Term
|
Definition
| bacteria with no cell wall, uses sterols from host in membrane... has very simple genome... uses adhesion proteins to bind to host cell, is not internalized |
|
|
Term
| mycoplasma pneumoniae kills cells by? |
|
Definition
| adheres to host cell and secretes peroxide and superoxide |
|
|
Term
| Mycoplasmal "walking" pneumonia |
|
Definition
| mild, atypical pneumonia and bronchitis... causes mild symptoms |
|
|
Term
| Why can't mycoplasmal pneumonia be treated by B-lactams? |
|
Definition
| no cell wall, can't be treated with anything that works on cell walls |
|
|
Term
| How is mycoplasmal pneumonia spread? |
|
Definition
| respiratory droplets... makes it common in school/college kids |
|
|
Term
| Be able to identify light/heavy chain and variable/constant region |
|
Definition
|
|
Term
| 6 functions of antibodies |
|
Definition
| nuetralization - occlude surface of toxin or pathogen :: Interfere with pili and flagella :: agglutination (makes for easier phagocytosis) :: Opsonization (enhances phagocytosis) :: compliment activation via the classical pathway :: tag for destruction - NK cells bind to Fc part of antibody and kill attached cell |
|
|
Term
|
Definition
| antibody-dependent cullular cytotoxicity :: NK cells seek out antibody-bound cells and kill them |
|
|
Term
| 5 different kinds of antibodies, classified based on Fc part |
|
Definition
|
|
Term
|
Definition
| first response, pentamer (allows for agglutination because it has so many binding sites) |
|
|
Term
|
Definition
| most common in blood, longest lived (21 days), can cross placenta |
|
|
Term
|
Definition
| main secreted in mucus, dimer, in breast milk - 1st line of defense in babies |
|
|
Term
|
Definition
| Dunno... found on memory B cells |
|
|
Term
|
Definition
| involved in allergic response, extension of Fc region allows it to bind to mast cells |
|
|
Term
|
Definition
| all start with IgM, some receive cytokine signals from Th cells which tells them to switch the heavy chain gene to IgG or IgA |
|
|
Term
| how is the class switching system involved in immune memory? |
|
Definition
| first exposure produces IgM, and eventually some IgG.. second exposure produces mostly IgG in larger amount and much more quickly -- this is the basis for vaccinations |
|
|
Term
| How can so few antibody genes result in so many antibody proteins? |
|
Definition
| somatic recombination - antibody genes are put together by combining parts (genetic cut and paste) :: Heavy chain v, D, and J regions and light chain V and J regions plus random imprecise joining |
|
|
Term
|
Definition
| pre-B cells, lymphoid stem cell precursors |
|
|
Term
| Each B cell produces how many types (VDJ combo) of antibody? |
|
Definition
| one -- so we have about a billion B cells |
|
|
Term
| When does somatic recombination happen? |
|
Definition
| before birth -- we are born with all the antibody-producing capacity we will ever have. |
|
|
Term
|
Definition
| B cells produce surface-bound antibodies before birth :: receptors bind antigens from a bacterium :: B cell engulfs antigen via endocytosis and presents it on MHCII :: If there is an activated Th cell nearby whose T cell receptor recognizes the same antigen, the Th cell binds to the B cell MHCII/antigen complex :: the Th cell secretes cytokines which causes the B cell to divide and produce clones of itself, some of which turn into plasma cells and some turn into memory cells |
|
|
Term
|
Definition
| when B cells divide to produce clones of itself (some are plasma cells and some are memory B's) |
|
|
Term
|
Definition
| secrete antibodies (IgM first, the IgG and IgA) |
|
|
Term
| Why do only specific B cells get activated and not just any? |
|
Definition
| because their surface receptors have to recognize the antigen |
|
|
Term
| Why are some B cells never used? |
|
Definition
| because they never run into the antigen that they have surface receptors for |
|
|
Term
| Why do some b cells recognize self? |
|
Definition
| VDJ joining is random - nothing directs it to make only antibodies |
|
|
Term
| Clonal deletion (negative selection) |
|
Definition
| Eliminating B cells that recognize self -- in bone marrow any B cells that bind antigen are made to die because the body assumes the bone marrow is not infected :: in circulation, any B cell that binds to an antigen but does not get activated by a Th cell becomes anergic and eventually dies |
|
|
Term
|
Definition
|
|
Term
| why do t cell receptors only have one antigen binding site, whereas antibodies have two? |
|
Definition
| because t cell receptors only have 1 arm |
|
|
Term
| Th cell surface molecule vs. Tc cell surface molecule. |
|
Definition
|
|
Term
| T_ bind to MHC2 and T_ bind to MHC1 |
|
Definition
|
|
Term
| MHC2 complexes are only on ___ cells, whereas MCH1 are on all cells |
|
Definition
|
|
Term
| Th cells secrete ___, whereas Tc cells secrete ____. |
|
Definition
|
|
Term
| MHC1 presents from ____, whereas MHC2 presents from. What significance is this? |
|
Definition
| cytoplasm (inside cell), exogenous antigens (didn't originally come from within cell) ... MHC1 can also present self antigens because it presents anything that might be in the cytoplasm |
|
|
Term
|
Definition
| 1. TCR binding to MHC2 and antigen, CD4 binding to MHC2 :: 2. Co-stimulatory peptide B7 binding to CD28 |
|
|
Term
|
Definition
| by APC upon binding of PMP to TLR |
|
|
Term
|
Definition
|
|
Term
|
Definition
| 1. TCR binding to MHC1 and antigen, CD8 binding to MHC1 :: 2. CD28 binding to B7 of APC OR cytokine (IL-2) is released from activated Th cells |
|
|
Term
| T cells bind ___ antigens, whereas B cells bind ___ antigens |
|
Definition
|
|
Term
| the 2nd signal in t cell activation ensures that? |
|
Definition
| t cells are only activated by phagocytes that have engulfed pathogens |
|
|
Term
| What happens to T cells that don't receive the 2nd activation signal? |
|
Definition
|
|
Term
|
Definition
| important to prevent random immune responses that can be harmful to the body |
|
|
Term
| naive vs. effector T cells |
|
Definition
| naive - haven't seen any "trouble" yet :: effector - activated, have an effect |
|
|
Term
| Activated Tc cell function |
|
Definition
| Bind to cell wtih correct antigen on its MHC1, release cytotoxins that induce apoptosis in target cell, release cytokines that help stimulate nearby macrophages |
|
|
Term
|
Definition
|
|
Term
| 3 functions of activated (effector) Th cells |
|
Definition
| stimulate proliferation and differentiation of B cells that have engulfed T-dependent antigens, binds to MHC2 of macrophage and secretes cytokines to boost the macrophage response, activates self to proliferate Th cells and clonal selection |
|
|
Term
| B cells can only engulf things bound to __ (#) receptor(s) |
