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93 Cards in this Set
- Front
- Back
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What is the difference between the non-specific resistance and specific immunity? |
specific = has to do with the intracellular foreign agents and defense against a particular foreign particle non-specific = first line of defense for foreign particles |
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What are some of the non-specific resistance mechanisms used by different organ systems? |
non-specific = lacks specificity and memory - normal microbiota - physical barriers - chemical mediators - intracellular immunity - phagocytosis - natural killer cells - inflammation |
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What are the characteristics of skin? |
has keratin and nails acting as a first line of defense |
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What are the characteristics of mucous membranes? |
has antimicrobial secretions has cilia |
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What are the antimicrobial secretions of mucous membranes? |
lactoperoxidase - creates a reactive oxygen species which is toxic to microbes lactoferrin - sequesters iron which limits multiplication lysosome - breaks down (hydrolyzes bonds), likely in gram positive bacteria |
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What is the difference between bacteriocins and cationic peptides? |
both have properties able to induce immune functions such as cytokines, chemotaxis, etc. bacteriocins are found on gram+/- bacteria and are lethal to similar species cationic peptides are produced by the host and made by positive cells which alter membrane permeability |
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What is the complement system? |
- ability to defend against bacterial infections by increasing phagocytosis (opsonization) - enhances antibodies and memory - punctures cell membranes causing cell lysis - promotes inflammatory response |
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What is a cytokine? |
a soluble protein or glycoprotein released by cell population and act as signalling molecules |
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What are some of the effects of cytokines? |
proliferation and differentiation activation of chemotaxis regulation of differentiation activation of specific molecules induction of apoptosis |
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What is chemotaxis? |
movements of leukocytes to a damaged area |
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What is inflammation? |
removal of foreign invaders - release of neutrophils - lactoferrin proteins - complement proteins - mast cells releasing histamines |
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What is the interferon response? |
prevents nearby cells from replicating and assembling |
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What are acute phase proteins? |
recognizing foreign material to release cytokines, liver stimulation, acute phase protein production - activates the complement system - enhance opsonization but more so phagocytosis - trap microbes and debris |
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What is phagocytosis? How does it happen? |
phagocytic cells will recognize, ingest and kill extracellular microbes - will fuse with a lysosome - helps destroy foreign invader by acid, lysosomal degradative enzymes and antimicrobial peptides |
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What is autophagy? |
destroy intracellular pathogens or pathogens escaping from phagosomes forms an autophagosome and is destroyed by chemicals as in phagocytosis |
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What is ubiquitin? |
a protein coat which tags the foreign particles for destruction |
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What is the role of natural killer cells? |
-release perforins to create holes in cell membrane - granzymes will induce apoptosis |
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What is opsonin-dependent phagocytosis? |
can be greatly increased by opsonization - complement, acute-phase and antibodies will bind to the surface of foreign cells |
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What is PAMPs? |
pathogen-associated-molecular-patterns |
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What are the four types of lymph organs? |
bone marrow: site of hematopoiesis spleen: filtration of blood lymph node: lymph filtration thymus: T-cell maturation |
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What is an epitopes? |
small 3-D portions of an antigen recognized by a single immune receptor |
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What is an antigen? |
molecules that confer immunogenicity which are recognized as foreign and unique |
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What is the mechanism of clonal selection? |
formation of large diverse lymphocyte pool that can bind to large range of antigenic epitotes - stimulated cells with proliferate and differentiate to produce clone cells which later form effector and memory cells |
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What is the MAC? |
membrane attack complex which is activated upon complement proteins - make pores on foreign particles - leads to cell lysis |
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What the the names of the different complement proteins? |
lectin alternative classical |
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What is the difference between the effector response and memory response? |
memory response is important for a second exposure to respond in a faster fashion and is long-lived effector: eliminates or renders foreign entity bacteria memory: upon second encounter with same foreign entity in a faster and more intense response |
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What is a antigenic determinant? |
epitote which is something that is recognized by the immune system |
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What is the function of antigen presenting cells in the specific immune system? |
helps present the antigens to cells such as cytotoxic or helper cells present antigens endogenously or exogenously |
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Why should cells not expressing MHC-I be targeted for destruction? |
these cells are unregulated, could be cancerous or infected with viruses but all cells will express MHC-I saying these are self-cells and should be left alone unless bound with an AOC |
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What is the significance of the light and heavy chain? |
regions of the antibodies which will can result or partake in rearrangement to generate diversity by using DNA splicing and hypermutuations |
