Micro 0580 Exam 2 – Flashcards
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| "-cide" |
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| kills organism (e.g. bactericide, fungicide) |
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| "-static" |
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| growth is halted |
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| sterilization |
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| an absolute process = killing/removal of all organisms (incl. bacterial spores) |
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| Will sterilization remove LPS? |
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| NO. sterilization does not necessarily remove bacterial procuts, especially heat-stable ones like endotoxin |
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| sanitization |
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| achieves clean w/ no pathogens (but does not imply sterilization or complete disinfection) |
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| Pasteurization |
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| elevated temp, follow by rapid cooling (e.g. kills pathogens in milk) |
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| Will Pasteurized milk be sterile? |
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| NO. pasteurization does not sterilize; some bacteria, spores, stable viruses may survive pasteurization mainly used to preserve and prevent spoilage |
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| antiseptic |
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| chemical used to kill organisms on the surface of skin |
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| aseptic technique |
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| means "without infection" |
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| What is the most effective means of preventing infection spread? |
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| hand washing |
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| barrier technique |
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| involves hand washing, gloves, gowns, masks, glasses, face shields, appropriate personal hygiene and cleaning of physician's equipment |
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| sterilization, disinfectant, preservatives list |
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| (see chart) |
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| antimicrobial |
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| a substance that interferes with proliferation of microorganisms (viruses, bacteria, fungi, protozoa, etc.) |
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| antibiotic |
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| a substance/compound of natural origin that demonstrates antimicrobial activity the source of which is often soil microorganisms (e.g. Streptomyces) |
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| bacteriostatic vs. bacteriocidal |
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| "-static" agents inhibit growth, but do not kill the organism "-cidal" agents kill the pathogen bacteriostatic agents normally rely on a healthy immune system, where they can boost immune function; whereas bacteriocidal agents may be needed especially in immunodeficient pt's |
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| narrow-spectrum antibiotics |
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| only affect certain classes (e.g. Gram-positive bacteria, or anaerobic bacteria) |
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| broad-spectrum antibiotics |
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| effective against many types of pathogens (usually bacteria) (e.g. both Gram-positive & Gram-negative bacteria) |
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| What are some situations when broad-spectrum antibiotics might be especially useful? |
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| life-threatening situations (before being able to identify a more specific sensitivity treatment), or in prophylaxis pre-surgery |
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| prophylaxis |
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| prevention of or protective treatment for disease |
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| Kirby-Bauer (aka KB testing, aka disk diffusion) |
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| a test which uses "wafers" containing antibiotics to judge the susceptibility of a certain pathogen (bacteria) to relevant antibiotics; this is a qualitative test the circles of poor bacterial growth ("zones of inhibition") around some of the wafers indicate antibiotic susceptibility in general, larger zones correlate with smaller MIC |
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| Minimum Inhibitory Concentration (MIC) |
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| a quantitative (#) measurement of the minimum antibiotic required to inhibit/prevent bacterial growth MIC < or = MBC |
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| Minimum Bactericidal Concentration (MBC) |
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| a quantitative (#) measure of the minimum concentration of antibiotic required to kill 99.9% of the patient's bacterial isolate; used to determine treatment regimens for life-threatening infections (e.g. meningitis) MBC is an extension of MIC |
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| Antimicrobial Serumcidal Concentration |
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| similar to MBC a quantitative (#) measurement of the minimum antibiotic required to kill a patient's isolate in their serum sample; this informs a patient-specific therapy |
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| How would an antibiogram be helpful to a clinician or to a public health advocate? |
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| antibiograms provide information (in table form) about antibiotic susceptibility and resistance trends of commonly used antibiotics, at a certain hospital these published reports are designed to help minimize resistance spread and provide cost-effective antibiotic use (b/c they list dose $ prices) |
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| How is effective chemotherapy limited by abscess formation? |
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| abscesses are low O2, low blood perfusion, so drugs may not be able to penetrate tissue necrosis favors replication of anearobic organisms effectiveness of the host immune system (phagocytes, antibodies, sulfonamides) is also limited the slowed-growth of the pathogens means drugs won't be as effective |
