotics, use full courses and rotate use of different antibiotics
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Microbial Decomposition and Time of Death
- Microorganisms decompose organic matter. Microorganisms in/on dead matter secrete enzymes to break it down so that they can respire (releasing CH4 and CO2)
- Time of death (TOD) can be determined by forensic scientists in 5 ways-
- Body temperature- After death, metabolic reactions which produce heat slow down, and eventually stop, causing body temperature to fall until it = environmental temperature. A body loses 1.5- 2 C per hour after death
- Cooling rate is affected by air temperature, clothing and body weight
- Degree of muscle contraction- After 4-5 hrs, muscles in a body start to contract and become stiff, this is rigor mortis.
- It begins when muscle cells become deprived of oxygen. Anaerobic respiration takes place, leading to a build up of lactic acid. The pH of cells decreases, inhibiting enzymes which produce ATP. No ATP means bonds between myosin and actin are fixed and the body stiffens
- Smaller muscles contract first- smaller ATP stores. Rigor mortis is affected by degree of muscle development and temperature
- Forensic entomology- The study of organisms present on a body. TOD can be estimated by looking at what insects are present, or by identifying the stage in a life cycle an insect is in (affected by drugs, humidity, oxygen and temperature)
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Microbial Decomposition and Time of Death 2
- Extent of decomposition- Immediately after death bacteria and enzymes begin to decompose the body.
- Hours to few days- cells and tissues broken down, skin turns greenish.
- Few days to few weeks- Microorganisms decompose tissues and organs, produces gases to bloat the body, skin blisters off.
- Few weeks- tissues liquefy and seep out.
- Few months to years- only skeleton remains.
- Decades to centuries- skeleton decomposes
- Affected by temperature and oxygen availability
- Stage of succession- 1. Conditions ideal for bacteria
- 2. As bacteria decompose tissues, conditions become favourable for flies and their larvae
- 3. Fly larvae feed -> conditions for beetles
- 4. As a body dries out, conditions not great for flies so they leave. Beetles remain to decompose dry tissue
- 5. When no tissue remains, conditions are not favourable for any organisms
- Affected by location of body (eg. above ground, underground, in water or sealed)
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