|
Definition
|
|
Term
| Th cells can activate B cells to produce ____. |
|
Definition
|
|
Term
| B cells usually need to be bound to ___ to avoid anergy, the exception to this rule is if they bind ____. |
|
Definition
| T cells, repeating antigens |
|
|
Term
|
Definition
| T-independent antigen conjugated to a protein |
|
|
Term
| How does a conjugate vaccine work? |
|
Definition
| A B cell binds to the T-independent antigen in the vaccine and internalizes the whole conjugate. It digests it and presents the protein on MHC2. A Th cells recognizes the protein and stimulates B cells to make antibodies to the original T-independent antigen. Also creates memory B cells and plasma cells. |
|
|
Term
| Why are conjugate vaccines so much stronger than polysaccharide vaccines? |
|
Definition
| polysaccharide vaccines bind on many B cell receptors, so the B cell cannot engulf the whole thing (it thinks its too big to engulf) -- thus it cannot create any memory B or plasma cells :: conjugate vaccines bind to only 1 BCR, so it can engulf it, present it on MHC2, and make memory and plasma B cells |
|
|
Term
| How to Th cells boost the macrophage response? |
|
Definition
| makes more lysosomes, nitric oxide is added to the oxidative burst, and giant cells and granulomas form -- basically, it enhances the phagocytic response |
|
|
Term
|
Definition
| long lived, can be reactivated by just binding an antigen (no need for CD28/B7 signal) |
|
|
Term
|
Definition
| AKA regulatory T cells - reduce the T cell response once antigen is gone (when infection is gone) |
|
|
Term
| T cell clonal deletion occurs where |
|
Definition
|
|
Term
| __% of T cells are selected against (deleted) |
|
Definition
|
|
Term
|
Definition
| T cells must bind to MHC1 in the thymus to be stimulated to develop, so T cells that fail to recognize MHC could never fuction and are left to die |
|
|
Term
| Negative T cell Selection |
|
Definition
| T cells must NOT bind to an antigen on the MHC in the thymus (because any antigens are self antigens), so if it does, the binding is too tight for them to be released into ciruclation |
|
|
Term
| Why do cancer and virus-infected cells proliferate? |
|
Definition
| they don't have MHC1, so they failt to cancel the kill signal |
|
|
Term
|
Definition
| they bind to Fc part of an antibody whos Fab parts are bound to a bacterium via ADCC, then bind to killer receptor on any other cell (kill signal), release cytotoxins to kill attached cell |
|
|
Term
| Why don't NK cells kill every cell in our body? |
|
Definition
| if MHC1 is also present, the "Kill signal" is canceled |
|
|
Term
| T-independent vs T-dependent antigens |
|
Definition
| T-dependent- B cell receptors need to bind to T cell |
|
|
Term
|
Definition
| produce by your own body in response to normal events |
|
|
Term
|
Definition
| produced by another, or inresponse to unnatural events |
|
|
Term
|
Definition
| you are producing your own Ig (vaccines, for ex.) ... takes time |
|
|
Term
|
Definition
| you are receiving someone else's Ig (antibodies) :: ex: IgG from placenta, IgA from breastfeeding, antiserum (snake antivenoms, etc) |
|
|
Term
| antiserums are ___, ____ immunity |
|
Definition
|
|
Term
|
Definition
| when there are enough people immune to an infection that the infection cannot spread rapidly for lack of hosts ... "enough people" depends on the disease |
|
|
Term
| antiserums, immunglubulin shots are ____-term only |
|
Definition
|
|
Term
| weakened form of the infectious agent that does not produce disease but DOES grow in the body |
|
Definition
|
|
Term
| how are live attenuated vacciens made? |
|
Definition
| passage through artificial host (something that it doesn't normally infect), which will weaken it ... or knock out genes associated with infection in lab |
|
|
Term
| Why are live attenuated vaccines more effective? |
|
Definition
| because the organisms actually grow in the body, it elicits a stronger immune response |
|
|
Term
| oral live attenuated vaccines |
|
Definition
| triggers B cell response in tissues -- results in IgA production ... can also be nasal spray |
|
|
Term
| Injected live attenuated vaccine |
|
Definition
| triggers circulating B cells - produces IgG |
|
|
Term
| How do you know how to give a vaccine (orally or injected)? |
|
Definition
| give the vaccine how the bug would normally be transmitted - if it's inhaled or injested, give it orally/nasally |
|
|
Term
|
Definition
| actual infectious agent is not present - usually elicits a weaker immune response by has no risk to even an immunocompromised patient. |
|
|
Term
| why do inactivated vaccines usually involve a series of shots? |
|
Definition
| because organisms are not actually living in your body, so it elicits a weaker immune response |
|
|
Term
| Inactivated vaccines usually include an adjuvant... why? |
|
Definition
| enhances B7 production by dendritic cells -- boosts immune response |
|
|
Term
|
Definition
|
|
Term
|
Definition
| pathogen inactivated with formalin |
|
|
Term
|
Definition
| vaccine against inactivated toxin, not whole bacterium |
|
|
Term
|
Definition
| isolate a specific PMP on the pathogen and just make the vaccine with these parts |
|
|
Term
|
Definition
|
|
Term
| Protein conjugate vaccines use T-independent or T-dependent antigens? |
|
Definition
|
|
Term
| All vaccines induce humoral immunity, Good (attenuated) vaccines induce ____ immunity |
|
Definition
|
|
Term
| attenuated/inactive vaccines have longer life |
|
Definition
|
|
Term
| two reasons to use inactivated vaccines |
|
Definition
| for immunocompromised patients, and for warm climates |
|
|
Term
| Edible vaccines are basically just ___ vaccines. |
|
Definition
|
|
Term
| how do dna-based vaccines provide immunity without exposure to a disease agent? |
|
Definition
| inject a pathogen's dna into the patient's cells, so you make the pathogen's proteins for a short time... then you can present the bad proteins on MHC and activate an immune response |
|
|
Term
| advantage of edible vaccines |
|
Definition
| you can have them wherever you can grow them ... for example norovirus vaccine in potatoes |
|
|
Term
|
Definition
| detecting antibodies for a pathogen in a patient who previously had none ... going from antibody negative to antibody positive titer |
|
|
Term
|
Definition
| maximum dilution that still gives a positive result for the antibody... so a titer of 1:256 is more concentrated (has more antibodies) than 1:16 |
|
|
Term
| Importance of antibody titer |
|
Definition
| compare convalescent serum to pre-immune serum to see if you have been infected |
|
|
Term
|
Definition
| PIS - serum before infection (average in population) |
|
|
Term
|
Definition
| antibody titer as you recover from disease |
