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207 Cards in this Set
- Front
- Back
define normal flora and state its purpose
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bacteria that is expected to colonize the body, helps protect from colonization by pathogens, can supplement host nutrition and provides immune stimulation
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define pathogenic bacteria
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technically limited to those virulent organisms where common exposure results in disease (Shigella, B. anthracis)
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define opportunistic pathogen
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an organism that does not normally cause disease (pseudomonas) causes a disease because the host has a pre-existing condition
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define and give an example of acute disease
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rapid onset, usually rapid resolution, e.g. cholera
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define and give an example of chronic disease
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slow onset, slow resolution e.g. tuberculosis
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define and given an example of a recurrent disease
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usually acute bouts without long lasting immunity, e.g. gonorrhea, E. coli UTI
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define and given an example of a pyogenic disease
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fever and large degree of white cell infiltrates (pus), e.g. Staph and Strep wound infections
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define and give an example of an immune mediated disease
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antibody or cellular responses to organism cause tissue damage e.g. rheumatic fever
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List 7 methods by which an organism can enter a host
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ingestion
inhalation trauma needles arthropod bites sexual transmission eyes Remeber: There Are Some Ewey Nasty Infection Incidents |
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How would organisms like Salmonella, Shigella, Vibrio cholerae, Listeria, and B. anthrasis gain entry into the host
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ingestion via contaminated food or water
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How would organisms like M. tuberculosis, Legionella pneumophila, Bordetella, B> anthracis, and Y. pestis gain entery into the host?
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inhalation
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Give some examples of species that can gain entry into the host via trauma
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Clostridia sp, B. anthrasis, Strep, Staph
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What pathogens commonly gain entry into the host via needlesticks
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Staph, Pseudomonas
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What pathogens are often transmited by arthropod bites
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Rickettsia, Yersinia pestis, Borrelia spp.
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List some pathogens that can be transmitted sexually
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Chlamydia trachomatis, Treponema pallidum, Neisseria gonorrhoeae, Shigella spp.
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List some pathogens that can gain entry into the host via the eyes
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Chalmydia trachomatis, N. gonorrhoeae, B. cereus, Pseudomonas spp.
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list the Molecular Koch's postulates
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1. the phenotype under investigation shoudl be associated with pathogenic members of a genus
2. specific mutagenesis of the gene(s) associated with virulence should lead to a significant decrease in virulence 3. complementation of the mutation should restore pathogenicity |
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What types of mutations are best for proving the molecular koch's postulates
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inframe deletions or point mutations
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How might a gene be complemented to restore pathogenicity when trying to prove the molecular koch's postulates
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on a plasmid or allelic replacement
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What adherence structures can serve as virulence/ disease mechanisms
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1. Pili/fimbraie
2. Non fimbrial surface proteins 3. Capsule 4. Lipoteichoic acids 5. flagella Sticky Pathogens Can Love Forever |
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Describe how a bacteria would normally be destroyed by a macrophage
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-bacteria becomes bound to cell surface
-induction of cellular events that leads to engulfment and formation of a phagosome -acidification of the phagosome and fusion with the lysosome -acid, destructive enzymes, and oxygen radicals destroy the bacteria |
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What are the four methods that bacteria can use to invade a cell and avoid being killed
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1. Cellular invasion with replication in the cytoplasm
2. invasion with replication in the late endosome 3. Invasion with replication in the phagosome 4. Special parasite vesicle |
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Cellular invasion with replication in the cytoplasm in a mechanism for cell invasion.Given an example of bacteria that do this
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Rickettsiae, Shigella, Listeria
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Invasion with replication in the late endosome is mechanism for cell invasion. Given an example of bacteria that do this
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Salmonella
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Invasion with replication in the phagolysosome is a mechanism for cellular invasion. Give an example of bacteria that do this
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Coxiella, Mycobacteria
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The use of a special parasite vesicle is an example of a cellular invasion mechaism. Give an example of bacteria that do this
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Chlamydia spp. use inclusion bodies
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Some intracellular bacteria like Shigella and Listeria spread from cell to cell in the host without an extracellular state. Explain how this occurs
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1. The cells enter the host and lyse the phagosome and then replicate in the cytoplasm
2. The cells organize polymerization of actin filaments and propel themselves into neighboring cells 3. They enter the new cells encased in a dobule membrane which they lyse for new rounds of replication |
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Describe the general structure of a bacterial exotoxin (AB subunit model)
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usually function as two discrete protein subunits or domains within a single protein, one subunit controls the ability to bind to the host cell receptors (B=bind) and the other carries out the toxic activity (A=activity).