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| antibiotics ; host immune system |
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| ideally, antibiotic agents should not harm the patient's immune system antimicrobials generally work best in the presence of an intact immune system drugs can't do it all |
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| superinfection |
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| develop one infection on top of another (e.g. vaginal yeast infection) this can be a limitation on the effectiveness of chemotherapy, since normal flora which were normally suppressed may be able to spread |
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| chemoprophylaxis |
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| administration of a drug to a patient who is not infected but who is at increased risk of acquiring infection (e.g. erythromycin/tetracycline drops for prevention of opthalmia neonatorium, aka neonatal conjunctivitis) |
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| When is chemoprophylaxis justified? (list some) |
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| (1) prevention of neonatal conjunctivitis, (2) for travelers facing malaria, (3) prevent Strept. In heart disease pt's, (4) against bacterial endocarditis in surgical procedures, (5) pre-surgery, (6) immunocompromised patents such as HIV, (7) UTI's, (8) animal and human bite wounds, (9) post-exposure to HIV, TB, or meningitis, (10) pre- and post-exposure in biological warfare |
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| What are some exaples of when chemoprophylaxis is not justified? |
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| (1) just to prevent secendory pneumonia in influenza, (2) just for clean surgery which does not cross mucosal surfaces, (3) just because patient insists on antibiotics for them or their children |
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| What are the five major classes of antibacterial chemotherapy drugs? |
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| (1) metabolic analogs - e.g. sulfa drugs (2) cell wall synthesis inhibitors - e.g. penicillins ; cephalosporins (3) cell membrane agents - e.g. Polymyxin B ; E (4) nucleic acid synthesis inhibitors - e.g. Rifampin (5) protein synthesis inhibitors - e.g. erythromycin ; tetracyclin |
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| TMP-SMX |
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| a combination therapy of trimethoprim and the sulfa drug sulfamtheoxazole used for uncomplicated UTIs and as the backbone therapy for pneumocystis jiroveci in HIV/AIDS (can be dually classified as metabolic analogs and DNA synthesis inhibitors) |
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| How do penicillins and cephalosporins work as chemotherapy drugs? |
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| by inhibiting the cross-linking of peptidoglycan in bacterial cell wall synthesis |
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| buy AT 30 SSCCELL at 50 |
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| 30S ribosome inhibitors = AT = aminoglycosides ; tetracyclines 50S ribosome inhibitors = SSCCCELL = streptomycin, streptogramins, chloramphenicol, clindamycin, clarithromycin, erythromycin, linezolid, lincomycin |
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| Dr. Spock and Mrs. Very against Strept |
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| Streptogramins (e.g. Synercid) used against: vancomycin-resistant enterococci (VRE) methicillin-resistant Staphylococcus aureus (MRSA) drug-resistant Streptococcus pneumoniae (DRSP) |
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| What protein synthesis inhibitors are used against intracellular bacteria, malaria, and as an anti-inflammatory? |
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| tetracyclines, minocycline, doxycycline, oxytetratcycline |
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| MRSA muppets |
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| mupirocin used topically to eliminate nasal carriage of staphylococcus aureus (esp. MRSA) |
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| GET on the MET |
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| metronidazole effective against anaerobic bacteria and certain protozoans giardia lamblia entamoeba histolytica trichomonas vaginalis |
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| Foxy Lady, Stop Gyrating! |
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| "floxacins" like ciprofloxacin and norfloxacin are used for UTIs (and lower respiratory tract infections) b/c they inhibit DNA packaging by DNA gyrase and promote cleavage of bacterial DNA |
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| Poly doesn't want a cracker |
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| Polymyxin B (neosporin) and Polymyxin E (colistin) are only used topically for skin, ear, and eye infections |
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| 5-FC 5 fungi before Christ |
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| 5-fluorocytosine is a cancer chemotherapeutic agent that inhibits nucleotide synthesis and interferes with fungal enzymes, also used for cryptococcal meningitis in AIDS patients |
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| What drugs affect fungal sterolsPIZAZ MAT |
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| polyenes (e.g. amphotericin B, nystatin) imidazoles & azoles (e.g. ketoconazole) morpholines (e.g. amorolfin) allyalmines & thicarbamates (e.g. terbinafie) |
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| Fluke AIDS patient |
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| fluconazole used for cryptococcal meningitis in AIDS patients, by inhibiting fungal sterol synthesis |
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| Tiny Turbo Ringworm infection |
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| terbinafine used for tinea ringworm infections (and onychomycosis) |
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| synergism |
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| 1 + 1 = 16 |
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| additive |
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| 1 + 1 = 2 |
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| antagonism |
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| 1 + 1 = 0.5 may be due to competition for a binding site or drug-drug interactions, opposing effects (e.g. tetracycline & penicillin) |
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| indifference |
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| 1 + 1 = 1 |
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| When would combination chemotherapy be used? |