|
|
Term
|
Definition
| produced from a single B cell |
|
|
Term
|
Definition
| produced from whole blood serum, contains IgG to many epitopes |
|
|
Term
|
Definition
| precipitate of an otherwise insoluble antigen due to antibodies cross linking antigens and forming large, insoluble aggregates -- requires an optimized antibody antigen ratio -- like agglutination |
|
|
Term
|
Definition
| Either an antibody or an antigen is loaded into center well in agar plate... load serum from patients in separate wells in circle around center... if the patient's serum reacts iwth the antigen/antibody in the middle, a precipitant forms as a line between the two |
|
|
Term
| Immunoelectrophoresis test |
|
Definition
| mixture of antiens separated by electrophoresis based on charge, a patient's serum is added to a trough in the gel... if the patient's antibodies react with the antigen, a line of precipitate will form |
|
|
Term
| 3 kinds of tests for precipitin |
|
Definition
| agglutination, immunoelectrophoresis, and immunodiffusion |
|
|
Term
|
Definition
| bind known antibodies with fluorescently tagged Fc ends to patient sample that may contain the antigen ... looks for antigen in the patient |
|
|
Term
| Indirect antibody testing |
|
Definition
| look to see if patient is making antibodies against a particular antigen... binds antibodies from the patient to a known antigen on the slide, then bind anti-Fc secondary antibodies (that are usually fluorescently tagged) to primary antibodies |
|
|
Term
| Why do indirect tests take longer to work? |
|
Definition
| because you're looking for an antibody, which takes a while to make. |
|
|
Term
| Why do indirect tests take longer to work? |
|
Definition
| because you're looking for an antibody, which takes a while to make. |
|
|
Term
|
Definition
| enzyme-linked immunosorbant assay... uses microtiter plates.. antibodies or antigens are tagged with enzyme that creates a certain color... change in color = positive |
|
|
Term
| example of an indirect ELISA test? |
|
Definition
|
|
Term
|
Definition
| confirmatory AIDS test if indirect ELISA is positive -- electrotransfer separates antigens |
|
|
Term
| Koch's postulates proved what? |
|
Definition
| how bacteria make you sick |
|
|
Term
| Koch's Postulates (and revisions) |
|
Definition
| The bacterium must be present in every disease case (toxins - bacteria aren't present, and idiopathology), The bacterium must be isolated from the disease case and grown in pure culture (most bacteria can't be grown in pure culture anyway, and diseases are often caused by multiple bacteria), The specific disease must be reproduced from pure culture in a healthy susceptible host inoculated with the bacterium (still do - except now we usually use animal model instead of humans -- problem with AIDS, we don't have a good animal model), The bacterium must be recoverable from the susceptible host. |
|
|
Term
| Derivative of Koch's postulates that we now use |
|
Definition
| Molecular Koch's postulate -- isolates infective GENE from bacteria |
|
|
Term
|
Definition
| organism is in your body and causing disease... more organism = more sick... kill organism = cure |
|
|
Term
|
Definition
| toxin produced by organism causes disease - organism doesn't have to be present at all -- antibiotics have no effect on course of disease |
|
|
Term
| First step in infection is ___ |
|
Definition
| adhesion of the organism to host cells |
|
|
Term
| how do bacteria bind to host cells? |
|
Definition
| pili with special adhesin proteins at the tip (called fimbriae) bind to specific receptors on your cells |
|
|
Term
| Why do our cells have receptors for bacteria? |
|
Definition
| we don't on purpose - the receptors are actually for something else and the bacteria have evolved to be able to use them. (ex: Nicerria Gonorrhea binds to CD46 whihc is usually a cancel kill signal for NK cells |
|
|
Term
| Pathogens must out-compete ___ to colonize successfully. |
|
Definition
|
|
Term
| How do pathogens outcompete native flora to colonize successfully? |
|
Definition
| IgA protease destroys IgA, iron siderophores steal iron from host, secreted effectors enhance binding and uptake via Type 3 SS (get taken up into cells quickly by causing ruffles in host cell membranes) |
|
|
Term
|
Definition
| produced by pathogenic strains and enhance invasion and/or colonization of host by bacterium (make a bacterium more virulent) |
|
|
Term
| Genes for Virulence factors are often passed between bacterial cells as a unit called ____... this is an example of _____. |
|
Definition
| pathogenicity island, horizontal gene transfer |
|
|
Term
| pathogenicity islands as compared to swapping homework |
|
Definition
| swapping one gene at a time would be like swapping one problem at a time, so they swap as pathogenicity islands (PAIs), which is like transferring an entire assignment at once |
|
|
Term
| ____ is well known for swapping virulence factors via PAIs... makes it hard to stop |
|
Definition
|
|
Term
| How bacteria get into body |
|
Definition
| Penetrate skin (often through trauma or insect bite), penetrate mucus membranes gut, urogenital, resp tract(via ruffling of epithelial cells, uptake by M cells, and direct phagocytosis) |
|
|
Term
| Why would you want to get phagocytized if you're a pathogen? |
|
Definition
| macrophages are much stronger once they've been activated by Th cells, so the bacteria can survive if they've been phagocytized BEFORE the macrophage is activated |
|
|
Term
| how do bacteria hide inside cells? |
|
Definition
| via actin rockets -- avoids humoral immunity (antibodies) which is outside the cells ... ex: shigella taken up by M cells, spread to epithelial cells via macrophags, spread within epithelial cells by actin rockets |
|
|
Term
| how do bacteria get the actin rockets? |
|
Definition
|
|
Term
| how do bacteria avoid complement? |
|
Definition
| host cells avoid alternate complement by blocking C3b... bacteria (esp Ng) steal the host C3b regulatory protein |
|
|
Term
| How do self cells avoid complement? |
|
Definition
| we have a C3b regulatory protein, which prevents activating complement |
|
|
Term
| ways to avoid phagocytosis |
|
Definition
| C5a peptidase - prevents PMN recruitment by digesting C5a :: Lysins - lyse phagocyte (leukocidins) :: capsules - special surface proteins such as M protein block PMPs :: Fc receptors (Staph protein A) bind the Fc part of Ig and presents "self" antigen to body |
|
|
Term
| 3 ways bacteria can live in phagocytes |
|
Definition
| break out of phagosome and live in the cytoplasm ... prevent phagosome/lysosome fusion ... live in phagolysosome |
|
|
Term
| How do bacteria avoid antibodies? |
|
Definition