There are also discrete elements of the protein necessary for secretion from the cell and for translocation across the plasma or endosomal membrane |
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Describe the 3 ways cytolytic toxins can act and give an example of each
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1. creation of a membrane pore e.g. alpha toxin of S. aureus
2. Enzymatic destruction of phospholipid bilayer e.g. sphingomyelinase of S. aureus, Beta toxin 3. Surfactant e.g. Delta toxin of S>. aureus |
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T/F hemolytic toxins evovled specifically to lyse RBCs
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false, they most likely evovled to lyse phagocytes
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describe type 3 secretion systems
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-directly delivers bacterial proteins into the host cell cytoplasm by injection
-proteins can affect cytossketal structure and second messenger pathways -example EHEC and petesal formation/ tight adhesion sites |
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List some examples of mechanisms to evade the host immune response
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capusles, antigenic variation, anti-immunoglobulin proteases, disruption of complement cascase, inhibition of opsonization, inhibition of phagocyte chemotaxsis, destruction of phagocytes by leucotoxins, intracellular replicaiton
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Discribe how disease is thought to occur in the three way interaction model
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When the pathogen enters the host, the homeostasis of the location is interupted and inflmation occurs. If the pathogen survives inflammation better than the normal microbiota, disease occurs
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Which cytokines are primarily responsible for the acute phase responses
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IL-6, TNF-a
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What are the three lines of defense against invasion by bacteria pathogens
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1. natural barriers like skin, mucous, cilliated epithelium, gastric acid, bile, normal flora
2. innate, pattern recognition and antigen non specific responses (fever, complement, iron binding proteins, antimicrobial peptides, phagocytes) 3. Memory responses based on antigen specificity (antibodies, T cells) |
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What defese mechanism is employed early in infection when bacterial attachement occurs
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innate defence mechanisms like antibodies to adhesins
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What defense mechanism is employed early infection when local proliferation occurs
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phagocytes, complement lysis, blocking of metabolite transport
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What defense mechanism is employed later in infection if invasion occurs
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antibody to aggressins, antibody to organism, complement lysis, phagocytes
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what defense mechaism is employed later in infection if a toxin is produce
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antibody to the toxin
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what defense mechaism is employed later in infection if intracelluar growth occurs
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cell mediated immunity
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What are the immune barrier defenses associated with the eyes
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washing of tears and lysozyme (catalyzes hydrolysis of bacterial peptidoglycan)
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What are the immune barrier defenses of the skin
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anatomic barrier, antimicrobial secretions
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What are the immune barrier functions of the digestive tract
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stomach acidity, normal flora, bile
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What are the immune barrier functions of the genitourinary tract
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washing of urine, lysozyme, vaginal lactic acid
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What are the immune barrier functions to the respiratory tract
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mucus, ciliated epithelium, alveolar macrophages
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lysozyme is a nonspecific humoral defense mechanism. What is its function and source
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function- catalyses the hydrolysis of bacterial peptidoglycan
source-tears, saliva, nasal secretions, body fluids, lysosomal granulas |
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lactoferrin and transferrin are nonspecific humoral defense mechanisms. What is their function and source
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function-bind iron and compete with MOs for it
source- specific granules of PMNs |
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lactoperoxidase is a nonspecific humoral defense mechanism
what is its source and function |
function- may be inhibitory to many microorganisms
source-milk and saliva |
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Beta lysin is a nonspecific humoral defense mechanism, what is its function and sourcce
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function- effective against gram positive bacteria
source- thrombocytes, normal serum |
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chemotactic factors are a nonspecific humoral defense mechanism, what is their function and sourcce
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function- induce directed migration of PMNs, monocytes, and other cells
source-bacterial substances, products of cell injury, denatured proteins, complement, chemokines |
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properdin is a nonspecific humoral defense mechanism, what is its function and sourcce
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function- activates complement in the absence of antibody-antigen complex
source-normal plasma |
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cationic peptides (defensins, etc) are a nonspecific humoral defense mechanism, what is their function and sourcce
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function-disrupt membranes, block cell transport activities
source- polymorphonuclear granules |
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what cell gives rise to all blood cells
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pluripotent stem cell
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what % of circulating leukocytes are neutrophils
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60%
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what % of circulating leukocytes are B lymphocytes and T cells
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33%
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What are PAMPs
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Pathogen Associated Molecular Patter, a bacterial product like flagella or LPS that trigger immune responses
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What type of receptors recognize PAMPs
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toll like receptors (TLRs)
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When circulating naive Th cells recognize their cognate antigen, they differentiate into one of several effector lineages. What are these lineages?