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| polymicrobic infection, to cover both aerobes & anaerobes, to enhance -cidal activity (synergism), to decrease doses of a toxic drug (additive or synergistic), life-threatening infection (full coverage), or to decrease risk of emergent resistance |
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| Riffman Hibernates |
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| Rifampin used to treat carriage of Hib and meningococcus, also MTB therapy; works b/c inhibits mRNA synthesis via DNA-dependent RNA polymerase |
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| drug efflux pump |
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| used by bacteria to avoid antibiotics the drug is actively pumped out of the cell, faster than it enters |
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| auxotroph |
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| organism that is unable to synthesize a particular organic compound e.g. yeast mutant with an inactivated uracil pathway e.g. auxotrophic humans must obtain vitamins and essential amino acids via diet |
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| tolerance |
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| a mechanism of bacterial resistance where there is no change in MIC but MBC is high; a rare phenomenon but may become more common in the future |
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| phenotypic tolerance |
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| evasion of killing by depression of bacterial growth rate |
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| genotypic tolerance |
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| evansion of killing by depressed production of murein (peptidoglycan) hydrolases |
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| What are some ways in which bacteria exhibit resistance to antimicrobial agents? |
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| (1) by altering the drug target site, (2) by preventing access of the drug to the target site, (3) by inactivating or destroying the drug, (4) by protecting the target site, (5) by overproducing the target, (6) bypassing antibiotic inhibition, (7) by developing tolerance |
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| What are examples of bacteria altering the target site of antimicrobial drugs? |
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| altering penicillin binding proteins (evades penicillin) altering DNA gyrace (evades fluoroquinolones) altering dihydrofolate reductase (evades trimethoprim) |
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| How do bacteria commonly acquire resistance? |
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| by mutation by destruction and/or inactivation of the drug by efflux of the drug |
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| capsule |
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| the "slimy football jersey" of bacteria => when a phagocyte tries to eat the bug, it can slip away bacterial cell capsule is a very large structure consisting largely of polysaccharides that lies outside the cell wall of bacteria; it is not easily washed off and can cause various diseases, a virulence factor some bacteria have capsule that resembles host polysaccharide, and this type of capsule is not immunogenic |
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| What do virulence factors enable bacteria to do? |
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| virulence factors are secreted by pathogens (bacteria, viruses, fungi, and protozoa) that enable them to: (1) adhere to and colonize a niche in the host (2) evade host immune response (3) suppress host immune response (4) enter/exit cells (5) obtain nutrition from host |
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| mucin |
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| mucin glycoproteins are the main component of the first barrier that bacteria encounter in the intestinal tract bacteria get stuck to the mucin because they have mucin-binding receptors, but some bacteria do not and others have enzymes to degrade mucin (virulence) |
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| defensins |
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| small cationic proteins found in (in)vertebrates that act as natural bactericidal proteins (also act against fungi and some fungi) defensins create pores in bacterial membranes, then diffuse through peptidoglycan to reach the cytoplasmic membrane (note: endotoxin/LPS binds to defensins, preventing them from reaching cytoplasm) |
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| sIgA |
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| secretory IgA is the main immunoglobulin found in mucous secretions (e.g. tears, saliva), protects against degradation from proteolytic enzymes sIgA contributes to mucin, making it stickier and simultaneously bingding bacterial antigens however, bacteria produce enzymes that cleave IgA, breaking the link between bacteria and mucin |
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| adhesins |
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| cell-surface components/appendages that facilitate bacterial adhesion/adherence to other cells or to inanimate objects; they are a type of virulence factor protein adhesins = fimbriae, pili, afimbrial, flagella, S-layer polysaccharide adhesins = cell wall, capsule |
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| S-layer |
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| part of the cell envelope that encloses the whole cell surface, resembles a tiled surface; can function as adhesins in Gram-negative bacteria, S-layers are associated with endotoxin/LPS, protect against complement and phagocytosis |
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| What kinds of signal transduction occur after adhesion of bacterial pili/fimbriae? |
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| activation/repression of virulence genes in the bacteria; or altering gene expression in the host |
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| pili |
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| rod-shaped, hair-like structures on surface of bacteria important for adherence, attach specifically to receptor, first initial "loose" contact, wait for tighter adherence important for conjugation, gene exchange mostly in Gram-negative bacteria pili are constantly lost and reformed, allowing altered antigenicity (see "fimbria") |
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| fimbria |
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| (see pili) |
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| Which would form a tighter adhesion - fimbrial or afimbrial? |
