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MIP 300- Unit 2
| Question | Answer |
|---|---|
| infection (definition) | when a parasite is multiplying in/on a host |
| infectious disease (definition) | when a host cannot function normally |
| pathogens (definition) | cause disease |
| pathogenicity (definition) | organism's ability to cause disease |
| virulence (definition) | degree or intensity of pathogenicity |
| three factors affecting outcome of host/parasite relationship | # organisms, virulence, host's resistance |
| symptoms | unobservable |
| signs | observable changes |
| disease syndrome | collection of signs and symptoms |
| infectivity (definition) | ability of an organism to start an infection |
| invasiveness (definition) | ability of an organism to spread |
| pathogenic potential (definition) | ability of an organisms to cause symptoms (toxins!) |
| 3 factors affecting virulence | infectivity, invasiveness, pathogenic potential |
| infectivity affected by (4) | ability to be transmitted, ability to adhere, ability to grow, ability to avoid immune response |
| fomite (definition) | inanimate objects that are contaminated (like a doorknob) |
| 4 ways of direct transmission | airborne, horizonal, vertical, vector |
| horizontal direct transmission | kissing etc |
| vertical direct transmission | pregnancy |
| vector direct transmission | insects |
| indirect transmission (3) | airborne (from soil etc), contaminated food/water, contact (fomites) |
| 5 places adhesins are found | fimbriae, capsule/glycocalyx/slime layer, s-layer, teichoic acid, viral capsids and envelopes |
| teichoic acid | for attachment; found in gram positive bacteria |
| s-layer | may be used for attachment; protein layer around cells |
| host must have correct ___ for parasite to grow | pH, oxygen, temperature |
| microbial products to avoid immune system (3) | IgA protease, leukocidins, capsule |
| IgA protease | cleaves IgA |
| leukocidins | kill lysosomes in WBCs |
| how to hide within a host cell? (2) | escape phagosome before fuses w/ lysosome; prevent phagosome from fusing with lysosome |
| M-cell targeting | (salmonella)-> releases enzyme that makes these ruffle (immune cells in GI tract) so bacteria sink into them and get taken up |
| macrophage targeting | (Tuberculosis)-> tricks cells into spreading across mucous membranes and into circulation (hides in macrophages) |
| microbial products involved in invasion (definition) | all break down tissue so more space for microbe |
| Leishmaniasis | protozoal skin infection that can become visceral |
| neurotoxin treatment | antiserum (aka antitoxin) AND antibiotics |
| botulism causes | flaccid paralysis |
| tetanus causes | spastic paralysis |
| tetanus toxin | tetanospasmin |
| enterotoxins (definition) | affect GI tract |
| enterotoxin examples (2) | Vibrio cholera, E. coli |
| cytotoxin (definition) | affects cellular functions |
| cytotoxin (examples) | Corynebacterium diptheriae, C. perfringens |
| Corynebacterium diptheriae | diptheria toxin; creates pseudomembrane of dead bacteria+neutrophils which clogs throat |
| Clostridium perfringens | releases a-toxin-> removes head from phospholipids, breaks down muscle tissue (causes gas gangrene) |
| superantigen (definition) | over-stimulates the immune system; causes similar response to endotoxins |
| superantigen example | S. aureus TSST1 (toxic shock syndrome); shock dilates blood vessels, causes rashes (>20% of T-cells activated) |
| exotoxin genes (3) | plasmid, lysogenic phage, chromosomal |
| which disease must have phage to be virulent? | Diptheria |
| toxoids | inactivated toxins |
| DPT vaccine | toxoids-> diphtheria, pertussis, tetanus |
| why is there no vaccine for lipid A? | the immune system doesn't recognize it and launch a response |
| septic shock cascade | caused by lipid A; blood clotting factor that over stimulates 4 systems; unregulated blood clotting which leads to organ failure **vasodilation |
| pelvic inflammatory disease | Neisseria gonorrhea; adhesins stick to sperm, scar tissue that blocks fallopian tubes |