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TH1, TH2, TH17
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What cytokines do TH1 cells produce? What innate immune effector mechanism does this trigger? What type of pathogen does this combat?
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TH1 cells produce IFN-gamma which stimulates macrophages to fight off intracellular pathogens
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What innate immune effector mechanism do TH2 cells trigger? What type of pathogen does this combat?
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TH2 help activate mast cells, basophils, and eosinophils, this helps combat hemolinth infections (parasites)
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What cytokines do TH17 cells produce? What innate immune effector mechanism does this trigger? What type of pathogen does this combat?
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TH17 cells produce IL-17 whihc helps recruit neutrophils to conbat extracellular bacteria and fungi
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What cytokines are important for fighting intracellular bacteria? Extracellular?
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intracellular-IFN-G (TH1 cells)
extracelllular- IL-17 (TH17 cells) |
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Which cytokine, produce by TH1, TH2, and TH17 cells is important for B cell proliferaiton and antibody production
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IL-4
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What cytokines are important in the acute phase response to bacteria?
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IL-1, IL-6, TNF
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Describe the immune response in terms of specificity, innateness, memory and cell type at 0-4. 4-96, and after 96 hours
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0-4 hours, nonspecific, innate, no memory, no specific T cells
4-96 hours- nonspecific and specific, inducible, no memory, no specific T cells post 96 hrs- specific, inducible, memory, specific T cells |
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Describe the barrier funtions of the immune system at 0-4hrs, 4-96 hrs, and post 96hrs
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0-4: skin, epithelia
4-96: local inflammation (C5a) and local TNF post 96:IgA antibody in luminal spaces, IgE antibody on most cells |
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Describe the immune response to extracellular pathogens at 0-4hrs, 4-96 hrs, and post 96hrs
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early- phagocytes, alternative complement pathway
middle-mannose binding protein, C reactive protien, T cell independent B B cell antibody plus complement late-IgG antibody and Fc receptor bearing cells, IgG, IgM antibody +, classical complement pathway |
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Describe the immune response to intracellular bacteria at 0-4hrs, 4-96 hrs, and post 96hrs
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early- macrophages
middle-T cell independent macrophage activation, IL-1, IL-6, TNF-a late- T cell activation of macrophages by IFN-G |
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Describe the immune response to virus infected cells 0-4hrs, 4-96 hrs, and post 96hrs
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early-natural killer cells
middle-interferon alpha, Beta, inferon activated NK cells late- cytotoxic T cells |
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What is the purpose of acute inflammmation and how is this achieved?
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purpose-contain infection, prevent, signal subsequent immune response.
Achieved by -capillary expansion to increase blood flow -increased permeability of microvasculature to allow escape of leukocytes -exit of leukocytes from capllaries |
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What are the symptoms of acute inflammation? What causes these symptoms
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rash/warmth- capillary expansion leads to increased blood flow
edema- increased permeabilty of microvasculature allows escapte of fluid, plasma proteins, and leukocytes pus- exit of leukocytes from capillaries to infection site |
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Where are actue phase proteins produced? What are they produced in response to? Where do these "triggers" come from?
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Actue phase proteins are produced by liver cells in response to IL-1, IL-6, and TNF, these cytokines are released by macrophages/ dendritic cells in reponse to PAMP ligands
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What are the acute phase proteins
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C-reactive protien (CRP), mannose binding protein ,(MBP) and fibrinogen
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WHat is the structure of CRP? WHat does it bind to? How does it contribute to the acute phase immune response
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stucture-pentameric disk
binds- phosphorylcholine on bacterial but not host membranes contribution-opsonizaiton and triggers classical complement pathway |
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What is the strucutre of MBP
WHat does it bind to? How does it contribute to the acute phase immune response |
structure- resemebles complement C1q
binds- mannose residues on bacterial cell surfaces common to forms of LPS and capsules contribution-opsonizatin, activates classical pathway (MBP binds MASP which then activates C4) |
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list the bacterial components that can directly activate protective responses
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LPS, lipoteichoic acid, lipoarabinomannan, glycolipids and glycopeptides, polyanions, N-formyl peptides
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list the bacterial components that are chemotactic
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peptidoglycan fragments,cell surface activation of alternative pathways of complemetn (C3a, C5a)
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What are the three pathways of complement activation? What triggers them?
Which pathway can begin before the immune response? |
classical-antibody antigen complex either IgG or IgM or CRP or MBP
lectin- mannose binding protein (MBSP replaces the C1 in the classical pathway then C4 to C2 the same way) alternative-directly on pathogen surface, can begin before the immune response because it doesn't require early complement components (C1, C2, C4 etc) |
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What are the three main consequences of complement activation
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1. opsonization of pathogens
2. recruitment of inflammatory cells via cytokines 3. direct killing of pathogens |
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Where do the three ways of activating complement converge?
