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114 Cards in this Set
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What are the basic differences between innate and acquired immune system?
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1. Innate immunity: non-specific defence.
- no 'memory', always working. - eg; external barrier defences (skin) - eg; internal cellular and biological defences. 2. Acquired immunity is specific, has the ability to remember previous exposure and is turned 'on' when needed. - eg; antibody-mediated immunity (humoral) - eg; cell-mediated immunity. |
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Describe the external (surface) entry barriers.
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External entry barriers; designed to block microbes from entering sterile internal tissues.
a) Structural defences (skin, mucous membranes); hard to penetrate, continuous loss of skin removes microbes. dry salty environment (of skin) limits growth of microbes. b) Mechanical defences: flushing action of fluids (tears, urine, saliva). ciliated cells in lungs move mucus & attached microbes - swallowed and eliminated. c)Microbial Defences: 'normal' microbial flora competition. d) Biochemical Defences: chemicals produced by body restrict microbial growth. - eg; acids, lysozyme in saliva, etc. |
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What are the internal defences after something gets past the entry barrier? (internal defences)
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second part of innate response.
come into action if pathogen overcome surface barriers. a) Phagocytosis. b) inflammation. c) Complement d) Fever |
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Describe Phagocytosis.
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Phagocytosis; a process by which certain cells (phagocytes) can digest and remove dead tissues and any foreign material that has penetrated an external barrier.
cells involved: (mainly white blood cells) * Monocytes, neutrophils and eosinophils (circulate in bloodstream). * *Macrophages** (monocytes which have migrated into deeper tissues and organs) - most important. * Dendritic cells (in tissues close to body surfaces, (skin, gut, etc.) Mechanism of Phagocytosis; 1. bacterium becomes attached to membrane evaginations called pseudopodia. 2. bacterium is ingested, forming phagosome. 3. Phagosome fuses with lysosome. 4. Lysosomal enzymes digest captured material. 5. Digestion products are released from cell. |
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How does a phagocyte know to go after a foreign microbe?
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Pattern recognition receptors (proteins located on the surface of phagocytes that recognized characteristics molecules in microbes but not found in host cells.
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How does a phagocyte kill a microbe?
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After ingesting a microbe, the phagocyte has various degradative enzymes and other toxic molecules contained in the lysosome compartment of the phagocyte.
the left overs are spit out, which are adsorbed and further degrade but may irritate surrounding tissue if in large amounts. |
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How do bacteria defend themselves against phagocytosis?
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1. produce capsular polysaccharide; making it harder for phagocyte to grab on and digest microbe.
2. secrete 'toxins' that target phagocytes. 3. Survive after being ingested; escape the phagosome-lysosome compartment and enter and grow cytoplasm. |
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What are other ways that cells can kill microbes?
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1. Eosinophils; secrete toxic proteins that perforate parasite wall. "extracellular killing".
2. Natural Killer cells: recognize a virus-infected cell and destroy it by secreting degradative enzymes. |
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What is the inflammatory response?
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Inflammatory response: a rapid biological response to tissue damage; indicates that the body is responding appropriate to the presence of microbes. purpose: attract phagocytes and other immune cells to the site of injury. Begin the processes that will repair and heal injured tissues. chemicals involved: - histamine; vasodialation, increases permeability of blood vessels, stimulates nerve endings (pain). - prostaglandins; vasodilation, fever, sensitivity to pain. attract phagocitic cells. -complement' proteins; stimulate release of histamine. enhance action of phagocytic cells. |
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what is the difference between chronic and acute inflammation?
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Acute vs chronic inflammation:
Acute: (GOOD) the immediate (beneficial) response to tissue injury &/or the presence of microbes. Neutrophils, plasma proteins and fluids accumulate in the damaged or infected area. resolves (usually <2 weeks) once the cause has been removed or the damaged tissue has healed. Chronic: (BAD) a longer-lasting (weeks, months) response that occurs if the microbe persists. an abnormal response that does not benefit the body. entry of macrophage and monocytes into the area. continuous macrophage attack results in further damage to tissues and the formation of fibrous tissues. |
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What are complement proteins?
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Complement proteins:
- a family of 30 different proteins found into he blood serum. 'complement' action of antibodies. - have three main functions: 1. Make phagocytossi more efficient via 'opsonization'. * coat bacterial cells surface. receptors on macrophage recognize the complement and promote more efficient 'swallowing of bacteria'. 2. Destroy bacteria by forming 'membrane attack complexes'. complement proteins insert into bacterial cell membrane to create pore. leakage of cytoplasmic contents... death. 3. Regulate Inflammation and other Immune Responses: cause vasodilation. help remove antibody and antigen complexes from circulation. |
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What is the purpose of fever?