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| afimbrial |
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| LPS |
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| in Gram-negative cell walls LPS triggers an innate immune response characterized by cytokine production and inflammation, possibly leading to septic shock |
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| cytokines |
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| small cell-signalling proteins secreted from numerous cells in the body (unlike hormones), immunomodulating agents |
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| How do bacteria acquire iron to survive in the body? |
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| some use siderophores, which chelate iron complexes in the blood, internalizing it inside the bacteria to be cleaved others bind and remove iron directly from host's transferrin and/or lactoferrin bacterial toxins kill cells, releasing iron finally, some bacteria exhibit "iron abstinence" or use substitute metals (e.g. Borrelia burgdorferi uses manganese) |
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| What is necessary for extracellular invasion of a host cell by bacteria? |
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| enzymes: elastase degrades extracellular molecules hyaluronidase cleaves proteoglycans streptokinase ; staphylokinase break down fibrin clots lipase degrades host oils nuclease digests RNA/DNA haemolysins lyse RBCs |
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| What pathogens have obligate intracellular lifestyles? |
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| Chlamydia spp. Rickettsia spp. Mycobacterium lepra Mycobacterium tuberculosis would be a factultative intracellular one, and it persists for years inside host |
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| Type III secretion |
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| a common strategy for pathogens to induce uptake into a host cell bacterial signalling proteins get injected into the cell, activating host to internalize the microbe e.g. Salmonella spp. ; Shigella spp. |
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| What three locations (intracellular niches) do bacteria generally inhabit while inside the cell? |
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| (1) phagolysosome - e.g. Coxiella burnetti, (2) phagosome - e.g. Chlamydia ; Salmonella, (3) cytosol - e.g. Shigella ; Rickettsia ; Listeria |
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| flavohemoglobin |
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| convert nitric oxide into NO3-, normally in the respiratory system E. coli bacteria use this enzyme to develop resistance to nitric oxide (NO) |
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| O antigen |
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| the presence of O antigen determines whether LPS is considered "rough" or "smooth", affects hydrophobic/hydrophilic nature in Neisseria gonorrhoeae, a sialic acid is bound to the O antigen, which helps evade host immune response |
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| How do bacteria evade the antibodies of host immune response? |
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| they can alter their pilus proteins, they can generate capsule which resembles host molecules, or they can coat themselves with host proteins such as firbonectin (which bind to the Fc portion of the antibodies, but do not lead to opsonization of bacteria =; no complement activation) |
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| two component signal transduction systems (TCSTSs) |
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| bacterial systems which detect external signals and direct the organism to make a response typically they have (1) a sensor protein and (2) a response regulator, which can either increase or prevent transcription of a gene involved in regulating many diverse cellular functions (incl. chemotaxis, quorum sensing, toxins, virulence) |
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| T/F: in bacteria, transcription and translation occur in the same compartment so protein formation can occur immediately as soon as transcription starts |
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| 1 |
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| shine-dalgarno sequence |
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| a ribosomal binding site in the mRNA, generally located 8 basepairs upstream of the start codon AUG in E. Coli, the sequence is "AGGAGG" participate in the formation of a polysome |
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| polysome |
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| a cluster of ribosomes, bound to a mRNA molecule |
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| operon |
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| a functioning unit of genomic DNA w/ a cluster of genes all under the control of a single regulatory signal or promoter helps speed and coordinate bacterial response/adaptation |
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| polycistronic |
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| a single mRNA can code for several different proteins |
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| bacterial mRNA vs. eukaryotic mRNA |
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| single compartment vs. nucleus-cytoplasm unstable vs. stable for several hours both have coding and non-coding regions eukaryotic is transcribed from DNA first 5'3' of triphosphate P-P-P ; last base vs. 5'3' of methylated cap ; poly-A tail |
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| regulons |
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| collections of genes or operons under regulation by the same regulatory protein (e.g. vir regulon of Streptococcus Pyogenes under activator Mga) multiple regulons can form a modulon |
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| sigma factor |
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| binds to core RNA polymerase, helping the core enzyme to recognize the promoter; sigma factor synthesis helps bacteria regulate gene expression once transcription is initiated, the sigma factor is released and can attach to another core polymerase |
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| what are some examples of sigma factors in action? |
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| sigma-38 helps regulate nutrient deprivation, oxidative and osmotic stress in Salmonella, E. coli, and Pseudomonas Aeruginosa sigma-32 is a heat shock protein important in the regulation of virulence of Vibrio cholerae |
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| terminator sequence |