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THey all result in the activation of C3 convertase
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What is the central step of the complement cascase, which can be reach by either the classical ,lectin, or alternate pathway? What is the result of this step?
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central step-activation of C3 convertase to cleave C3 to C3a and C3b
Cleavage of C3 and subsequently C5 (triggerd by C3b) genearates anaphylatoxins (C3a and C5a) and MAC (C5-9) |
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which two complement activation pathways are triggered by bacterial surfaces
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alternative and lectin
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Which complment activation pathway is triggered by antibody-antigen complexes
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classical
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Which proteins of the complment cascade are anaphylotoxic
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C3a, C5a
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which complement protein is responsible for opsonization
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C3b
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which bacteria are killed by the terminal complement lytic structure
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gram negative
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Who discovered phagocytosis
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Elie Metchnikoff
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Describe the process by which neutrophils migrate from the bloodstream to the site of bacterial elicited inflammation
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1. endothelial cells respond to IL-1 and TNF-a which results in upregulation of selectins leading to neutrophil tethering and rolling adhesion
2.ICAM is induced on the endothelial sufrace which is the receptor for neutrophil LFA1, this results in firm adhesion 3. Neutrophil flattens and pseudopods reach between endothelial cells. The cytoskeleton rearragnes and the cells squeezes into the interstitial space 4. A gradient of chemotactic substances results in migraiton to the site of injury |
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What cytokines are important for the expression of selections which are necessary to faciliate neutrophil tethering and rolling adhesion
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IL-1 and TNF-a
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Which receptor-ligand system is essential for neutrophil firm adhesion
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endothelial cell ICAM and neutrophil LFA1
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What proteins can serve as opsonins
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mannose binding protein, IgG, C3b
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list the oxygen dependent antibacterial compounds found within the phagolysosome
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hydorgen peroxide (NADPH oxidase, and NADH oxidase)
superoxide hydroxyl radicals activated halides nitrous oxide |
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list the oxygen independent compounds of the phagolysosome
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acids, lysozyme, lactoferrin, defensins and other cationic protiens, proteases, elastase, cathepsin G
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What does TLR1 recognize and where is it located
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lipoprotein, located on plasma membrane
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What does TLR2 recognize, and where is it located
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petidoglycan, zymosan, LAM (bacteria, fungi), located on plasma membrane
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What does TLR 6 recognize
Where is it located |
mycoplasma lipoprotein, located on plasma membrane
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What does TLR 4 recognize, Where is it located
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enterobacterial LPS, located on plasma membrane
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What does TLR5 recognize, Where is it located
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flagella, located on plasma membrane
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What does TLR 3 recognize? Where is it located?
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recognizes dsRNA ( viruses) , located on the endosomal membrane
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What do TLR7 and TLR 8 recognize, where are they located
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recognize ssRNA (viruses) located on endosomal membrane
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What cytokine facilitates the anti-inflammatory function of macrophages
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IL-10
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Immune memory is an accessory function of macropahges. What are the two ways this is acheive and what cytokine is invovled in 1 of the pathways?
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1. antigen processing and presentation
2. T lymphocyte activation via IL-12 |
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What are the two pathogen recognition and inflammatory functions of macrophages? What cytokines are involved?
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1. cehmokines
2. inflamation w/ IL1, IL6, TNFa |
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What are the 4 effector functions of macrophages?
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1. nitric oxide
2. oxidative burst 3.antimicrobial peptides 4. opsonization via C3b and IgG Fc receptors then phagocytosis "NAPO" the microbes (nitric, oxidative, antimicrocial, phagocytosis |
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What are the four main categories of macrophage functions?