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Fever; a biological response to external or internal pyrogenic (fever-inducing) agents.
benefits: 1. slows growth of temperature-sensitive microbes. 2. reduces availability of nutrients required by microbes for growth. 3. increases metabolic activity of phagocytic cells. 4. stimulates the acute inflammatory response. |
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What are pyrogens?
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Pyrogenic; fever inducing.
External pyrogens; bacterial LPS, fungal wall components, etc. internal pyrogens - chemicals released from phagocytes. pyrogens cause the hypothalamus to produce prostaglandins, which then act to re-set body's thermostat to a higher level. |
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What are the main characteristics of acquired immunity?
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Acquired immunity (third line of defence)
characterized by; discrimination; able to distinguish foreign & self. Diversity: able to recognize all possible foreign molecules. Memory: able to remember previous exposure. Two major components: 1. Humoral immunity: production of antibodies by B-cells (lymphocytes made in the bone marrow) in response to antigens. 2. Cell-mediated immunity (lymphocytes which develop in the thymus) for the control of 'intracellular microbes'. |
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Explain antibodies and antigens.
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Part of humoral immunity.
Antigen; any substance that stimulates b-cells to make antibodies. can be something completely foreign to the body, or abnormal substance. If an antigen is too large, only a small portion of it able to stimulate the antibodies. Antibody: proteins produced by B-cells which are able to specifically recognize and bind to only that antigen. a single bacterial cell will contain many differnt epitopes to which antibodies may be made. |
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Describe the structure of antibodies.
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Antibodies (immunoglobulins)
- a single antibody has four polypeptide chains and two 'ends'. - one end is 'constant' same structure in all imunoglobulin molecules. - other end is 'variable' (differs in structure in imunoglobulin). - Variable end is designed to specifically recognize and bind to a unique antigen. - a single antibody can bind two antigens at one time. |
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How do antibodies bind to antigens?
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1. agglutination; antigen and antibody 'clump' due to the two binding sites on each antibody (two per antibody) - the immune system can make an antibody for every possible antigen = antibody diversity. |
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How does the body make so many different antibodies?
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How does thebody make so many different antibodies?
- Antibodies areproduced by B-cells, but one B-cell can only make one type of antibody thatrecognizes one antigen. - Therefore: Humans carry a complete collection ofmany different B-cells, each one able to recognize only one specific antigen,and make the antibody corresponding to it. - Est.to be 109 - 1010 different B-cells in the body. 1. B-cells circulate, waiting to encounter the antigen towhich they are destined to make an antibody against. 2. When a B-cell encounters its antigen, it istriggered to divide and differentiate. Some differentiate into antibody-producing“plasma” cells. Pumpout lots of Ig into the circulation. Some differentiate into long-lived “memory”cells. Available to produce more antibody if thissame antigen is ever encountered again in the future. |
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What is the timing of antibody production.
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Timing ofAntibody Production
1) First-time exposure leads to production of first IgM, thenIgG (not immediate → may take 3 - 6 days before first IgM appears). 2) Antibodylevels decline if antigen is no longer present (Ig-producing plasma cells dieoff if not continually re-stimulated) 3) Second exposure to the same antigen gives a stronger &faster IgG response - Pre-existing memory cells rapidly detect antigen andbegin to produce more Ig |
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what are the five main types/classes of antibodies.
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MADGE
1. IgG - Mainantibody found in circulation (80% of total antibody) - Able to cross theplacenta (& therefore protect the fetus) 2 2. IgA - 10 - 15% of total antibodies - Found insecretions (breast milk, mucus, saliva, etc.) - Blocks attachment of microbesto mucosal tissue surfaces 3. IgM - 5 - 10% - Forms large complexes withantigen which are easily cleared 4. IgD - < 0.2% - Function unclear (may helpregulate immune system) 5. IgE - <0.01% - Involved in development of allergies |
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What does the binding of an antibody to its antigen actually accomplishes.
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1.Agglutination - clumping of antigen + antibody → Occurs because each Ig has 2binding sites → Large clumps are better phagocytosed or filtered out of bodyfluids
2.Opsonization - coating bacteria with antibody enables better phagocytosis 3.Neutralization - blocks attachment of virus, bacteria, or toxin to host cellsurface 4. Interacts with, and strengthens, parts ofthe innate immune system (Triggers complement production; Helps theinflammatory response, etc.) |
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What is the purpose of cell mediated immunity?
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1. Toeliminate cells infected with a bacteria or a virus (Antibodies mostlycirculate freely and can’t enter cells – including a cell containing a microbeinside it).