| IgA protease, antigenic variation (Ng pilus "cassette switching"), hyaluronic acid (self antigen) capsule |
|
|
Term
| 5 ways bacteria can hide in the body |
|
Definition
| avoid antibodies, live in phagocytes, avoid phagocytes, avoid complement, and avoid immune system by living in cells |
|
|
Term
| ___ is the only endotoxin, and it's only found in gram pos/neg bacteria |
|
Definition
|
|
Term
| The vaccine for LPS is only against what part? |
|
Definition
|
|
Term
| How does LPS endotoxin lead to septic shock? |
|
Definition
| serum protein LBP (lipid-binding protein) binds LPS from lysed bacterial cells, then binds to lymphocyte surface protein CD14 and TLR4.This induces citokine secretion which increases WBC production and capillary permeability (diapedesis)... systemic infection = septic shock |
|
|
Term
| components of septic shock |
|
Definition
| hypovolemia, organ failure, DIC (disseminated intravascular coagulation), death |
|
|
Term
| how do you make sure IV fluid is LPS-free? |
|
Definition
| Limulus amoebocyte assay (LAL) test -- amoebocytes are motile RBCs in the horseshoe crab... even very small concentrations of LPS causes these to clot |
|
|
Term
| Endotoxin effect on host vs exotoxin effect |
|
Definition
| endotoxin - always same effect, exotoxin - variable. |
|
|
Term
| Endotoxin/exotoxin induces fever |
|
Definition
|
|
Term
| Where are the genes for endotoxin carried? exotoxin? |
|
Definition
| endo - on chromosome, exo- on plasmid or PAI |
|
|
Term
| Where is endo/exotoxin is secreted whereas endo/exotoxin is part of cell membrane |
|
Definition
|
|
Term
| Why is there no vaccine against endotoxin? |
|
Definition
| because the only vaccine is against the o-polysaccharide part of LPS, but the toxic part is Lipid A |
|
|
Term
|
Definition
| B- binding part... binds to receptor, is not toxic itself.. often used as subunit vaccine (cholera) :: A- active (Toxic) part |
|
|
Term
| 3 ways the A part of A-B toxin works |
|
Definition
| mess up cell signaling via signal kinase, alter cAMP concentration by affecting H2O balance in cell, interferes with translation |
|
|
Term
| How are A-B toxins named? |
|
Definition
| AB5 = 1 A part, 5 B parts... A2B = 2 A parts, 1 B part |
|
|
Term
| How does anthrax kill cells? |
|
Definition
| 2 A parts - one is lethal factor - cytotoxin interferes with sensor kinase :: one is edema factor - messes with cAMP to cause edema |
|
|
Term
| The B part of anthrax is called |
|
Definition
|
|
Term
|
Definition
| A-B, cellulolytic, tissue damaging, superantigen |
|
|
Term
| 2 types of cellulolytic toxin |
|
Definition
| hemolysins and phospholipases |
|
|
Term
|
Definition
| B - totally kills blood cells, highly virulent, a - kills some blood cells, those that aren't killed are oxidized and turn kind of greenish, gamma - no hemolysins (basically hemolysin negative) |
|
|
Term
| what kind of hemolysin is naturally occurring in the human throat? |
|
Definition
|
|
Term
| How do phospholipases kill cells? |
|
Definition
| remove phospholipid head group so water can't bind -- basically creates a cell with a water layer and a lipid layer... not a cell at all |
|
|
Term
| 2 types of tissue damaging toxins |
|
Definition
| expoliative and hyaluronidase |
|
|
Term
|
Definition
| sloughs off outer layer of skin -- Stapholococcus scalded skin syndrome (SSSS) |
|
|
Term
|
Definition
| Stapholococcus scalded skin syndrome - not dangerous unless bacteria get in, easily spread, mostly in babies and boys who first start shaving... destroys connection between epidermis and dermis |
|
|
Term
|
Definition
| tissue damaging toxin that destroys connective tissue between cells (hyaluronic acid)... allows bacteria to penetrate deep within tissues - often used for anesthesia |
|
|
Term
| How does superantigen toxin work? |
|
Definition
| Crosslinks TCR to MHC2 without antigen (links T cells nonspecifically), results in massive T cell activation which causes Septic shock (patient usually bleeds to death) |
|
|
Term
| 2 examples of superantigen toxin |
|
Definition
| Toxic shock syndrome toxin and necrotizing fasciitis |
|
|
Term
| How can your immune response kill you via inflammation? |
|
Definition
| phagocytes recruited by inflammation (Type III and Type IV HS) damage tissue ... meningitis and PID (N.g. and chlamydia) |
|
|
Term
| How can your immune response kill you via antibodies? |
|
Definition
| immune complexes stick in glomeruli after infection (acute golmerulonephritis), or immune mimicry |
|
|
Term
| Acute glomerolonephritis is a Type ___ HS |
|
Definition
|
|
Term
|
Definition
| bacterially-induced autoimmune disease - bacteria mimic own antibodies so closely that your body starts attacking them :: ex: rheumatic heart disease (acute rheumatic fever) caused by antibodies to strep M recognizing the autoantigen on heart muscle |
|
|
Term
| 4 ways viruses can avoid inactivation by the immune system |
|
Definition
| produce IFN repressors (stop cell cynthesis of IFN), produce p53 inhibitors (inhibit apoptosis), Produce MHC analog (UL18) which reverses NK-mediated killing of viral infected cells, cause cell fusion into syncytia to avoid exposure to serum antibodies |
|
|
Term
| What is an example of a disease that produces p53 inhibitors to inhibit apoptosis |
|
Definition
| papillomavirus E6 protein |
|
|
Term
| How does cytomegalovirus work? |
|
Definition
| produces MHC analog (UL18) to reverse Nk-mediated killing of viral infected cells |
|
|
Term
| 3 types of fungal infections |
|
Definition
| toxins, dermatophytes produce keratinase, inhaling spores |
|
|
Term
| most serious fungal infections are caused by? |
|
Definition
| inhaling spores of dimorphic fungi |
|
|
Term
| dermatophyte fungal infections |
|
Definition
| invade superficial skin (ringowrm, athlete's foot) |
|
|
Term
|
Definition
| aflatoxin and ergot poisoning |
|
|
Term
| Malaria, and how it avoids immune system |
|
Definition
| protozoal infection - plasmodium lives in RBC so it's not exposed to humoral immunity... no MHC, so not exposed to cellular immunity |
|
|
Term
| How do trypanosomes avoid the immune system? |
|
Definition
| protozoa - surface antigen variation |
|
|
Term
| How do schistosomes (protozoa) avoid the immune system |
|
Definition
| surface receptors for host proteins |
|
|
Term
|
Definition
| normally keeps us from getting respiratory infections by: goblet cells secrete mucose in nasal passages, which trap bacteria then cilia sweep it out |
|
|
Term
| 3 methods of respiratory protection |
|
Definition
| mucociliary escalator, native flora, lysozyme and blinking |
|
|
Term
| the mucociliary escalator can be paralyzed by |
|
Definition
| tobacco smoke, alcohol/alcoholism, narcotics |
|
|
Term
| the eustachian tube connects the ___ and the ____. |
|
Definition
|
|
Term