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1. anti-inflammatory
2. accessory 3. pathogen recognistion and inflamation 4. effector functions |
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What 4 important inflammatory cytokines are produces by macrophages
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IL1, IL6, IL 12,TNFa
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Which immunoglobulin is produced first after a primary antigen challenge
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IgM
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How does the secondary response to a second antigen challenge differe from the primary response to a primary antigen challenge
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The secondary response consists mainly of IgG whereas the primary response is IgM first. The secondary response (anamnestic response) reaches a higher titer and lasts longer
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list the 4 postulates of lymphocyte clonal selection
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1. each lymphocyte beras a single type receptor of a unique specificity
2. inteaction between a foreign molecule and the receptor with high affinity in the proper context triggers activation 3. The activated cell differentiates into clones with the same receptor specificity 4. lymphocytes beraing receptors specific for self receptors are deleted early in lymphoid development |
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What is the structure, site of action and effector functions of IgM antibodies
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structure- classic Y shape with heavy and light chain, bound in pentameric structure with disulfide bonds joining the 5 induvidual antibodies
site of action- intravascular effector functions- complement activation, agglutination, important for responses to polysaccharides on bacterial surfaces |
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What is the structure, site of action and effector functions of IgG antibodies
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structure- Y shpae with heavy and light chains
site- intravascular, intersitial fluid, transplacental function- complement activation, neutralization, opsonization, neonatal immunity |
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What is the structure, site of action and effector functions of IgA antibodies
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structure- Y shape with heavy and light chains, dimeric secretory IgA
site- luminal secretions, breast milk, mucosa function-neutralization at body surfaces, intestinal immunity in neonates |
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What is the structure, site of action and effector functions of IgE antibodies
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structure- Y shape with heavy and light chains
site- subcutaneous, submucosal function-mast cell sensitization, eosinophil acitvation |
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What is the structure, site of action and effector functions of IgD antibodies
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structure-Y shape with heavy and light chain
site- B cell surface function-unknonw, possibly B cell antigen receptor |
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list 3 bacteria surface structures that antibodies can bind to
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1. fimbriae
2. lipoteichoic acid 3. capsule |
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How important (-, +, ++, +++) is complement for fighting extracellular bacteria? Intracellular?
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extracellular +
intracellular - |
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How important (-, +, ++, +++) is interferon for fighting extracellular bacteria? Intracellular?
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it is not important for either (-) interferons are important in defending against viral infections
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How important (-, +, ++, +++) are neutrophils for fighting extracellular bacteria? Intracellular?
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extracellular +++
intracellular - |
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How important (-, +, ++, +++) are macrophages for fighting extracellular bacteria? Intracellular?
|
extracellular ++
intracellular +++ |
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How important (-, +, ++, +++) are CD4 TH1 cells for fighting extracellular bacteria? Intracellular?
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extracellular -
intracellular ++ |
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How important (-, +, ++, +++) are CD cytotoxic T cells for fighting extracellular bacteria? Intracellular?
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extracellular -
intracellular ++ |
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How important (-, +, ++, +++) are antibodies for fighting extracellular bacteria? Intracellular?
|
extracellular ++
intracellular + |
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What are the 5 properties of a good candidate for vaccine development
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1. organism causes significant illness
2.organism exists as only one serotype 3.antibody blocks infection or systemic spread 4. organism does not have oncogenic potential 5. vaccine is heat stable |
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What are the 5 properties of a good vaccine
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1. generates memory response without disease
2. elicits a strong response (adjuvants) 3. the correct response is elicited (systemic vs mucosal route, antibody vs. T cell) 4. resonable cost 5. safe |
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Compare and contrast live and inactivated vaccines in terms of route of administration
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live- natural or injection
inactive- injection |
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Compare and contrast live and inactivated vaccines in terms of dose
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live- low
inactive- high |
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Compare and contrast live and inactivated vaccines in terms of number of doses
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live- single
inactive- multiple |
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Compare and contrast live and inactivated vaccines in terms of need for adjuvant
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live-no
inactive- yes |
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Compare and contrast live and inactivated vaccines in terms of duration of immunity
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live-long term
inactive- short term |
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Compare and contrast live and inactivated vaccines in terms of antibody response
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live- IgG, IgA
inactive- IgG |
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Compare and contrast live and inactivated vaccines in terms of cell medaited immune response
|
live-good
inactive- poor |
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Compare and contrast live and inactivated vaccines in terms of heat lability
|
live- yes
inactive- no |
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Compare and contrast live and inactivated vaccines in terms of interferance and side effects
|
live- occasional interferance and occasional mild side effects
inactive- no interfereance, occasional sore arm |
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Compare and contrast live and inactivated vaccines in terms of reversion to virulence
|
live- rare
inactive- none |
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What type of immune response is generated from the naked DNA vaccine model? How is this done?
|
A cytotoxic T cell response is illicited by injecting naked DNA coated on gold particles into muscle cells. This resulted in production of the encoded proteins and an immune response towards those proteins
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What is the gram stain morphology of Staphylococcus?
|
gram positive cocci
two plane division gives grape like clusters |
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Is Staph motile?