2. To eliminate “self” cells which have become athreat to the host (eg. cancerous cells), or foreign cells introduced fromanother human (eg. transplanted tissues). 3. To regulate the function of cells involved ininnate immunity (macrophage) and humoral immunity (B-cells). |
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How are T-cells involved?
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Mediated by T-cells (T-lymphocytes)
- Lymphocytes which are produced in the bonemarrow (like B-cells) but further develop and mature in the thymus. - Two types of T-cells are produced in the thymus: * HelperT-cells (TH) * CytotoxicT-cells (TC) - Both types enter the circulatory system in aninactive state. -T-cellsmust first be “activated” before they can function. *The TH orTC cell makes contact with a specific antigen via a protein on its surface(“T-cell receptor”). *Contactof receptor + antigen triggers the TH or TC cells to divide and differentiateinto two forms: “Functional” TH or TC cells “Memory” TH or TCcells |
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What are the types of activated t-cells, and what do they do?
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If it’s a Helper T-cell:
- Secretechemical signals (“cytokines”) that “help” other immune system cells workbetter * increase the phagocytic activity of macrophage *stimulate development of B-cells (and moreT-cells) - Memory TH cells persist and allow for a fasterresponse if the same antigen which originally activated it is encountered inthe future · If it’s a Cytotoxic T-cell: - Searchfor other cells carrying the same antigen which originally activated it (eg.virus-infected host cells, cancerous cells, transplanted foreign tissues, etc.) - TC attach to the target cell and releasetoxin-containing granules ⇒ Toxins form pores in membrane oftargeted cell & kill it. - TC itself is not harmed and can be re-cycled tokill again. - Note: TC cells can directly kill avirus-infected cell; TH cells do not have any killing ability on their own(only help other cells)i |
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What are cytokines?
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Cytokines are chemicals that regulate and signal between the different parts of the immune system.
o Regulate the intensity and duration of theimmune response o Regulateproper development of immune systemcells |
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What is the disease potential for cytokines?
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Disease potential (if the cytokine balance isupset)
Eg. Some cancers gives abnormal levels of cytokineproduction → Lymphoid tumors result in over-production of lymphocytes andtherefore over-production of cytokines Eg. Some persistent or chronic bacterial infections(tuberculosis) stimulate prolonged, low-level production of cytokines →Long-term physiological effects (eg. muscle & fat mobilization ⇒weight loss) Eg. Some bacterial toxins & virus infectionstrigger a sudden, massive over-production of cytokines (aka. “Cytokine Storm”)→ Fever, shock, widespread blood clotting → Potential for tissue & organdamage (& may be lethal) Eg. The “cytokinestorm” caused by some strains of Influenza virus |
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What is the therapeutic potential for cytokines?
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a) Cytokines used as drugs Eg. Interleukin-2(Proleukin) Stimulates production ofT-cells - Treatment of renal cell cancers, melanoma b) Drugswhich block cytokine activity Eg. Adalimumab (Humira™) - Antibody against TNF →depresses TNF activity → Reduces inflammation due to some autoimmune diseases(eg. Rheumatoid arthritis, Crohn’s disease, etc.).But → Cytokines have multiple effects &interact with each other ( ⇒ targeting one may upset another)
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what is agglutination? |
Agglutination: the antigen and antiody 'clump' due to the two binding sites on each antibody (two antigens per antibody) |
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what is opsonization? |
Bacteria is coated with antibody to enhance phagocytosis. |
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What is neutralization? |
Neutralization blocks the attachment of a virus, bacteria or toxin to the host cell surface. |
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What is does interaction do? |
Interaction strengthens the innate immune system via 'complement production' and helps the inflammatory response. |
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what do antibodies look like? |
one single antibody has 4 polypeptide chains and two ends. once constant, one variable. constant; same structure in all antibodies. variable; different between each antibody. |
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What types of cells make antibodies? |
the plasma B-cells. - but only one B-cell can make one type of antibody that recognizes one antigen. there are thus many b-cells in the body. b-cells wait to encounter antigen that they are 'destined' to produce an antibody against it. |
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what are memory B-cells, and why do we have them? |
When the B-cells encounter an antigen, it divides and conqueres. - if we are exposed a second time to the same antigen, we will get stronger, faster. the antibody response is due to 'memory cells' |
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What is the timing of antibody production? |
after the first exposure, IgM needs to be made first 3-6 days, then IgG. BUT: after second exposure to an antigen, there is stronger and faster response because of pre-existing memory cells. These cells rapidly detect antigen and produce more Ig. |
