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INFECTION Contents OUTLINE THE PATHOGENESIS OF INFECTION, ITS EFFECTS ON THE HOST AND THE ROLE OF HOST FACTORS IN THE DEVELOPMENT OF DISEASE ...................................................................................... 1 Step 1 External Barriers to infection ........................................................................................ 2 Step 2 Spread ............................................................................................................................. 3 Step 3 Evasion of Host Defences at many stages ....................................................................... 4 Step 4 Damage ........................................................................................................................... 6 Step 5 Resolution ........................................................................................................................ 6 EXPLAIN HOW BACTERIA SPREAD BOTH WITHIN A HOST AND BETWEEN HOSTS ................................. 8 REFERENCES.................................................................................................................................... 8 OUTLINE THE PATHOGENESIS OF INFECTION, ITS EFFECTS ON THE HOST AND THE ROLE OF HOST FACTORS IN THE DEVELOPMENT OF DISEASE Steps involved in pathogenesis of infection: i. Access & Entry – Acquisition, colonisation, penetration A pathogen must overcome the body’s external defences: ii. Skin e.g. skin secretions (sweat, sebum etc), keratin (protection against bacterial enzymes) Natural flora providing competition for space and nutrients Shedding of epithelia Mucociliary clearance from airways Spread – Local & Systemic Transmission A pathogen must immediately overcome local defences. This includes the evasion of the innate immune system. iii. Evasion of Host Defences at many stages Evasion of host defences. Includes previously described barrier defences of the host, other defences include: Innate immunity: Complement and physical barriers. Acquired immunity: T- cell mediated. iv. Damage – Direct effects of the pathogen, and those secondary to the host response of the process A pathogen is then shed from body (exit). Pathogens can be spread between hosts, e.g. passing through the gastrointestinal tract, droplet spread from the respiratory system, direct spread from the urogenital system. Jess Q – Week 6 – Out Damn’d Spot Page 1 v. Resolution – Activation of the Innate & Acquired Immune Response ± Medical Treatment As a result of being infected with a pathogen, the acquired immune response will develop specificity to recognise if the same pathogen invades the body a second time. This way, a person will not be diseased from the same pathogen a second time. Basic overview of immunity Step 1 External Barriers to infection External barriers An invading microorganism initially encounters ‘external’ defences, such as enzymes in secretions that can damage or destroy microorganisms (e.g. lysozyme in saliva and tears, low pH in the stomach, sticky mucus on many surfaces, and the presence in the gut and genital tract of normal bacterial flora that are able to prevent the growth of pathogenic organisms Jess Q – Week 6 – Out Damn’d Spot Page 2 Step 2 Spread Pathogens can be transmitted both locally and systemically. mechanisms are required. They are characterised by; To combat this, innate defence Rapid, first line of defence against infection Non-specific (do not distinguish between different pathogens) Always present at low levels May be rapidly activated early in an infection or after tissue damage They slow or prevent the development of infections during the several days that it takes for the acquired immune system to develop a specific response A body’s defence system distinguishes certain characteristic molecules on the surface of some invaders, called pathogen-associated molecular patterns (PAMPs), which acts as flags to identify bacteria as opposed to the eukaryotic host cells. If a pathogen passes the initial external defences, internal non-specific defences come into play. Activation of the complement cascade has three main consequences: 1. Induction of local inflammation, increasing vascular permeability at the sites of infection and attracting phagocytes to sites where complement is bound 2. Facilitation of the engulfment by phagocytic cells of microbes or cells with complement bound to them 3. Lysis of cells and damage to bacteria with complement bound to their surface (by ‘punching’ holes through the cell membrane) The inflammatory response When the external barriers are breached, resulting in injury and the introduction of microorganisms, an integrated, non-specific response called the inflammatory response occurs. Chemicals released in the damaged or infected tissue, such as histamine released from stimulated