Can it form spores? catalase rxn? oxygen relationship? |
non-motile, non spore forming, catalase positive, facultative anaerobe
|
|
What are the three staph species that are important to humans
|
S. aureus
S. epidermidis S. saprophyticus |
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How is Staph normally grown? How can S. aurues be selected?
|
Can grow Staph species on blood agar plates at 37, colonies form within 24 hrs
S. aureus can be selected for with manitol salts agar which contains 7.5% salt as a selective agent. Fermentation of the mannitol turns the media yellow (differential and selective media) |
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What are the two important diagnostic enzymes for Staphylococcus
|
1. coagulase- S. aureus is coag +
2. catalase- all are catalse + , differ from strep wich are calatase negative |
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What are the 4 staphylococcol tissue destryoing enzymes
|
1. hyaluronidase
2. lipase 3. nuclease 4. fibrinolysin (staphylokinase) Staph Never Have Love |
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What is staphylokinase and how does it help Staph avoid the immune response
|
Staphylokinase is a Staph enzyme that activates plasminogen to form plasmin which digests fibrin clots. This disrupts the fibrin meshwork which is used to localize an infection. Staphlyokinase also cleaves C3b and IgG which prevents the bacteria from being opsonized efficicently
|
|
How does fibrinogen protect Staph from the host immune response?
|
It binds C3b and prevents lysis by complement
|
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What are 3 mechanisms used by Stahylococcol species to evade the host immune response
|
1. staphylokinase
2. fibrinogen 3. protein A |
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What are the 5 ways protein A functions as a virulence factor?
|
1. binds to Fc fragment of antibodies
2.Binds to TNFa receptor 3. Binds von Willebrand factor 4. Binds B cell surface IgM variable regions 5. Aids in cell agglutinatino/ biofilm formation "A Fears Very Tiny Bugs" (Aggultination, Fc binding, Von Willebrand, TNF, B Cells) |
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One of the ways that protein A acts as a virulence factor is by binding the Fc portion of antibodies. Explain the net effect of this process
|
-twarts accute immunity by tying up the antibodies in an unproductive way
-prevents opsonization |
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One of the ways that protein A acts as a virulence factor is by binding the TNFa receptor. Explain the net effect of this process
|
binding of the TNFa receptor leads to induction of cytokines and subsequent inflammation
|
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One of the ways that protein A acts as a virulence factor is by binding von Willebrand factor. Explain the net effect of this process
|
von Willebrand factor is a serum glycoprotein that mediates platelet aggregation at sites of endothelial damage. Protein A can bind to this factor which facilitates infection and adhesion at invaded sites like catheters etc
|
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One of the ways that protein A acts as a virulence factor is by binding to vraible regions of B cell surface IgM. Explain the net effect of this process
|
This induces B cell apoptosis and thus poor antibody response
|
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How is protein A used commercially?
|
IT can be coupled to small beads and Ig specific for a target protein can be added. An antigen-antibody- bead complex is formed which can then be centrifuged out of a lysate
|
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What is cogulase's (bound and free) function and how does it benefit S. aureus?
|
converts fibrinogen to fibrin
bound form causes staphylococci to clump, free form reacts with globulin plasma factor to form staphylotrhombin may form a protective layer of fibrin around stahylococcal abscesses |
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How are S. epidermidis and S. saprophyticcus differentiated?
|
novobiocin suceptibilit, S. saprophyticus is resistant
|
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Which portion of LPS is antigenic? Which is toxic?
|
the o antigen is antigenic
lipid A is toxic |
|
Describe the alpha and beta toxins associated with S. aureus? What do they do?
|
alpha- disrupts smooth muscle in blood vessels, oxic to many different cells types, forms pore in host cell emembrane resulting in an influx of ions and cell lysis
beta (sphingomyelinase C)-catalyses hydrolysis of membrane phospholipids (sphignomyelin) together the two toxins are responsible for tissue descrtion and abscess formation |
|
Describe the Staphylococcal toxin Panton-Valentine Leukocidin
Why is the dose significant? How is it aquired by the strain? What is unique about is strain distribution |
-PVL leads to the secretion of two proteins LukS and LukF. These combine on the phagocyte cell membrane and form a pore that leads to leukotoxicity (signifiance in pathogenesis is controversial)
-low dose leads to apoptosis but high dose leads to lysis releasing inflammatory mediators and ROS which cause tissue necrosis -it is encoded by a prophage -PVL is made by 5% of S. auerus strains but nearly all MRSA strains |
|
What are Phenol-soluble modulins (PSMs)
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small (20-25 AA) surfactant peptides produce by MRSA ans some S. epidermidis.