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the antibody involved in the development of allergies is: a) IgM b) IgA c) IgD d) IgG e) IgE |
e) IgE is involved in the development of allergies. |
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the antibody that blocks the attachment of microbes to mucosal tissue is; a) IgM b) IgA c) IgD d) IgG e) IgE |
b) IgA - 10 - 15% of total antibodies - Found insecretions (breast milk, mucus, saliva, etc.) - Blocks attachment of microbesto mucosal tissue |
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the antibody that forms large and easily cleared complexes with an antigen is: a) IgM b) IgA c) IgD d) IgG e) IgE |
a) IgM - 5 - 10% - Forms large complexes with antigen which are easily cleared |
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What is cell-mediate immunity for? |
cell mediated immunity is used to eliminate infected cells, eliminate 'self' cells that have become threats, and to regulate the function of cells. |
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What are the cells involved in cell-mediated immunity? |
T-cells; lymphocytes which are produced in the bone marrow but further develop and mature in the thymus. |
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What is the difference between helper t-cells and cytotoxic t-cells. |
helper t-cell; - secrete chemical signals to help others do their job, - increase phagocytic activity of macrophage. - DO NOT have the ability to kill cell on their own. Cytotoxic t-cell: - has the direct effect on infected cell. - attaches and releases toxin-containing granules. - have the ability to directly kill cell BUT: both need to be activated. |
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what are cytokines? |
cytokines: - a set of many chemicals that regulate and signal between different parts of the immune system. - 'chemical messengers'. - if the balance of cytokines is upset, there is disease potential. - cytokines can be used to treat diseases. |
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What is hypersensitivity disorder? |
Hypersensitivity disorders; - are overly aggressive immune response to an antigen. |
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what is immediate hypersensitivity? |
Immediate hypersensitivity - Anaphylactic reactions - 1st contact with allergen triggers B-Cells, TONS of IgE producedwhich bind to mast cells. - 2nd contact with same allergen; allergen binds to mast cell, mast cells “de- granulate” and releaseinflammatory chemicals such as histamine |
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What is delayed hypersensitivity? |
Delayed hypersensitivity - Does not involve antibodies, allergen+Helper T cells only. - 24hrs beforereaction due to time required for Helper T cells to kick in. - 1stexposure with allergen activates helper- T cells and production of memoryhelper T cells. - 2nd exposure- memory cells activated, helper T cellsrelease cytokines that bring macrophage and Cytotoxic cells to allergen - inflammation occurs; |
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What is the difference between localized and generalized anaphylaxis? |
Localized; reaction only at site were allergen enters/contacts body. Generalized: contact allergen causes a reaction throughout the body. |
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What does delayed hypersensitivity involve? give an example |
Antigen and helper t-cells only. eg: the tuberculin skin test |
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What are immunodeficiency disorders? |
Immunodeficiency disorders are the failure to mount an effective immune response to foreign allergen due to a defect in the innate or adaptive immune immune system. |
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What does immunodeficiency mean? |
Either congenital (genetic) or acquired failed immune response to an allergen. |
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What are some examples of congenital immunodeficiencies? |
1. agammaglobulinemia; b-cell deficiency (fail to form) 2. DeGeorge Syndrome; T-Cell deficiency (abnormalities in the thymus) - Severe combined immunodeficiency (SCID); precursor for T and B cells fails to form. |
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what sorts of things cause immunodeficiency? |
Immunodefiency causes; - microbial or chemical (most common) eg; HIV - Drugs (corticosteroids) - stress, malnutrition, alcoholism (all cause stress that can lead to increased susceptibility to microbial infections) |
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What is meant by autoimmunity? |
Autoimmunity: - a damaging immune reaction to your own cells due to an inability to distinguish self from non-self. - antibodies are produced, activate T-cells which recognize antigens on NORMAL cells. |
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What is rheumatic fever? |
Rheumatic fever; - an autoimmune disease, from untreated strep throat. - There is a cross reaction between cell wall proteins and antigens on heart valves; causes damage and inflammation of heart valves. |
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What causes rheumatoid arthritis? |
Rheumatoid arthritis: - autoimmune disease - T-cells activated by unknown self-antigen. Ig+antigen deposits in joints. - can lead to damage in joints. |
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How do serological assays work? |
Serological assays: - look for antibodies in the blood. - the antigen-antibody interaction is very specific. - If we know/have the antibody available to us, then we can use it to detect the antigen and vice versa. The antigen can be anything (microbe, drug, hormone, etc.) ELISA tests are based on this principle. |
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What is the principle behind the ELISA test. |