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| lies just 3' to the stop codon short inverted repeats form a hydrogen-bonded, stem-loop structure that causes RNA polymerase to pause/stop transcription |
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| active repressors |
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| interfere with RNA polymerase, turning transcription off |
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| inducers |
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| bind to and block repressor molecules, turning transcription ON |
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| activators |
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| bind directly to specific sequences adjacent to the promoter site or directly to RNA polymerase, to promote gene transcription (e.g. cAMP receptor) |
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| co-repressors |
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| native repressors have no affinity for the operator site, so the default mode of gene transcription is ON, but when a co-repressor binds to the repressor, this actually leads to repression of gene transcription (e.g. trp operon) |
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| accidental gene rearrangements |
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| e.g. repair, mutation, transposition, plasmid, phage, foreign DNA |
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| programmed gene rearrangements |
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| are part of a genetic program, largely predictable genes must be moved to an active "expression locus" repeating the program over and over is the source of consistent antigenic variation e.g. amplification, deletion, assembly of genes from gene segments e.g. moving a gene from silent storage to an active site |
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| silent genes |
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| must be moved to an active site where transcription and translation occur before they can express 'new gene' |
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| Phase variation |
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| switches on/off the expression of some component, like surface proteins |
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| Antigenic variation |
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| alters the antigenic nature of component such as surface proteins |
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| DNA inversion |
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| a type of phase variation for gene expression vvv = ON. ^^^ = OFF. |
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| slipped-strand mispairing |
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| a type of phase variation for gene expression strand slippage leads to frame shift, premature termination, truncated protein product |
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| DNA recombination |
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| a type of antigenic variation for genes uses homologous recombination to "suffle" the antigenic make-up of product (e.g. type IV pilus of N. gonnorhoeae) |
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| Point mutations |
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| a type of antigenic variations for gene expression simple mutations can give rise to antigenic variants no longer recognizable to host immune system (e.g. HIV & influenza A virus) |
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| Epigenetic variation |
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| a type of antigenetic variation where variation occurs in the phenotype of the organism, but not the genotype (e.g. methylation of surface structures) |
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| antigenic drift |
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| hugh mutation rates associated with viruses, produces variants, some of which may not be reactive to antibodies anymore (virulence) |
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| antigenic shift |
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| large scale change in a particular pathogen now, prior exposure will yield no beneficial sensitivity advantage b/c the pathogen appears as "new" (e.g. influenza pandemics of 1918) |
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| plasmids |
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| are non-chromosomal/extrachromosomal genetic elements that usually encode traits that are not essential for viability and replicate independently of the chromosome, most are supercoiled & linear cell-to-cell transfer, direct contact = conjugation intentional uptake of "naked" gene = transformation => horizontal gene transfer |
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| copy number |
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| the average number of molecules of a given plasmid per bacterial chromosome is called its copy number smaller plasmids usually are nonconjugative, and have high copy numbers large plasmids are often conjugative, have small copy numbers, carry other genes as well as the operon, and code for all functions required for their replication |
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| vector |
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| a DNA molecule used as a vehicle to transfer foreign genetic material into a cell the four major types of vectors are plasmids, viruses, cosmids, and artificial chromosomes |
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| conjugative plasmids |
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| mediate conjugation, usually large, autonomous replication and transfer of DNA to recipient (e.g. genes for sex pilus) |
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| nonconjugative plasmids |
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| do not mediate conjugation, usually smaller, they lack one or more of the genes needed for transfer of DNA |
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| F-factor |
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| a conjugative plasmid that controls sexual functions of bacteria the first episome discovered |
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| col factor |
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| aka bacteriocinogenic plasmids code for substances that kill other bacteria (bacteriocins or colicins) |
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| R-factors |
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| aka resistance plasmids carry antibiotic resistance genes |
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| degradative plasmids |