| damage caused by inflammation | macrophages/neutrophils release toxic molecules that cause tissue damage |
| damage caused by antibodies | antigen/antibody complexes settle in kidneys and joints that elicits an immune response -> tissue damage |
| how does herpes evade immune system? | prevent MHC I on cell surface |
| skin as an innate physical barrier | keratinocytes (keratin is H2O repellant), dry, top layer is dead, acidic, salty |
| fungal infection that invades skin | ringworm |
| Streptococcus pyogenes | exotoxin A= shock; exotoxin B= melts tissue/muscle underneath skin |
| mucosa | columnar cells that form barrier, release mucous (prevents adhesions and traps microbes) |
| problems that weaken mucous defense | smoking (kills cilia), asthma, cystic fibrosis |
| mucociliary escalator | ciliated cells and mucous trap and propel microbes away from lungs and into throat |
| how microbes evade GI tract (4) | resist saliva, strong adhesins, capsules, slime layers |
| microbes response to stomach acid | pH resistant (produce base), resistant spores |
| cervical mucous, prostatic fluid, tears contain ___ | lysozyme and lactoferrin |
| defensins | punch holes in membrane |
| lactoferrin/transferrin | sequester iron away from microbes |
| bacteriocin | produced by normal flora; kill other bacteria |
| complement 3 functions | opsonization, MAC, inflammation |
| cytokines | protein communication molecules |
| interferon response | infected cell releases it, other cells have receptors and synthesize antiviral proteins |
| granulocytes (definition) | contain toxic molecules |
| agranuloytes (definition) | do not contain toxic molecules |
| macrophages are called ___ in blood | monocytes |
| dendritic cells | phagocytosis; present in skin and mucosa |
| neutrophils | first responders (in blood) |
| inflammation (4) | bacteria introduced; histamine released; neutrophils roll and stop; extravassation |
| death from fever occurs at ___ | 109.4 degrees F |
| two substances that cause fever | pyrogens (exogenous= LPS etc; endogenous=interleukin-1) |
| why are fevers good? (4) | slows microbial growth, inactivates some toxins, increases immune activity, forces person to feel ill |
| two immunological responses | primary= first exposure; secondary= memory response |
| antigen | a substance that the body sees as foreign and mounts an immune response |
| epitopes | short AA sequences that are recognized by antibodies and T-cells |
| when active, CD8 cells are called (and activated by whom?) | CTL (cytotoxic T lymphocytes) *activated by t-helper CD4 |
| CD4 aka | (bossy) T helper cells |
| CD8 cells are important for | fighting viruses and tumor cells |
| how do C8 cells kill? | make pore, insert enzymes, apoptosis |
| B-cells | recognize and bind to antigen using the BCR (surface bound antibody) after receiving cytokine signal |
| memory B cells | stay in lymph nodes until second infection |
| IgM | secreted after infection, pentameric |
| IgD | unknown function, stays bound to B-cell |
| IgG | most abundant during 2nd infection, *crosses placenta (monomeric), blood! |
| IgA | mucosal surfaces (dimeric) |
| IgE | allergies (binds to mast cells), monomeric |
| 5 functions of antibodies | complement fixation, neutralization, opsonization, (agglutination, precipitation) |
| complement fixation | antibodies trigger complement cascade |
| opsonization (antibodies) | same process as complement does |
| neutralization | antibodies surround microbe and prevent it from binding to a cell |
| live attenuated vaccines | live culture no longer pathogenic (vaccine) *can mutate and be virulent |
| activated/killed vaccines | killed with heat or chemicals |
| toxoids | inactivated toxins (vaccines) |
| polysaccharide capsules | vaccine type; copy of the coat of microbes |
| what do B-cells do? | recognize an epitope, and make an antibody (IgM initially, IgG later) |
| protein vaccines | recombinant or native (new) |
| DNA vaccines | inject plasmids that express antigens in host tissues (in clinical testing) |
| recombinant vector vaccines | use of viruses or bacteria to deliver genes of interest (in clinical testing) |