ELISA is a test that detects and measures antibodies in your blood. Thistest can be used to determine if you have antibodies that are related to certain infectious conditions. Antibodies are proteins that the body produces in response to harmful substances (antigens) based on serological assays. 1. antigen attached to solid support. 2. patient serum added; antibodies (if present) will bind to the attached antigen. 3. a second antibody is added, which recognizes human immunoglobulin and is 'tagged' with an enzyme. 4. substrate added for the tagged enzyme; coloured reaction is prouced if anti-human antbody has bound to complex. |
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How would you interpret an ELISA test result? |
If test is positive; - you have antibodies against that particular virus in your blood serum. - you have either a current infection, previous infection or current vaccine. |
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How do external actions affect the immune response? |
- one can manipulate or adjust the immune responseby external actions - there are drugs which canstimulate or suppress parts of the immune system - Immunosuppressive, immunostimulatory, but many have side effects and arenon-specific nutrients are important in maintaining a strongimmune system - deficiency in some nutrients impairs immune function (Ex: zinc, selenium,copper, vitamins, folic acid |
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Discuss the basic principles behind vaccines. |
to inducememory B/T Cells against a microbe so that future exposure to that same microbereults in a rapid immune response that will eliminate the microbe before itcauses disease |
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What is the difference between passive and active immunization? |
passive; temporary,short-term, results when antibodies are administered to a person active; longer-term, a true immune response occurs following an exposure to antigen |
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Why can can maternal antibodies affect vaccines? |
maternal antibodies give partial protection against microbes for the first 4-6months of life |
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What is the difference between whole cells and sub-unit vaccines? |
whole-cell vaccines: entire microbes and theirantigenic parts are given- both killed and live (but weakened) sub-unit vaccines: consist only of those partsof the microbe that are the most antigenic/ are needed to cause disease and animmune response |
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What are adjuvants? |
Adjuvants: - non antigenic components, enhance the immune responseto the antigen. - They trap antigen and promote slow release, more efficientactivation of T-Cells, non- specific immune stimulant provide better responses. |
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What is herd immunity? |
Herd immunity: - pseudo immunity, achieved by being part of agroup. - Not necessary to vaccinate entire population. Instead, only vaccinatecertain percentage so that infected and susceptible people are unlikely to meet |
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What is commensalism? |
Commensalism- microbebenefits by being associated with a human, but the human is unaffected. |
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What is mutualism? |
Mutualism- both thehuman and the microbe benefit from the interaction |
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What is parasitism |
Parasitism- themicrobe benefits, but the human host is harmed |
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What is normal flora? |
Normal Flora- totalmicrobial population that is consistently found associated with a healthy human |
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What is the difference between; colonization, infection and disease? |
Colonization- microbebecomes established and begins to grow on external surface Infection- amicrobe penetrates a body surface, enters and multiplies within tissue andtriggers immune response Disease- aninfection that results in damage to the body |
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Describe Normal flora in an infant. |
Foetus gut is sterile Normal flora originates at birth, when infant isexposed to microbes from: environment, mother’s genitals, medical personnel. Itis constantly changing depending on many factors (environment). |
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Describe the different types of Normal Flora |
Skin; lessspecies diversity than other anatomical sites, always shedding. - Can causedisease if introduced to underlying tissues Respiratory Tract; greatdiversity of species b/c of different sites (mouth, tongue, saliva, teeth,nasal area, lower resp. tract) Genito-Urinary Tract- Urine inbladder has NO normal flora (inhealthy people). Intestinal Tract- stomach,SI, colon. Has the greatesttotal#and diversity of flora and species. NOTE: diagnostic tests (eg. blood cultures) cansometimes be affected by the presence of normal flora. blood culture- patient’s blood inoculated into broth mediato test for presence of pathogens in the blood (aka bacteremia). Specimen iscollected via puncture to skin.c |
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What is an opportunistic infection? |
“Opportunistic Infection"; amicrobe which is not pathogenic under normal conditions, but may cause diseaseif introduced into a normally sterile body site, or a host with a compromisedimmune system |
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What are benefits from Normal Flora? |
A key element in human nutrition, a defencemechanism against infection, used therapeutically. Eg; Fecal transplants; - to treat C. Diff. Feces from a normal, healthyperson is given to affected patient via NG tube or enema. Up to 90% success inre-establishing intestinal flora and suppressing C. Diff.!! )Pm |