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| enable the digestion of unusual substances |
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| virulence plasmids |
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| turn the bacterium into a pathogen (e.g. siderophores for iron uptake, toxins) |
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| What is the medical significance of plasmids? |
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| they control many important properties of pathogens (resistance, toxin production, adherence, colonization) and compairing profiles can help identify pathogens epidemiologically |
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| exotoxins |
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| toxic bacterial proteins found in both Gram-positive and Gram-negative bacteria important for survival and propagation (e.g. evasion or iron acquisition) but some toxins have no known benefit (e.g. botulinum toxin) some have been used in vaccines, some used in treatment |
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| T/F: toxin genes are not normal components of the bacterial genome |
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| TRUE (for many bacteria) carried in on bacteriophages (e.g. diptheria toxin) or found on plasmids from other bacterial species |
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| 1-2-3 … SMAB! |
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| Type I toxins = Superantigens Type II toxins = Membrane-acting Type III toxins = A-B toxins |
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| cytokine storm |
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| Type I toxins bind to MHC and receptors on T cells to stimulate a super-normal immune response of excessively high levels of IL-2 cytokines (e.g. toxic shock syndrome toxin from Staph. Aureus) |
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| pore-forming cytotoxins |
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| Type II toxins that insert into host membrane and make an open channel, swelling and rupture |
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| enzyme cytotoxins |
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| Type II toxins that destabilize host cell membrane, by removing charged groups on phospholipids or cleave at other sites (e.g. Staph. Aureus alpha-hemolysin used to kill host phagosomes) |
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| How do A-B toxins exert effect? |
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| B subunit binds to membrane receptor, then translocates the A portion into the host cell, catalyzing an ADP-ribosylation reaction which either inactivates or damages the host cell protein (e.g. diptheria toxin does this to elongation factor EF-2) |
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| diptheria toxin |
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| a Type III A-B toxin that targets heparin-binding epidermal growth factor (HB-EFG) to inactivate enlongation factor EF-2, stopping protein synthesis => diptheria involves damage to heart & neurological symptoms (difficulty swallowing) |
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| botulinum toxin |
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| a Type III A-B toxin that does not involve colonization, but rather intoxication, targets neurons and peripheral nerve endings, blocking Ach release, causing => generalized "flaccid paralysis" where muscles don't get stimulated, atrophy (e.g. food-borne botulism) |
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| Which type of botulinum toxin is used off-label for cosmetic treatment of wrinkles? |
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| C1 = botox C2 and C3 = are less toxic |
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| tetanus toxin |
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| a Type III A-B toxin that targets the CNS, blocking the release of inhibitory interneurons that would normally be responsible for relaxing muscles after contraction =; tetanus "lockjaw" is a spastic paralysis, constant contraction |
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| zinc-requiring endopeptidases |
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| cleave a set of proteins called "synaptobrevins" that are normally found in synaptic vesicles of neurons responsible for release of neurotransmitter and inhibitory mediators botulism ; tetanus toxin share a considerable amount of genetic similarity to the enzymes that cleave these proteins |
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| Why do botulinum toxin and tetanus toxin cause such different effects? |
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| botulinum toxin targets peripheral neurons; while tetanus toxin acts on the CNS |
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| alpha-toxin |
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| a Type II membrane-disrupting toxin that targets many cell types, hydrolyzing the lipid "lecithin" and has phospholipase activity =; kills host cells and causes tissue damage (aka gangrene) w/ an expanding zone of dead tissue |
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| toxic shock syndrome toxin (TSST) |
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| a Type I superantigen toxin that targets T cells and macrophages =; causes nonspecific binding of T cells and macrophages; elicits cytokine production by T cells, which help produce fever and other symptoms of toxic shock syndrome |
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| Pasteurellosis toxin |
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| a Type III A-B toxin that binds ganglioside receptors and enters cells via endocytosis, turns on G protein permanently, disrupting hormone regulation of cellular activities =; causes bone loss, weight loss, destruction of lung |
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| biofilms |
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| collection/mixture of microorganisms (bacteria, fungi, and/or protozoa, with associated bacteriophages and other viruses) embedded in a polysaccharide matrix, which is secreted by one or more member(s), attached to a solid biologic or non-biologic surface |
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| T/F: more than 99% of all bacteria live in biofilm communities |
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| 1 |
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| extracellular polymeric substances (EPS) |
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| slimy substance secreted into biofilms to facilitate attachment and matrix formation and to become irreversibly attached (permanent adherence) |
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| how is microorganism behavior more complex in a biofilm community? |