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What are superantigens? |
bacterial and viral proteins which stimulate a stronger immune than normal by tricking variants of the T-cells into activation stimulates the release of massive quantities of cytokines from T-cells and results in a hyper reaction |
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What contributes to generating genetic diversity? |
- rearrangement of antibody-gene segments - generation of different codons during splicing or gene segments - insertion of nucleotides during splicing - hypermutations - combination of light and heavy chains |
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What is the secondary antibody response? |
B and T cells will mount a heightened memory-based response with a shorter lag time, rapid log phase and binds with a higher affinity |
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What does the secondary antibody response need? |
reserves of memory cells IgM --> IgG heavy chain switch somatic hypermutations of the V regions |
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What are the types of acquired immunity? |
natural or artificial and later active or passive |
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What is microbiota? |
the normal mixture of microbes in the host body |
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What is used to determine the different microbiota in hosts today? |
use of metagenomics: - isolate DNA from samples of specific body regions - amplify DNA fragments using PCR and random primers - sequencing DNA fragments |
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How has our knowledge of microbiota been expanded? |
use of genetic sequencing (cheap, easier, and quicker) |
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Why is it best to use metagenomics? |
not all microbiota are culturable |
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Where is the largest population of microbiota in the body and why? |
large intestine because of elimination due to peristalsis, replaced rapidly due to reproduction and regular food intake, microbes present are anaerobes or facultative anaerobes |
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What are the metabolic benefits of intestinal microbiota? |
- produce neurotransmitters - produce nutrients that can be used - convert nutrients into short chain fatty acids to feed microbes - convert billirubin |
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What are superorganisms/holobionts? |
- emerge when gene-encoded metabolic processes of the symbiont become integrated with those of the host - blend of host and microbial traits where host and microbial cells co-metabolize various substrates |
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What is the normal immune function of microbiota? |
- prevent colonization by pathogens - environmental control - microbial warfare |
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What is the the hygiene hypothesis? |
living in too clean of an environment = - immune system does not mature properly - may not react properly - immune related health problems - may overact |
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What is the difference between probiotics and prebiotics? |
pro: certain living organisms meant to be applied or ingested with providing health benefits pre - certain foods will be ingested to provide optimal conditions for growing beneficial microbiota |
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Why is the significance of C. difficile? |
- an infection occurring in the hospital - host in immunocompromised - host may lack normal microbiota - production of endospores (difficult to kill) |
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What is the difference between an experimental or correlational study? |
experimental: manipulate and independent variable to see if there is an effect on the dependent variable correlational: observe two groups that differ in one variable and see if there is any correlation with another variable |
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What is the difference between in vivo and in vitro? |
vivo: living organism vitro: in a lab on a petri dish |
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What is a cytokine storm? |
release of massive quantities of cytokines from T-cells (can be done by superantigens) |
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How can an infectious disease not be communicable? |
a communicable disease is something that can be passed directly or indirectly through a contract, vehicle or vector not communicable would be unable to be spread in this manner ie. food poisoning |
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How can a carrier spread disease without being ill? |
having a delayed prodromal period, some people can still be carriers during the convalescent stage of illness |
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What are the two forms of direct contact transmission? |
horizontal: person to person through contact or sexual disease vertical: mother to baby |
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What is a fomite? |
inanimate objects which are involved in spreading pathogens |
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What is the difference between external and internal vector transmission? |
external: carried outside on body of vector internal: carried within the vector |
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What are the two kinds of internal vector transmissions? |
haborage: does not undergo changes within vector biologic: pathogen undergoes changes within vector |
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What are the two types of ways to exit a host? |
active: actual movement of pathogen to exit site passive: fecal movement, vomitting, etc |
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What is the chain of infection for the plague? |
rat reservoir --> human + rat feces = human infection --> bloor/airborne deposits --> next human victim |
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What are the important factors in determining risk from infectious disease? |
virulence agent exposure susceptibility dose |
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What is the relationship among factors determining chance and severity of disease once exposure has occured? |
change & severity (a) #pathogens x virulence over host resistance |
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What is the ID50? |
infectious dose 50 which states that 50% of the experimental hosts will become infected |
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What are the virulence factors? |
attachment, colonization and growth invasion resistance to host defenses production of toxins |
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How do pathogens adhere? |