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What are prebiotics? |
Prebiotics- Non-digestible food additives that stimulate growth of pre-existing beneficial bacteria, have prolonged stay in the gut |
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What are pro-biotics? |
Probiotics- Livingbacteria consumed alone or with food products. Thought to stimulate intestinaland urogenital cells to secrete protective mucus, interact with human immunesystem, occupy space on host tissue so that pathogens cannot becomeestablished. ***Many claims have not been tested. |
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What is the infectious disease cycle? |
Infectious Disease Cycle:cycle between reservoir, transmission, and host |
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What is a reservoir? A carrier? |
Reservoir: the source of infection, natural habitat ofa microbe Carrier: aninfected human not showing signs ofdisease, but still able to transmit |
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What are ways in which microbial disease can be transmitted? |
Contact: - most frequent mode of transmission** - either direct or indirect. - Direct; physicalcontact. - Indirect; via anintermediate. - (vehicle- food/water, fomite- inanimate object,vector- animal/ insect) Droplet: - immediately inhaled, large drops of mucus, travel <1 meter away from source. Airborne: - microbes remain suspended in the air for hours, - can float freely >1 meteraway from source, - very similar to droplet but require different infectioncontrol precautions |
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What are vehicles, fomites and vectors? |
Methods of microbial disease transmission through contact. vehicle; food/water fomite; inanimate object Vector; animal/insect |
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How can transmission be controlled? |
1. Controlthe Reservoir/ Source (whether it’s an animal, human, orenvironment) 2. Controlthe Amount ofNew Hosts (Limit Susceptible Population):improve living conditions & general health/ nutrition to strengthen immunesystem, publicly educate, etc. 3. Control Transmission:**FOCUSon this step** use appropriate methods for different types of transmission. Eg:For Indirect, provide clean water, prevent food contamination. For Airborne,use a negative pressure room. For Droplet, use barrier precautions (PPE). |
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What is a disease control network? |
“DiseaseControl Network” - (to which all of you belong) - A network of individuals andorganizations who identify, track, and control infectious diseases. - Eg: publichealth organizations, health care workers, epidemiologists, diagnostic labs,etc. |
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What are nosocomial infections? |
healthcare-associated infections: infections that occur during a stay in the hospital, akaNosocomial, hospital- aquired. |
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What are factors that put patients at risk? |
Factors that put patients at risk: - the state of patient(immunocompromised) - type of medical procedure(anything that passes thenormal flora), - the type of microbe that patient is exposed to(opportunisticpathogen), - patient’s environment(overcrowding, housekeeping, sanitation,etc.) |
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Factors that put health care workers at risk. |
Factors that put us (HCP) at risk: - Acquiring an infectionfrom our patient (via droplet, airbourne, contact,etc.), - infection acquiredafter an accidental exposure (‘sharps’ injury) |
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What are routine practices? What are additional precautions? |
Routine: 1- assess the risk before an encounter. 2-Use PPE asrequired and hand hygiene. 3-Educate and demonstrate proper techniques of PPE andhygiene, promote immunization. Additional: When routine practicesare not enough, based on the assessed risk. |
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What is the most important elements in infection control? |
Hand hygiene. hand hygiene is one of the most important elements ininfection control, both in the workplace and at home, and when hand hygiene mustbe done in a healthcare setting. - Before initialpatient encounter, before aseptic procedure, after body fluid exposure, afterpatient encounter. |
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Define: Pathologenicity, virulence and virulence factor. |
Pathogenicity- the ability of a microbe to cause disease Virulence – the degree of pathogenicity, as indicated by mortality rates Virulence factor- any microbial component that is required for/ contributes topathogenicity |
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Define localized, system and subclinical infections. |
Localized (microbe restriced tocertain site in body) systemic(microbe has spread to several areas in the body) subclinical (infection with very few obvioussymptoms) |
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What are the 5 steps that bacteria must undergo in order to cause disease? What are the associated virulence factors? |
1. Transmission/Entry intoHost - determined by mechanism of transmission, most pathogens have a‘preferred’ portal of entry 2. Avoid Being removed afterEntry - use pili for attachment (others include bacterial cell surfaceproteins and capsular polysaccharide) 3. Migrate to a Site Suitablefor Growth; - **only optional step. - “Invasion” of surface tissues and moving within the host
4. Overcome host defences andMultiply at Preferred Site bacteria need to be able to: - obtain nutrients from the host (via hemolysins), - evade host’s immune systemdefenses (via bacterial capsule and toxins)