| The lacrimal duct connects the ___ and the ___. |
|
Definition
| tear gland and the nasopharynx |
|
|
Term
|
Definition
| pain, fever, hard to swallow, red throat, patches of pus.. NO cough or runny nose |
|
|
Term
| Strep throat is caused by? |
|
Definition
| S. pyogenes (Group A strep) |
|
|
Term
| virulence factors associated with Group A strep |
|
Definition
| C5a peptidase (damages complement), Hyaluronic acid capsule (looks like self), M Protein (C3b protease damages complement and antigen responsible for late sequelae), G protein - Fc binding protein, exotoxins, hymeolysins, streptokinase |
|
|
Term
| late sequelae of strep throat |
|
Definition
| rheumatic fever develops if strep is untreated |
|
|
Term
| How can untreated strep throat lead to bacterial endocarditis in dental patients? |
|
Definition
| rheumatic fever is late sequela, then antibodies are made against the M protein, the antibodies erode heart valvues, which allows a rough surface for biofilm attachment, viridian group strep (which is normal mouth flora) can now colonize the heart valve, causing bacteria endocarditis |
|
|
Term
|
Definition
| toxin affects heart and kidneys, dead cell sin throat form pseudomembrane which blocks the airway |
|
|
Term
| How is diphtheria developed? |
|
Definition
| AB toxin is produced in host when there is low Fe content, the B part binds to cells in heart, kidneys, and back of throat... A part stops protein synthesis |
|
|
Term
| why do people die of diphtheria? |
|
Definition
|
|
Term
| How do you prevent diphtheria? |
|
Definition
| spread by resp droplets, so stay away from someone with it - also vaccines (DTaP, with booster every 10 years) |
|
|
Term
|
Definition
| antitoxin - via passive immunity - DIG (diphtheria immunoglobulin) |
|
|
Term
| 2 bacteria that ALWAYS cause ENT infections |
|
Definition
| haemophilus influenzae type b, strep pneumoniae |
|
|
Term
|
Definition
| Pinkeye - lost of pus, caused by H. influenzae, strep pneumonia, n. gonorrhoeae, psudomonas from cosmetics |
|
|
Term
| What is characteristic of pseudomonas infections? |
|
Definition
|
|
Term
|
Definition
| middle ear infection - bacteria in pharynx travels up eustachian tube to ear canal - very painful, may cause eardrum to rupture, no fever, caused by H. influenzae and s. pneumoniae |
|
|
Term
| Why do little kids get ear tubes? |
|
Definition
| Because their eustachian tubes are too small to let bacteria drain out |
|
|
Term
|
Definition
| headache, swelling, pus in nasal secretions, caused by s. pneumoniae and h. influenzae |
|
|
Term
| when would you use antibiotics for ENT infections? |
|
Definition
| only for recurring infections (3x/6mos) |
|
|
Term
|
Definition
| filling of lungs with fluid... inflammatory response to lung infection, high fever, shortness of breath, pink sputum |
|
|
Term
| why do you have pink sputum in pneumonia? |
|
Definition
| PMNs and diplococci present in lung serum (indicative of infection) |
|
|
Term
|
Definition
| 23-valent (polysaccharide, not great)... only for adults |
|
|
Term
| Most common cause of community-acquired bacterial pneumonia |
|
Definition
| strep pneumonia (LRT pneumonia) |
|
|
Term
| 2 major causes of the common cold |
|
Definition
| rhinovirus and adenovirus |
|
|
Term
|
Definition
| causes about 50% of colds, is a picornavirus, naked, ssRNA, ok with high pH in URT, but not in low pH of stomach |
|
|
Term
| How does rhinovirus work? |
|
Definition
| binds to epithelial cell receptors, causes cell death induces immune mediators, secretions, swelling |
|
|
Term
| ___ is the most common infectious disease at about 3 cases/yr/person |
|
Definition
|
|
Term
| How can the same person get several rhinovirus colds each year? |
|
Definition
| there are over 100 different rhinoviruses, and you are only immune to one for 5-10 years after you've gotten it |
|
|
Term
| potentially effective treatment for the common cold |
|
Definition
| pleconaril - binds to capsid and inhibits receptor binding and uncoating (phase II trials) |
|
|
Term
|
Definition
| naked, dsDNA virus... causes cold AND fever, pus may be present |
|
|
Term
| 2 diseases caused by adenovirus, other than colds |
|
Definition
| viral conjunctivitis and diarrhea (some strains can survive stomach) |
|
|
Term
| How is adenovirus spread? |
|
Definition
| resp droplets during acute phase, feces several weeks afterwards |
|
|
Term
| how do you treat adenovirus? |
|
Definition
| just treat symptoms -- vaccine available, but not commercially |
|
|
Term
|
Definition
| virolent paroxysms of coughing, so sever that vomiting occurs.. try to catch breath between coughs = whooping |
|
|
Term
| Why is pertussis currently on the rise in the US? |
|
Definition
| it was thought of as a childhood disease (bc symptoms usually occur in children) so we stopped immunizing adults only to find out that adults can still get it asymptomatically and spread it to kids |
|
|
Term
| What causes pertussis? and what effect does it have? |
|
Definition
| Bordetella pertussis toxin (AB5 toxin) -- A part ADP-ribosylates an inhibitor of cAMP synthesis (knowck out inhibitor of cAMP = increased fluid production) |
|
|
Term
| Why did we switch from the DPT vaccine to DTaP? |
|
Definition
| DPT - whole cell vaccine, some people had allergic response to it, DTaP is acellular pertussis |
|
|
Term
| Tuberculosis is caused by? symptoms? |
|
Definition
| mycobacterium tuberculosis - fatigue, fever, weight loss, blood tinged cough |
|
|
Term
| How can infection with mycobacterium tuberulosis lead to granuloma formation? |
|
Definition
| initially produces exudative lesion (typical inflammatory response), then may lead to a productive lesion (granuloma) because it gets inside a machrophage but doesn't die - so the macrophage keeps activating more and more t cells -- can lead to dissemination or lung fibrination |
|
|
Term
| What might happen to non-granulomous TB infections? |
|
Definition
| either heals or necrotizes lung |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| How might TB be diagnosed (pre- and post-death) |
|
Definition
| spots on liver (granulomas) or lungs (fibrination) ... or upon autopsy a hole in bones |
|
|
Term
| How is TB spread and what does it do once its in the body? |
|
Definition
| resp droplets - invade alveolar macrophages and prevent phagolysosome fusion |
|
|
Term
| Why is TB on the rise in the US? |
|
Definition
| AIDS - proliferates in immunocompromised people |
|
|
Term
|
Definition
| chemo with multiple drugs :: DOT - directly observed therapy (bc people will sell the drugs on the street) :: MDR - multiple drug resistant :: XDR - extremely drug resistant (virtually untreatable) |
|
|
Term
| How is TB prevented in most of the world? |
|
Definition
| BCG vaccine - live, non-pathogenic strain |