fimbriae, capsules, slime layers, spikes |
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How do pathogens colonize? |
find favourable conditions in the host which allow for suitable environment |
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How does a pathogen invade its host? |
- have ability to spread to adjacent or other tissues - can penetrate through substances - attack extracellular matrix, basement membranes, membranes and intestinal walls - can degrade the attachments between cells |
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What is septicemia? |
having both pathogens and toxins in the blood |
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What is the difference between extracellular and intracellular pathogens? |
extra: multiply outside of cells intra: multiply within ccells |
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What is the difference between a faculative or obligate intracellular pathogen? |
faculative: can live within or outside a host obligate: must live within a host to survive |
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How does a pathogen resist host defenses? |
- hide latent within host cells - fusing host cells to adjacent cells to prevent expose to microbial proteins - mutations to change antigenic sites or alter expression of antigens - interfere with interferon response |
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What is a biofilm? |
a layer on top of bacterial pathogens which makes for cells to become less sensitive to antibiotics and antibodies |
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What is zoonosis? |
the transmission of animal pathogens to humans |
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What is a holobiont? |
host and their microbiota |
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How would cellular mechanisms be impacted by an anti-inflammatory response? |
- prevent prostaglandins - block cytokines, histamines - no recruitment of neutrophils - no lactoferrins = keep iron relevant and prevent proper immune response |
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How do APCs carry out bacterial recognition, digestion and presentation? |
macrophages, dendritic cells and B-cells will attach to antigens later binding to proper MHCs to later promote an immune response |
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What two different proteins carry out opsonization? |
completment system acute phase proteins |
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What are the two types of leukocytes that use perforins? |
natural killer cells cytotoxic T-cells |
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What are the cardinal signs of inflammation? |
redness, swelling, pain, warmth and altered functions |
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How does the innate respond to pathogens invading cells and pathogens invading tissue spaces? |
cells invasion: use phagocytosis, lysis, etc tissue invasion: use of first line of defense (inflammation) |
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Why do some vaccines require boosters? |
provoke a memory response and later a stronger immune response and to protect for future infection |
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Why would proteins be suitable for use as antibodies? |
- many amino acid combinations - primary and secondary structures - can be put together in different ways - varying size |
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How does the immune system combat extracellular vs intracellular infections? |
extra: done through inflammatory response intra: cell-mediated and cytotoxic responses |
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How does the healthy immune system make so many different antibodies specific for many different antigens? |
- rearrangement of antibody gene segments - different codons during splicing - somatic hypermutations |
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What are six examples of how the innate and adaptive immune system work together? |
- complement system - inflammation - macrophages - phagocytosis - lysis - many more... |
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What are the various T-cells? |
T-helper: cytokines which later will direct other immune responses T-cytotoxic: kill infected/transformed cells T-regulatory: suppress immune responding to self |
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Why would a defect in MHC-I protein would affect the immune response? |
all cells should be expressing MHC-I, if not we're un sure which cells are ours and which are not |
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What are the five ways antibodies help destroy pathogens? |
opsonization - adds opsin/substrate to help phagocytosis agglutination - come together and clump neutralization - inactivation and block binding capacity complement fixation - lysis precipitation - formation of a new insoluble product |
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Why would it be beneficial that lymphocytes will require two types of signals for activation? |
creates a regulatory response? ensure a proper immune response will occur |
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What is the difference between NK cells and cytotoxic T-cells? |
NK: lack specificity and memory cytotoxic: will be there to kill host cells expressing MHC-I |
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What is clonal selection? |
a generation of diversity of the lymphocyte pool which can bind to many epitotes to stimulate recognized cells later becoming effector or memory cells |
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Is a pathogen always a pathogen under any circumstance? |
pathogens are what cause disease (pathogenicity) therefore a pathogen is always a pathogen but can be active or inactive based on the viable host or mode of transmission |
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What the factors determining tissue tropism of a pathogen? |
tissue tropism: depending on how the pathogen wants to enter the tissue: - kinds of tissue of an organism affects - route of transmission - adhesion factors - growth requirements - invasiveness - adhesion factors |
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A higher ID50 would mean a higher or lower virulence? |
A higher ID50 would be a lower virulence because it would take MORE to actually infect an organism |
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What are some ways that a pathogen is able to evade the host immune system? |
- hiding (becoming latent) - mutating antigenic sites - lack/prevent the interferon response - resistance to host defenses |
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What would be characteristics of a good reservoir? |
- cannot be killed - can be moved around easily - easily transmitted |