5. Exit host and Transfer to aNew Host - required for long-term survival of pathogen. |
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What is an 'infectious dose?' |
Infectious dose: numberof organisms needed to start an infection *depends on point of entry |
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What is the difference between exotoxin and endotoxin? |
Endotoxins - “lipid A” portion in lipopolysaccharide (LPS), only present in gramnegative bacteria. - part of the outer portion of the cell wall of gram-negative bacteria. they are liberated when the bacteria die and the cell wall breaks apart. - Causes fever+shock= TOXIC SHOCK Exotoxins - toxic proteins secreted by bacteria, - may be by both gram negative and positive bacteria. - exotoxins are produced inside mostly gram-positive bacteria as part of their growth and metabolism. - they are then released into the surrounding medium - HIGHLYPOTENT in SMALL amounts. - Are soluble and can be carried by the bloodstream toact at a different site than infected site. |
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What are the pros and cons for the lab diagnosis using gram stains and miscroscopy? |
Pros: - fast and easy - good for specimins that should be sterile in healthy people. Cons: - not very sensitive. not very useful if normal flora present - only tells that bacteria are present. doesn't ID them. |
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What are the pros and cons for the lab diagnosis using non-growth tests, such as ELISA and nucleic acid based tests? |
Pros: - fast, very sensitive. cons: - require that you know exactly what to look for (does not screen) - complex and expensive |
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What are the pros and cons for the lab diagnosis using growth tests. (most often used) |
Pros: - good 'screening' test cons: - slow (24-72hrs) - contamination with normal flora can cause difficulties. |
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What are some skin infections? |
Caused by staphilococcus: Folliculities; small red bumps on the skin (minor) furnuncles; boils. Infection spreads to the adjacent tissue (pus, pain, swelling, redness) carbuncles; furuncles merge and give multiple sites of draining pus. scalded skin syndrome; caused by 'exfolliation' toxins in some strains of S aureus. Redness and soft blisters all over the body. Common < 2yrs |
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True or false: Folliculities are boils. |
False; Folliculities; small red bumps on the skin (minor) furnuncles; boils. Infection spreads to the adjacent tissue (pus, pain, swelling, redness) |
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How do these skin infections start, what is the reservoir, and how are the prevented/treated? |
Reservoir- skin and nasal passages of humans. Transmission- directcontact, fomites, droplets* can survive for weeks on surface. Prevention-careful hand washing, antiseptic washes, extra care around patients within-dwelling devices. Treatment- antibiotics, surgical drainage. |
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True or false
CA-MRSA and HA-MRSA are big public health concerns (community and hospital acquired MRSA) |
True |
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What are gastrointestinal infections caused by? |
Gastrointestinal infections- caused by “enteric” bacteria(bacteria that causes GI disease afterusing food or water as entry into the gut) |
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What is the differencebetween food poisoning and food infections? |
Food Poisoning: need tointake the exotoxin growing in the food, not necessarily the food. - Symptoms occur in 4-6hrs because toxins are alreadyin the food. - Consumption of live bacteria is not required. Food Infections: bacteriaenter gut, multiply in gut, and release exotoxins there. - Therefore, takes 18-24hrs for symptoms to occur. Consumption of live bacteria required. |
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What types ofhousehold practices are implicated as factors in food-borne diseases? |
inadequate refrigeration,food sits for too long, inadequate reheating, inadequate cooking, infected foodhandlers, raw foods and ingredients… many examples. Staph Aureus as anexample of a food poisoning: anything high in salt and sugar favours the growthof Staph. Also, Ham/Pork/Beef count for 40% of cases. |
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Discuss Staphlococus Aureus |
Staph Aureus - an exampleof a food poisoning: anything high in salt and sugar favors the growth ofStaph. - Also, Ham/Pork/Beef count for 40% of cases.- How does it get intofoods? - If contaminated food isleft at room temperature, Staph grows and releases exotoxins. - **Ifrefrigerated, bacteria can’t grow and will not release toxins. And what happens when youconsume the toxin? - Has no taste or odor, - Symptoms happen within 4 hrs because toxin is pre-formed. - Recovery occurswithout treatment- gut just needs to be cleared. |
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Discuss E. Coli 0157 |
E. coli O157 as an example of a food infection - reservoir; Intestinal tract of cattle. what does the toxin do? - Secretes exotoxins (while growing) that kill epithelial gut cellsand damages lining of intestinal tract. Treatment: Fluid Replacement to avoid dehydration, Anti-Diarrhea andantibiotics are NOT recommended. possible complication(eg. HUS) and how does this arise? More at risk for HUS if using antibiotic astreatmentà arises ifverotoxin enters the blood, causing the lysis of RBC and possible kidneydamage. **potentially fatal** |
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Discuss Genitourinary Tract infections. |