| conjugate vaccines | link toxoid to polysaccharide component to help target T-cells |
| how does HIV work? | kills CD4 cells (no antibody, no CTL) **increased cancer and opportunistic infections |
| how does Epstein-Barr virus work? | over proliferation of B and T cells |
| how do herpes/measles work? | hide antigens from surface of presenting cells |
| how does the flu work? | changes antigens each year |
| How does Tuberculosis work? | reproduce inside WBCs |
| our definition for organic | 2 or more carbons |
| heterotrophs | use reduced organic molecules as carbon source |
| trace element function | help in metabolic functions |
| phototrophs reduce or oxidize CO2? | reduce |
| bioremediation | cleaning/plastic making using microbes |
| Exxon Valdez oil spill | add P and N to stimulate oil-eating bacteria |
| chemical work | molecule synthesis |
| E0 values | more negative= give electrons; positive= receive electrons |
| epidemiology | the study of distribution and determinants of disease frequency in human populations |
| outbreak | higher than expected occurrence in a small group (WWII vets pneumonia) |
| pandemic | occurrence higher than expected worldwide (influenza) |
| nosocomial infection | illnesses associated with hospitalization |
| endemic disease | steady but low frequency (herpes) |
| epidemic | occurrence higher than expected (index case) |
| zoonoses | animal disease transmitted to humans (80% of known diseases) |
| prairie dogs transmit | the plague |
| deer mice transmit | hanta virus (sheds) |
| vectors and ___ are the same thing | carriers |
| hepatitis A/E | transient |
| hepatitis B/C | chronic |
| convalescent | getting better, large # of microbes |
| most infectious w/ flu when? | prodromal |
| passive mechanical vector | vector carries it outside of its body |
| passive biological vector | animal carries it inside its body |
| active biological vector | bite, defecate, regurgitate in tissue |
| antigenic drift | example mixing up H's and N's of influenza |
| antigenic shift | example mutations in H and N antigens |
| when do you for sure want antibiotics (4) | rash/stiff neck/fever, sore throat that doesn't go away, skin infections, bladder infections |
| what did Bonnie Bassler study? | squid that used bacteria to hide its shadow; pumped 95% of them out in the morning; enough for quorum sensing by night time |
| types of quorum sensing | species-specific and species-nonspecific |
| what is the system that removes microbes from the lungs? | mucociliary escalator |
| infections that one gets at hospitals | nosocomial |
| mice= infected but cannot transmit to cats; fleas carry disease to cats and they get sick: mouse= ___; flea=____ | reservoir; vector |
| you travel to Africa and develop Ebola, which antibody most effective in helping to clear it? | IgG (blood) |
| 2 antigens and 7 epitopes for a parasite- how many B cells specific for it? | 1 for each epitope (7) |
| 2 different antibodies specific for same epitope- they will have different __ | constant regions on the heavy chains |
| roommate has hep A; you get gamma globulin shot; if they develop it 3 years later will you be protected? | no, it likely mutated (it's also acute) |
| asked to develop a toxoid specific for the C difficile toxin- what will you create? | the toxin that is deactivated by chemicals or heat |
| what would happen w/ complement deficiency? | lack of pore production on pathogens |
| smoker gets lung infections why? | smoking kills cilia |
| 3 ways TSST an LPS are different | exotoxin/endotoxin; actively secreted/not; made of protein/made of lipopolysaccharides |
| 2 ways TSST and LPS same | both lead to shock and both have no vaccine |
| which antibody inhibits toxin binding to receptors in the liver | IgG |
| H2S-> S could be done by | aerobic chemolithotrophy or anaerobic chemolithotrophy |
| NO3- -> NO2- could be done by | anaerobic chemolithotrophy or anaerobic respiration |
| final electron acceptor in methanogenesis | CO2 |
Created by:
melaniebeale
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