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| they break down complex nutrients by pooling their biochemical resources; they alter their phenotype (growth rate, gene regulation); and they demonstrate enhanced survival with nutrition availability, defense mechanisms, resistance to physical force, evasion of phagocytosis ; antibiotics ; disinfectants |
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| conditioning layer |
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| in the first attachment phase of a biofilm life cycle, a sediment of organic molecules help to form a "conditioning layer" on the biofilm surface; the first colonists are usually bacteria |
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| how can biofilms propagate? |
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| biofilms can spread around and creep along a surface they can propagate through detachment of clumps or by a type of "seeding dispersal" that releases individual cells |
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| T/F: the susceptibility of biofilms to antimicrobial agents can be determined by MIC/MBC |
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| FALSE!!!!!! These tests rely on the response of planktonic ("free") microorganisms rather than biofilm-associated ones |
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| how do biofilms affect chronic wounds? |
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| they prevent wound healing biofilms are especially found on many medical devices and pieces of hospital equipment such as catheters, prostheses, heart vales, shunts, dental implants, ventilators, hemodialysis machines, etc. |
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| What are the ways in which biofilms are intrinsically resistant to antimicrobials? |
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| it's difficult for drugs to diffuse through the EPS matrix ("capsule"); biofilms have a lower growth rate, minimizing the rate that antimicrobial agents would be taken in effectively; and the environment surrounding biofilms may provide further protection |
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| Why make biofilms? |
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| prevents detachment, stay in a favorable niche, more opportunities for gene exchange, more cell-to-cell communication and/or cooperation, more exposure to moving water, more nutrient adsorption; plus defense against mechanical force, predation, and immune response |
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| What are some "good biofilms"? |
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| in earth's sediment and bedrock, there are recycling elements and leaching minerals and soil-forming bacterial biofilms that help; there is mutual exchange of nutrients among plant roots and microbes; and we could use bioremediation in sewage treatment and/or toxic waste sites |
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| quorum sensing |
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| (listen to audio) |
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| Does direct testing involve cell culture? |
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| NO. direct testing involves microscopic (e.g. gram stain) and macroscopic (e.g. agglutination) techniques to get rapid identification of a pathogen |
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| agglutination |
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| the aggregation by antibodies of suspended cells or similar-sized particles (agglutinogens) into clumps that settle (immunological/serological method of pathogen identification, where epitope + Ab = clumps) |
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| immunoassay |
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| extremely sensitive tests that permit rapid and accurate measurement of trace Ag or Ab (incl. RIA, ELISA, EIA) |
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| thioglycolate |
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| selective media for anaerobic bacteria (e.g. Clostridium, Bacterioides) |
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| chocolate agar |
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| selective media for fastidious organisms (e.g. Haemophilus) |
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| Thayer-Martin media |
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| selective media for Neisseria addition of antibiotics kill off other organisms |
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| Blood agar |
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| differential media that differentiates b/w alpha, beta, and gamma hemolysis of Streptococcus |
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| MacConkey media |
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| both selective and differential media, used a lot for Salmonella ; Shigella |
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| Eosin Methylene Blue (EMB) |
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| both selective and differential media, produces metallic green sheen for lactose-positive |
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| How is phage typing used to identify pathogens? |
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| only certain kinds of phages infect certain bacteria this method is good for outbreak scenarios, identify down to subspecies |
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| Western Blot |
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| a procedure for separating and identifying Ag or Ab mixtures by electrophoresis in polyacrylamide gel, followed by immune labeling identifies specific antigen, detects proteins |
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| complement fixation |
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| immunological method of testing for certain antibodies or specific antigen uses Ab + Ag + complement + sheep RBC |
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| ELISA |
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| enzyme-linked ammuno-sorbent assay a very sensitive serological test used to detect Ab's in such diseases as AIDS |
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| Why would you order immunoelectrophoresis? |
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| this test can detect disorders in Ab production serum samples are electrophoresed, then proteins are reacted with antibodies, diffuesion produces arc pattern representing major serum components |
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| PCR |
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| polymerase chain reaction specific DNA gene amplification |