|
|
Term
| How is TB prevented in the US? and why don't we do what everyone else does? |
|
Definition
| PPD or Mantoux Skin test (if you have TB, you'll have activated T cells that create a skin rxn)- because TB isn't a big enough problem to need to vaccinate everyone, and those who have been vaccinated present a positive skin test (Type IV HS), so it's impossible to know who actually has it... we'd rather know who has it. |
|
|
Term
|
Definition
| orthomyxovirus, enveloped ssRNA in 8 segments - two envelope proteins, hemagglutinin and neuraminiduase |
|
|
Term
| why is it important that flu is a segmented virus? |
|
Definition
| allows genetic reassortment - why theres a new strain every year |
|
|
Term
| hemagglutinin and neuraminidase |
|
Definition
| H allows binding, N allows release ... of flu virus |
|
|
Term
| what causes antigenic drift |
|
Definition
| minor changes in flu virus because it is an RNA virus - no proofreading |
|
|
Term
|
Definition
| in flu virus - major changes when RNA segments are reassorted in alternate host (human or pig)-- responsible for major flu epidemics (1918) |
|
|
Term
| 3 major flu pandemics of the last 100 years |
|
Definition
| 1918 (spanish flu) - H1N1 - most deadly, killed healthy adults :: 1957 (asian flu) - H2N2 - very old people immune because it was common in 1870s :: 1968 (Hong Kong flu) - H3N2 - mild |
|
|
Term
| Why isn't the bird flu a problem yet? |
|
Definition
| H5 doesnt bind well to human cells -- needs about 2 more mutations |
|
|
Term
|
Definition
| amantadine (blocks binding of hemagglutinin and virus uncoating) :: oseltamivir and tamaflu (prevents neuraminidase from relasing the virus so it can't spread |
|
|
Term
|
Definition
| vaccines annually (50-70% effective, whereas normal vaccines are 95%) -- usually injected killed virus, new flu-mist vaccine a little better bc its live attenuated |
|
|
Term
| #1 cause of LRT infection in babies |
|
Definition
| respiratory syncytial virus |
|
|
Term
| what kind of virus causes RSV |
|
Definition
|
|
Term
|
Definition
| Sin Nombre - fever muscle aches nausea and loss of lung function shock and death = very rapid pneumonia and hypovolemia |
|
|
Term
| Hantavirus in what region |
|
Definition
| SW USA - Navajo population --- inhaled in dust aerosols from infected rodents |
|
|
Term
|
Definition
| fungal disease - mold spores enter lung and develop into pherules, which release endospores --- symptoms from immune response to endospores, most severe in immunocomp. |
|
|
Term
| what do Histoplasmosis spores look like? |
|
Definition
|
|
Term
| Where is histoplasmosis common? |
|
Definition
| Ohio/Mississippi river valley - most common in cavers |
|
|
Term
| How is histoplasmosis treated? |
|
Definition
| antifungals - amphotericin, azoles |
|
|
Term
| F plasmid... "F" stands for? |
|
Definition
|
|
Term
| Resistant bacteria develop naturally through ____. |
|
Definition
|
|
Term
|
Definition
| Cell with F plasmid inserted in it |
|
|
Term
|
Definition
| F plasmid is inserted in HFR cell, then when it leaves it takes with it the genes around it, some of which may have antibiotic resistance |
|
|
Term
|
Definition
| F plasmid with multiple (2 or 3) antibiotic resistance genes in it |
|
|
Term
| Responsible for rapid transfer of multiple antibiotic resistance between bacterial cells |
|
Definition
|
|
Term
| What problem do R plasmids cause? |
|
Definition
| If you have one R plasmid with resistance to a certain antibiotic and you get sick and are treated with that antibiotic, it's no big deal because you only have 1 R plasmid in 1 bacterium... but lots of other cells (bacteria) will be killed off in the infection, leaving room for the R plasmid bacterium to replicate... now you have lots of cells with that R plasmid. If you are treated with that antibiotic again, it will no longer be effective because you have too many resistant bacteria. |
|
|
Term
|
Definition
| furuncle (boil) - inflammatory response to growth of S. aureus |
|
|
Term
| Key enzyme in staph infections |
|
Definition
| coagulase - prevents immune system cells from getting to infection by blocking off area that's infected |
|
|
Term
| Staph infection of hair follicles |
|
Definition
|
|
Term
|
Definition
| scalded skin syndrome (bullous exfoliation), toxic shock syndrome (superoxide) |
|
|
Term
| What staph has coagulase? |
|
Definition
|
|
Term
| When does S. epi cause infections? |
|
Definition
| people with catheters or implanted medical devices (metal plates)... s. epi forms biofilm on foreign devise and cannot be treated |
|
|
Term
| How are staph infections spread? |
|
Definition
| contact and fomites (sheets and clothing) -- kids may get it by sleeping in daycare centers |
|
|
Term
| Notorious MDR staph infection |
|
Definition
|
|
Term
| Antibiotic specifically for MRSA |
|
Definition
|
|
Term
|
Definition
| strep skin infection - very painful infection of fat tissue underneath skin and causes inflammation |
|
|
Term
|
Definition
| Usually strep skin infection, also can be staph... crusty rash found most often in preschoolers, spread by fomites and contact... problem comes from late sequelae (autoimmune) |
|
|
Term
| Problem with most strep infections |
|
Definition
| Late sequelae - autoimmune disease, immune mimicry -- caused when we start making antibodies against an infection |
|
|
Term
|
Definition
| Rheumatic fever, acute glomeruli nephritis (AGN) |
|
|
Term
|
Definition
| Strep infection with superantigen and tissue activating toxins - bacterial and cytokine induced tissue damage -- common in IV drug users who share drugs |
|
|
Term
| Why should strep infections be treated quickly? |
|
Definition
|
|
Term
| Treatment for strep skin infections |
|
Definition
| keep from spreading, isolate carriers, penicillin (except for toxins), anti-inflammatory drugs |
|
|
Term
| ____ infections are opportunistic skin infections in wounds and burns. ___% of deaths in burn patients is caused by this. |
|
Definition
|
|
Term
| Telltale sign of pseduomonas infections |
|
Definition
| green... either green color to skin, green sputum in resp infections, etc |
|
|
Term
| Pseudomonas causes about 85% of deaths in what resp disease? |
|
Definition
|
|
Term
| #1 complication of RK and Lasik surgery |
|
Definition
|
|
Term
| common cause of nosocomial UTI after catheritization |
|
Definition
|
|
Term
| horizontal gene transfer of R plasmids is common in ____. |
|
Definition
|
|
Term
| Major problem with pseudomonas |
|
Definition
|
|
Term
| Treatments of pseudomonas |
|
Definition
| focused on prevention, not much you can do once biofilm is established... topical antimicrobials on wounds... used multiple drug therapy for long term treatment because of R plasmids |
|
|
Term