mast cells and cytokines initiate a series of local changes including; 1. Widening of capillaries, causing an increased blood flow to the area 2. Increased permeability of the capillaries, causing a release of plasma into the surrounding tissue 3. Attraction of phagocytes, monocytes (which develop into macrophages) and neutrophils to the site and their migration into the surrounding tissue This results in: Redness Swelling Pain Increased warmth all at the side of the affected area. The phagocytes attracted to the area attack and engulf bacteria and remove cell debris. Antibodies and complement move to the site and lead to the development of the specific immune response. Jess Q – Week 6 – Out Damn’d Spot Page 3 Step 3 Evasion of Host Defences at many stages Adaptive Immune System Takes time to develop Therefore, important in recovery from disease more than preventing infection initially Specific response. E.g.: distinguishes between different infecting microorganisms or strains of the same microorganisms. Has immunological memory o Primary response person vaccinated against disease, immune system recognises it o Secondary response person comes contact with disease again, system recognises disease and is more efficient in preventing infection second time around Cells involved in specific acquired immunity There are two distinct kinds of immune response that are usually effective against different kinds of microorganisms: a cellular response (mediated by T cells type of acquired immunity is achieved through the formation of large numbers of activated T lymphocytes that are specifically crafted in the lymph nodes to destroy the foreign agent.), and a humoral response (in serum – mediated by antibodies produced by B lymphocytes - the body develops circulating antibodies, which are globulin molecules in the blood plasma that are capable of attacking the invading agent.) Cells involved in immune response: Jess Q – Week 6 – Out Damn’d Spot Page 4 Cells of immune response in more detail: Jess Q – Week 6 – Out Damn’d Spot Page 5 Step 4 Damage Damage results from direct effects of the pathogen and those secondary to the host response of the process. Pathogens can be spread from various means, namely through i. ii. iii. iv. v. vi. Contact (eg. Touching surfaces contaminated by Hep B) Inhalation (eg. Breathing in airborne droplets infected with Step. Pneumoniae) – Horizontal Ingestion (eg. Eating food contaminated with Salmonella) Inoculation (eg. Transmission of Hep C from sharing needles) Transplacental (eg. Tetratogens, like Leukaemia, crossing the placenta from mother to child) – Vertical Transmission Vectors (eg. Mosquitoes carrying Malaria) Step 5 Resolution Activation of the Innate & Acquired Immune Response ± Medical Treatment If a person is exposed to the same pathogen a second time, the acquired immune response will be activated to enhance the immune defences of the body. This can be achieved with vaccination or from being exposed to the pathogen and recovering from infection Jess Q – Week 6 – Out Damn’d Spot Page 6 Clinical features of acute inflammation Jess Q – Week 6 – Out Damn’d Spot Page 7 EXPLAIN HOW BACTERIA SPREAD BOTH WITHIN A HOST AND BETWEEN HOSTS Bacteria spread within a host the following ways: 1. The ability to use motility and other means to contact host cells and disseminate within a host. 2. The ability to adhere to host cells and resist physical removal. 3. The ability to invade host cells. 4. The ability to compete for iron and other nutrients. 5. The ability to resist innate immune defences such as phagocytosis and complement. 6. The ability to evade adaptive immune defences. Bacteria spread between hosts the following ways: Some bacteria produce adhesion molecules called invasins that activate the host cell's cytoskeletal machinery enabling bacterial entry into the cell by phagocytosis. Advantages of entering a human cell include: a) Providing the bacterium with a ready supply of nutrients b) Protecting the bacteria from complement, antibodies, and other body defence molecules In addition, some pathogenic bacteria: a) Invade phagocytic cells, neutralize their killing ability, and turn them into a safe haven for bacterial replication b) Kill phagocytic dendritic cells once they are engulfed and prevent those dendritic cells from activating the T4-lymphocytes and T8-lymphocytes required for adaptive immunity REFERENCES Abbas, A & Litchtman, A. (2011). Basic Immunology. Philadelphia: Elsevier. Colledge, N., Walker, B.& Ralston, S. (2010). Davidson’s Principles and Practices of Medicine. Philadelphia: Churchill Livingstone. Knox B, Ladiges, P., Evans, B. & Saint, R (2007). Biology – An Australian Focus. Australia: McGraw Hill. Sherwood, L. (2004). Human Physiology: From Cells to Systems (5th Edition). Australia: Thompson. Jess Q – Week 6 – Out Damn’d Spot Page 8