Genitourinary tractinfections: - very sensitive microbes that require directcontact transmission Ex: Neisseria gonorrhoeae (“flow of seed”)- - - Direct Transmission What happens when it getsinto the GU tract: - invades epithelial cellsand enters into sub- epithelial tissues. - Releases endotoxin (LPS). - Tissuedamage allows release of free bacteria into genital secretions. - Leads to moretransmission. What symptoms seen in males vs. females: FEMALE - mild vaginal inflammation,dysuria, - often asymptomatic (potentialto become carriers). MALE= urethral canal inflammation, dysuria, discharge ofpus, more easily recognized and treated What are possiblecomplications? - usually occur if left untreated. MALE= urethral scarring,infertility. FEMALE= bacteria ascend into uterus and fallopian tubes(inflammation, fever, abdominal pain, scarring of fallopian tubes- infertility) How is it diagnosed? Molecular PCR test on urine specimens (NOT a swab) |
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Discuss Streptococcus pyogenes. |
Streptococcus pyogenes - (an upper resp. infection) Reservoir; HUMANS. Transmission; Respiratory Droplet How does it cause diseaseonce it gets into your throat? - it enters throat andattaches to epithelial cells. - In the throat, it multiplies, evades hostdefences, secretes hemolysin and exotoxins. Complications: - scarlet fever, glomerulonephritis, rheumatic fever. - not all strains of S pyogenes can cause complications. - Necrotizing fasciitis is also a complication, but only when S. Pyogenes (strep) gets into cuts. Not a respiratory-spread disease. Diagnostic procedure: throat swab; blood agar media; look for hemolytic colonies. |
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Bacterial pneumonias. |
bacterial pneumonias (alower resp infection) - What are some commonfeatures found in all bacterial pneumonias (specific names of the bacterial speciescausing pneumonia is not important) o usually associated withpre- disposing risk factorso Bacterial Capsules areimportant virulence factors (block phagocytosis)o Bacteria trigger the immunereaction (inflammation, air-spaces filled with fluid & phagocytes)o Some are preventable withvaccination (only given to some populations) ider%IT |
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Scarlet fever: |
o Scarlet Fever: (strep symptoms and skinrash) if left untreated, certain strains of Strep produce “ErythrogenicExotoxin”à which damages small blood vessels and causes inflammation. It is very rare. |
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Glomerulonephritis |
Glomerulonephritis: Strepantigens and anti- Strep antibodies accumulate in the blood vessels of thekidneysà causes fever, blood in urine, increase BP. Occurs during recoverystage of untreated Strep. |
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Rheumatic Fever |
Rheumatic Fever: Autoimmunedisease, antibodies cross- react with antigens found in heart and joint tissuesà causes fever, inflammation of joints and heart valves. Scarringof heart tissue can also lead to HF. Occurs 3-4 weeks after self- limited Strepinfection. Rare |
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Mycobacterium Tuberculosis |
Mycobacterium Tuberculosis “acid-fast”, slow-growing microbe, with humans as the only known reservoir Cancause disease even though it does not have typical virulence factors seen in otherbacteria (eg. toxins, pili, etc.). - therefore, all symptomsare due to hosts’ immune system response two forms of tuberculosis: 1. Primary TB: a first time infection 2. Secondary TB: mainly a delayedhypersensitivity reaction following reactivation of the bacteria) - “tubercle” - walled off lesions or stimulated macrophages that enclose M.tband prevent further spread (they remain alive, but cannot grow further).- Diagnosis: - Acid- fast stain of sputum - Lab culture of M.tb fromsputumà takes 2-4 weeks for growth. SLOW. - Skin test (Mantoux test): non- infectious protein extract is injected under skin. Redding=positive skin test. BUT may be due to a current TB infection, a previous TBinfection, prior exposure OR prior vaccination. (follow up test recommended)- Treatment: - through anti- mycobacterial drugs used in combination. - ** Isoniazid+ Rifampin.- - “directly observed therapy” DOTS- Directly Observed Therapy, Shortcourse- where you watch thepatient take the pill. |
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Describe the differencebetween generalized vs. localized signs and symptoms that indicate that someone has amicrobial infection. |
Generalized Signs: fever, chills,nausea, shock, low BP, aches/pains, neuro abnormalities Localized Signs: Resp. distress,inflammation, GI disease, skin lesions, draining sinuses, pulmonaryinfiltrates, abnormal WBC counts |
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List the two main functionsof the clinical laboratory |
1. To provide information as to the presence or absence of microbesin a patient specimen - Is there a microbepresent? If so, what is it? 2. To provide information asto the susceptibility of the microbe to antimicrobial agents - Helps guide proper therapy: how will we get rid of the presentmicrobe? |
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What are the 3 rights of specimen collection? |
specimen collection is oneof the most critical aspects of laboratory diagnosis: needs to be TheRight Specimen, collected at the Right Time (before treatment), and collectedthe Right Way.- |
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List some of the mainreasons why specimens are rejected by the clinical lab. |
Unlabeled or improperlylabeled Collected with the wrongswab, container, materials, etc. Leaked while beingtransported Inadequate Volume Single specimen submittedfor multiple tests Delayed in transit to lab/improperly stored |