| Bacterial disease caused by spirochaete (cork-screw bacteria) called borrelia burgdorferi |
|
Definition
|
|
Term
| How do you get infected with lyme disease? and how do you know you have it? |
|
Definition
| nymph of deer tick (almost impossible to see)... bull's eye rash develops |
|
|
Term
| Problem wtih lyme disease |
|
Definition
| late sequelae - heart conduction abnormalities, arthritis |
|
|
Term
| 2 main places where you find lyme disease |
|
Definition
| new england states and minnesota down through chicago |
|
|
Term
|
Definition
| avoid vectors (wear long pants and sleeves), antibiotics (tet and pen derivative) |
|
|
Term
| ___ is caused by an anaerobic spore-former called clostridium tetani |
|
Definition
|
|
Term
|
Definition
| AB toxin where B part binds to presynaptic neruons and A part inhibits neuroinhibitors, so ALL muscles contract |
|
|
Term
| Most cases of tetanus come from? |
|
Definition
| bad tattoos and piercings, stepping on a rusty nail -- any deep penetration wound |
|
|
Term
|
Definition
| vaccination (DTaP) and boosters every 10 years (tetanus shot), tetanus immune globulin antitoxin given immediately after injury, surgical debridement, muscle relaxants, NOT CNS depressants |
|
|
Term
| gangrene is caused by what bacterium |
|
Definition
|
|
Term
|
Definition
|
|
Term
| What kind of accident would cause gangrene |
|
Definition
| blunt trauma injuries, especially under anaerobic conditions |
|
|
Term
| Death from gangrene happens because? |
|
Definition
| bacteria releases gas, which is toxic and causes toxic shock |
|
|
Term
|
Definition
| usually just have to cut off bad tissue |
|
|
Term
|
Definition
| bacteria in animals that is transmitted to us when we are bitten by them... causes edematous abscess within a few hours after bite |
|
|
Term
| Why do dog and cat bites cause inflammation so quickly? |
|
Definition
| because our body is not used to that bacteria, so our immune system takes longer to respond to it |
|
|
Term
| pasturella in chickens causes? |
|
Definition
|
|
Term
| pasturella in cattle causes |
|
Definition
| shipping fever - copious nasal discharge, septicemia, pneumonia, death in 18 hrs. |
|
|
Term
| pasturella in rabbits causes |
|
Definition
| snuffles - progresses to lethal hemorrhagic pneumonia (bloody lungs) |
|
|
Term
|
Definition
| cat scratch disease - lymph node swelling |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| why are about half of kittens infected wtih bartonella henslae? |
|
Definition
| it lives in cat RBCs - so its easily transmitted by fleas |
|
|
Term
| How is cat scratch disease treated? |
|
Definition
|
|
Term
| disease caused by a variety of herpes virus called varicella-zoster virus, a ds DNA enveloped virus |
|
Definition
|
|
Term
| Chickenpox causes a ____ rash, meaning all three stages are present at once |
|
Definition
| maculo-papulo-pustular (flat spots, raised spots, leaking pus) |
|
|
Term
| Chickenpox is varicella-zoster virus... what does that mean? |
|
Definition
| varicella = chickenpox, zoster = shingles |
|
|
Term
| Chickenpox as a latent virus |
|
Definition
|
|
Term
|
Definition
| stillbirth or serious developmental problems |
|
|
Term
| ___ is a known reactivator of herpes virus. It reactivates along a ____, which is fed by one neuron. |
|
Definition
|
|
Term
| Chickenpox in early teens (9-15 yr olds) who took aspirin for the chickenpox come down with ____, which is a ____ disease. |
|
Definition
|
|
Term
|
Definition
|
|
Term
| what kind of virus is measles |
|
Definition
|
|
Term
|
Definition
| choria (runny nose), cough, and conjunctivitis |
|
|
Term
| about 50% of people with measles get ___ in pharynx, caused by? |
|
Definition
| Koplik's spots... caused by dead cells in resp epithelium |
|
|
Term
| ____ are pathonomic for measles, meaning? |
|
Definition
| Koplik's spots -- if you have Koplik's spots, you have measles |
|
|
Term
| Measles grows in ___ cells, which results in? |
|
Definition
| T cells - reduced cellular immunity |
|
|
Term
|
Definition
| vaccine (MMR) required in developed world, 2 injection regimen |
|
|
Term
| ___ is AKA Rubella and is caused by a small enveloped ssRNA togavirus |
|
Definition
|
|
Term
| symptoms of german measles |
|
Definition
| slight fever, mild symtpoms, very fine rash |
|
|
Term
| german measles spread by ? |
|
Definition
|
|
Term
| Problem with German measles |
|
Definition
| vertical transmission - from mom to baby - causes congenital rubella syndrome = blind, deaf, heart disease, retardation |
|
|
Term
|
Definition
| human papillomavirus (HPV) |
|
|
Term
| how does HPV work to cause warts? |
|
Definition
| replicates in epithelial cells, causing abnormal cells with the E6 protein... causes wart |
|
|
Term
|
Definition
| HPV virus produces it, prevents p53 from checking DNA for abnormalities - causes wart |
|
|
Term
| 2 kinds of HPV that cause cervical cancer, and how? |
|
Definition
| type 16 and 18... are proviruses (integrate DNA into host DNA) to cause chromosomal abnormalities |
|
|
Term
| Candida albicans infections |
|
Definition
| yeast infections - diaper rash, thrush (white cheesy growth in mouth, common in infants and AIDS patients), vaginal yeast infections .. normal flora that grows in moist places |
|
|
Term
|
Definition
| produce cutaneous fungal infections (below surface of skin) - tinea infections (athlete's foot, ringworm, etc) |
|
|
Term
| Sporotrichosis infections |
|
Definition
| AKA "Rose gardener's disease" fungal infection caused by punctures from plant thorns, which introduces dimorphic spores... nodules form along lymph nodes |
|
|
Term
|
Definition
| no VDJ joining - no B or T cells |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
| Type of antibody that would be most effective for agglutinating bacterial cells? |
|
Definition
| IgM - because its a tetramer |
|
|
Term
| Breast fed babies recieve what antibodies that bottle fed babies dont? |
|
Definition
|
|
Term
| What happens if you are exposed to an antigen which none of your B cell receptors recognize? |
|
Definition
| Your innate immune system will deal with it. |
|
|
Term
| What happens if you have a B cell receptor that recognizes an antigen but no T cell receptor recognizes that same antigen? |
|
Definition
|
|
Term
| What happens if you produce a B cell that does not recognize any antigen you're exposed to? |
|
Definition
| nothing - the b cell just doesn't replicate |
|
|
Term
| Can T cells agglutinate bacteria? |
|
Definition
|
|
Term
| What type of cell produces the surface protein B7? |
|
Definition
| Phagocytes after they have phagocytized a foreign cell |
|
|
Term
A cancer vaccine that has recently passed phase I clinical trials uses adenovirus that's been genetically engineered to carry the B7 gene. How does this work?