At high conentration they can lyse neutrophils and RBCs at low concentrations their "modulin" activity stimulates neutrophils to produce cytokines and to positivley chemotax towards a loal inflammatory site (example is delta toxin) |
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What two forms of hemolysis can S. aureus display
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beta and non-hemolytic
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Describe the staphylococal exotoxin exfoliatin
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-causes splitting of the epidermnal layers of skin via disruptionof the intracellular junctions, results in desqumation of the epidermis
~%5 of S. aureus -the cause of staphylococcal scalded skin syndrome |
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What Staphylococcal product causs SSSS
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exfoliatin
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Describe the Staphylococcal exotoxin Toxic Shock Syndrome Toxin (TSST)
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-associated with TSS cuausing S. aureus strains
-binds host cells and induces cytokine and inflamatory produces "cytokine storm" IL-1, IL-6, IL-12, TNFa |
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Describe the Staphylococcal enterotoxin. What disease does it cause? How does it act?
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-heat and acid stable
-ingestion of toxin without bacteria is sufficient to cause illness -leads to food poisioning -binding of toxin to host cells leads to release of cytokines and inflammatory products -example of a super antigen |
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What is a super antigen?
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A superantigen acts as a polyclonal T cell activator. In contrast to the normal pathway where an antigen leads to the activation of one specific T cell population, superantigens can activate many different types of T cells beause they facilitate binding of TCR and MHC2 outside of the antigen binding domain
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How does the immune response ellicited by a superantigen differ from that induced by a "normal" antigen
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when a normal antigen is presented to a T cell, recongition leads to cytokine (IL-2) secretion and proliferation of that specific type of T cell. The T cell then ineracts with the B cell resulting in antibody production. When a superantigne activates a T cell the same pathway occurs but in addition, excess IL-2 stimulates the produciton of TNF and other cytokines, eventually leading to shock
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Toxic shock syndrome is caused when a localized staphylococci infection produces TSST-1. What are the symptoms of TSS? What can cause the disease to reoccur? How is the disease caused?
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Sxs- sudden fever, hypotension, diffuse erthematous rash, if untreated can lead to multiple organ failure and death
-disease can reoccur if antibiotics do not clear infection or pt. fails to develop an antibody to TSS-1 -disease associated with use of hyper-absorbant tampons |
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T/F S. aureus associated food poisoning results from ingesting a bacteria
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false, the posoning is the result of ingesting a heat resistant enterotoxin not the bacteria itself
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describe S. aureus associated food poisoning
Cause? Severity? Sxs? Tx and recovery? |
Caused by ingestion of heat stable enterotoxing. Manifests 4-12 hours after ingestion of contaminated food. Sxs include vomiting, diarrhea, abdomnial pain, and nausea. The disease is self limiting and recovery begins post 24 hrs. Rarely seroius except in elderly
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Describe Staphylococcal Scalded Skin Syndrome (SSSS) aka Ritter's disease
age group? cause? Sxs? Tx? |
occurs in small children
abrupt onset of erthema (skin inflammation), large bullae (cutaneous blisters) NO WBCs or bacteria clears 7-10 days, no lasting scarring caused by the exofoliatin toxin note that Bullous impetigo has localized blisters also but these are culture positive |
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What two organisms can cause impetigo
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S. aureus and Group A Strep (S. pyogenes)
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Describe impetigo
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result of Group A strep or Staph aureus infection. Formation of multiple pustules on the skin which often rupture and form crusty lesions
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Describe Folliculitis
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result of S. aureus infection. Pus filled infection of hair follicules. Folliculitis of the eyelash is called a stye
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What organism causes furuncles/boils/ carbuncles. Describe these infections. Are there any serious complications?
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S. auerus. Furuncles/ boids are a progression of folliculitis where larger reddened nodules develop. Carbuncles are groups of furuncels that join togeter and progress deeper into the subcutaneous tissue. This progression canlead to bacterimia.
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S. aureus is a common cause of bacterimia. What are two ways this organism can get introduced into the blood?
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-indwelling catheters
- IV drug use |
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Describe S. aureus associated pneumonia
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life threatening infection. Can result from aspiration of oral secretions or by spread from the blood (hematogenous). Especially probelmatic consequence of viral influenza or cystic fibrosis
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Staph epidermidis is coagulase negative (diff from S. aureus). What are the most common sites of infection by this organism
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-infection of replaced heart valves
-infection of catheters and prosthetic joints |
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What type of infection is commonly associated with Staph Saprohyticus? (coagulase negative)
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Uriniary tract infection (cystitis= bladder, urethritis= urethra)
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What is the significance of small colony varients
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A strain of S. aureus that may live intracellulary. Allow the bacteria to avoid host immune response and resist antibiotics
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What is the purpose of lancefield grouping?