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| why is DNA hybridization called "checkerboard hybridization"? |
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| large DNA samlpes are hybridized against large numbers of DNA probes on a single support can identify bacterial species contained in a sample with many species |
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| RFLP |
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| restriction fragment length polymorphism aka "DNA fingerprinting" where DNA is digested, fragmented, electrophoresed, labeled probes => only a few strains will be genetically similar |
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| PFGE |
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| pulsed-field gel electrophoresis large segments of DNA separated by rotating the electric field, does not require special fluorescent dyes good for when you have a lot of DNA |
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| RIA |
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| radioactive isotope label used in immunoassays, very sensitive |
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| indirect ELISA |
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| detects the Ab to a specific Ag w/ radioactive labels or enzyme labels |
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| captured ELISA |
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| detects the Ag w/ radioactive labels or enzyme labels |
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| what is the goal of most genome projects? |
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| to produce a finished contiguous DNA sequence of the chromosome (or genome) |
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| ORF |
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| open reading frame any stretch of codons (longest) that does not contain chain termination (STOP) codon |
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| what is the challenge now facing scientists studying genomics/bioinformatics? |
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| how to organize and catalog the vast amount of information, interpret large amounts of information into a usable form (e.g. identifying and characterizing genes or identifying the combination of genes that make an organism pathogenic) |
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| is bioinformatics studied in vivo or in vitro? |
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| in vitro it's biologically-derived information, statistical analysis |
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| in silico |
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| using computers to carry out biological experiments virtually allows researcher to look at the bigger picture |
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| what are the three components of basic genomic information? |
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| gene content gene organization gene dynamic (e.g. horizontal gene transfer in bacteria) |
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| pan-genome |
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| the entire gene pool for a pathogen sp. (incl. genes that are not shared by all strains) core = all strains dispensable = more than 1 strain-specific = only 1 |
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| transposons |
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| segments of DNA that can move/jump within a genome/plasmid, propagation depends on physical integration with a genome replicon (unlike plasmid) in the process, they may cause mutation or decrease the amount of DNA in genome (aka mobile genetic elements or "jumping genes") |
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| what is the simple structure of a transposon's insertion elements (IS)? |
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| simple structure of a transposon includes a gene producing an enzyme that catalyzes insertion, a repeated sequence ("inverted terminal repeat") marking the end of insertion, and a short stretch of genomic DNA ("target site repeat") that's repeated on either side of the insertion element |
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| Copy + Paste mechanism |
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| first transcribe the DNA into RNA then use reverse transcriptase to make a DNA copy of the RNA to insert to a new location as opposed to the Cut + Paste mechanism where DNA moves directly from place to place |
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| 1,2,3 = Classy Retro hairCUT MINI-me! |
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| Class I transposons = RETROtransposons (copy + paste mechanism) Class II transposons = (CUT + paste mechanism) Class III transposons = Miniature Inverted-repeats Transposable Elements (aka MITEs) |
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| transposon mutagenesis |
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| transposons that carry a selectable marker (such as antibiotic resistance) have been used to make random mutations in the genome of a pathogen; the mutant is screened for loss of virulence |
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| pathogenicity islands (PAIs) |
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| genomic islands acquired by horizontal gene transfer which collectively contribute to virulence of the pathogen; similar to transposons in that they carry functional genes associated with tRNA genes, targets for DNA integration high in C's and G's found mainly in Gram-negative, but a few Gram-positive e.g. adhesins, toxins, iron uptake systems, invasins, etc. |
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| SNPs |
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| single nucleotide polymorphisms are small genetic changes, sources of variation within a person's DNA sequence serve as biological markers ("SNP profiles") |
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| microarrays |
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| analyze host and microbe gene expression during infection to tentatively identify the genes whose expression is turned on (or off) under certain conditions; the array is hybridized with mRNA, DNA or cDNA from the organism grown under different conditions; can help identify expression of virulence factors advantage = largen number of genes in small space |
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| hybridization probing |
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| a technique that uses fluorescently labelec nucleic acid molecules as "mobile probes" to identify complementary molecules (sequences that are able to base-pair with one antoher) |