a. stimulate antibody production from B cells
b.enhance actiation of Tc cells by nonAPCs
c. enhance phagocytosis of tumor cell
d. allow effector Th cells to secrete antibodies |
|
Definition
| Enhances activation of Tc cells by nonAPCs |
|
|
Term
| live attenuated polio vaccine is given orally whereas attenuated flu vaccine is given as a nasal mist, why? |
|
Definition
| memory mucosal B cells exist at the site of infection |
|
|
Term
| What do immunodiffusion and ABO blood typing have in common? |
|
Definition
| antibody-antigen complexes form |
|
|
Term
| A patient has been exposed to TB but has formed granulomas. He gets tested every 6 mos to determine whether the TB has broken out of the granuloma. What type of test should be used? |
|
Definition
| Direct fluorescent antibody |
|
|
Term
| IN a direct ELISA test, antibodies are attached to the bottom of a microtiter well. HOw can we be sure the Abs have the Fab part pointing up? |
|
Definition
|
|
Term
| EHEC is E. coli that has acquired toxin and pilus genes from Shigella. This is an example of? |
|
Definition
| HGT of pathogenicity islands |
|
|
Term
| Pt. had strep 3 weeks ago and now present with cardiac insufficiency and valve malformations. what has happened? |
|
Definition
| he is producing anti-strep antibodies |
|
|
Term
What is a characteristic of a chronic illness?
prevalence much higher than incidence, or prevalence only slightly higher than incidence? |
|
Definition
| prevalence much higher than incidence |
|
|
Term
| Atypical pneumonias differ from typical pneumonias, in that atypical pneumonias require more/less treatment? |
|
Definition
|
|
Term
|
Definition
| to avoid humoral immune system |
|
|
Term
| A patient with a cold also has a fever, and red itchy eyes. She is most likely infected with what? |
|
Definition
| adenovirus - cold, fever, conjuctivitis (rhinovirus is JUST cold) |
|
|
Term
| 2 bacteria that cause biofilms |
|
Definition
| pseudomonas and staph epidermidis |
|
|
Term
During the course of an acute illness, an indirect ELISA will...
a. only detect the antigens associated with the illness
b. become positive sooner in an illness than a direct ELISA would
c. become positive but return to negative shortly after illness is cured
d. be developed by adding a second antibody that recognizes the first
e. need to be done 4 or 5 times to determine with what the patient is infected |
|
Definition
|
|
Term
A classic allergy response (Type I HS) requires two exposures to the allergen. After one exposure, what happens?
a. Th cells becomes activated
b. IgM is secreted into the tissues where it waits for the second exposure.
c. Mast cells become caoted with IgE
d. smaller than usual immune complexes form
e. nothing happens until the second exposure |
|
Definition
|
|
Term
A pathogenicity island is a?
a. cluster of virulence factors that can be transmited by HGT
b. group of pathogenic bacteria boudn to an M cell
c. patch of membrane receptors to which pathogenic bacteria bind
d. plasmid on which multiple antibioti resistance genes are located
e. tissue or organ that commonly serves as a site for bacterial portal of entry |
|
Definition
|
|
Term
| What is the function of Staph protein A? |
|
Definition
|
|
Term
| Why are scientists concerned that the overuse of a signel antibiotic might select for multiple antibiotic resistnaces in bacteria? |
|
Definition
| R plasmids mean that selection of any antibiotic resistance selects for them all. |
|
|
Term
| What type of cell do NK cells kill? |
|
Definition
|
|
Term
|
Definition
| if any lines are present, it means the disease is present |
|
|
Term
In the disease Lupus, autoantibodies are directed against:
a. DNA,
B. B cells
C. epithelial cells
d. Acetylcholine
e. anything you touch or eat |
|
Definition
|
|
Term
| The most common immune disorder in the US is selective IgA deficiency. People who suffer from this will be more likely to get ___ that other people? |
|
Definition
| resp and digestive illness |
|
|
Term
| Which of the following is not a signal that a pathogen's 2-component regulatory syustem recognizes to induce virulence factor genes? low pH, high free iron concentraiton, presence of cytokines, increased temperature, binding to receptors on macrophages |
|
Definition
|
|
Term
| M cell ruffling is in response to? |
|
Definition
|
|
Term
| How is LPS toxic to humans? |
|
Definition
| It binds strongly to macrophages, causing a response that can lead to hypovolemia |
|
|
Term
Which of the following is a method for viruses to evade the host immune defenses?
a. produce a protein that prevents host cell apoptosis in response to dna damage
b. use host actin to spread intracellularly
c. produce antiphagocytic lipid capsule
d. prevent recruitment of MAC
e. survive nad replicate within phagolysosome |
|
Definition
|
|
Term
Which of the following is not used as a target for antiviral drugs?
a. nucleic acid synthesis
b. receptor binding
c. proteolysis of a polyprotein
d. viral budding from host cell
e. viral folic acid metabolism |
|
Definition
|
|
Term
| What do tetanus and gangrene have in common? |
|
Definition
| They both require anaerobic conditions to grow |
|
|
Term
| What do measles and german measles have in common? |
|
Definition
| both spread via resp droplets |
|
|
Term
| Haemophilus influenzae type B causes most common respiratory infections (sinusitis, conjuntivitis, otitis media, etc.), but you aren't supposed to be treated with antibiotics unless it recurs more than 3x in 6 mos. why do you need antibiotics at that point? |
|
Definition
| chronic Hib infections can cause ear damage and even meningitis |
|
|