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serological groupping of streptococci based on cell wall carbohydrages (C groups), note that some species do not have C group antigens (like S. pneumoniae)
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What speicies belongs to group A strep and gives a Beta hemolytic reacion?
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Group A- S. pyogenes
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What species belongs to group B strep and gives a Beta and occasionally alpha and non hemolytic reaction
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S. agalactiae
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What lancefield group does S. pneumoniae belong to?
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none, it does not have a C antigen
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What is the viridans strep group? What disease do they cause
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Oral commensal speceis that are alpha hemolytic
usually not pathogenic but can cause endocarditis if they are introduced into the blood stream |
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List the 8 virulence determineants of Group A strep, S. pyogenes
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1. capsule
2. M protein 3. Lipoteichoic Acid 4. F protein 5. Streptolysin O and S 6. C5a peptidase 7. Ig binding protein 8. tissue destroying enzymes |
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What sugar is the group A C antigen?
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rhamnose, N-acetylglucosamine
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List 6 suppurative group A streptococcal diseases
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1. pharyngitis
2. Scarlet fever 3. Streptococcoal toxic shock 4. impetigo "Strep Is Careful Never to Pass" (scarlet, impetigo, cellulitis, necrotizing faciitis, toxic shock, pharyngitis) 5. cellulitis 6. nercrotizing fasciitis |
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T/F Group A strep can be carried in teh throat without disease
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True, 15 to 20% of children and adults are carriers
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List two non suppurative group A streptococcal diseases
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1. rheumatic fever
2. Acute glomerular nephritis |
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Describe rheumatic fever
cause? age group? |
believe to be casused by antibodies to group A strep that cross react with connective tissue leading to local complement activation and destructuion, usually mannefests on hear valves
-usually occurs in children ages 5-15 |
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Describe acutue glomerular nephritis
cause? sxs? |
inflammation of the glomeruli, loss of filtering ability, accumulation of waste in system and loss of protein in the urine
-believe to be caused by an accumulation of antibody-antigen compelxes to group A strep in the glomeruli |
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How is group A strep cultured and presumptivley identified
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-culture on BAP plate
-ID- recongize hemolytic colonies, sensitive to bacitracin |
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How is group B strep culture and presumptivley identified
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-culture on BAP with beta hemolysis
-resistant to bacitracin -hydrolyses hippurate |
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What two diseases are associated with group B strep
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neonatal sepsis and meningitis
postpartum sepsis |
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List 4 diseases that are caused by Streptococcus pneumoniae
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1. pneumonia
2. otitis media and sinusitis 3. meningitis 4. bacteremia |
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T/F S. pneumoniae is a strict human parasite
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true
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How is S. pneumoniae cultured and presumptivley identified
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-readily grown
-forms large goey colonies (capsule) that exhibit alpha hemolysis, -sensitive to optocin -note that serological identification of the capsular type is not a routine laboratory test |
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What type of hemolysis?
Group A strep (S. pyogenes) Group B strep (S. agalactiae) S. pneumoniae |
Group A- beta
Group B- beta S. pneumonaie- alpha |
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What does the S. pneumoniae vaccine consist of and who is it recomended for?
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-consists of the most common types of capusular carbohydrates
-recomended for elderly |
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What is the difference between active and passive immunity?
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active- result of an infection,a person forms their own antibodies
passive- a person is given antibodies from anther source (IV, injection etc) |
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Is MBP an opsonin?
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Yes
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What are the 4 steps of phagocytosis
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1. formation of the phagosome
2. acidification of the phagosome 3. fusion with the lysosome 4. killing |
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What are the antigen presenting cells?
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macrophages, dendritic cells, B cells
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Listeria monocytogenes is motile intracellularly in infected cells and the motility results in the infection of neighboring cells. What host molecule is rearranged and what listerial protein mediates the rearrangement?
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Actin, ActA
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What are the Staphylococcal immune evasion enzymes / binding proteins
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1. stahylokinse- activates plasminogen to form plasmin which digests fibrin clots and allows the infection to spread. Also cleaves C3b and IgG
2. fibrinogen binding protein- binds C3b and IgG 3. Protein A |
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List 2 Staph virulence factors that can bind IgG
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Staphylokinase, Protein A
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List2 Staph virulence factors (enzymes or binding proteins) that interfere with complement
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1. Staphylokinase cleaves C3b
2. Fibrinogen binding protein binds C3 |
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Which streptococcal virulence factors interfere with complement?
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1. M protein degrades C3b
2. C5a peptidase degrades C5a |
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Which steptococcal virulence factors have lytic activity?
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Streptolysin S and O
Streptokinase |
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Which streptococcal virulence factors are antiphagocytic
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1. capusle
2. M protein |