Micro, Ass 3, Renee’s Questions

1.     What is a broad spectrum antibiotic?
1.     one the is active against several types of microoorganisms
2.     What is an antibiotic that is active against one or a very few types or microorganisms?
2.     Narrow spectrum
3.     What type of antibiotic inhibits bacterial growth but does not kill?
3.     Bacteriostatic
4.     When bacteriostatic drugs are withdrawn can bacteria continue to grow?
4.     yes
5.     How do most bacteriostatic drugs inhibit growth?
5.     inhibit protein synthesis
6.     What type of antibiotic kills bacteria?
6.     Bactericidal
7.     Why are bactericidal drug actions inhibited by a –static drug?
7.     requires bacterial growth in order to impair
8.     What are some advantages to –cidal drugs?
8.     Reduces the number of bugs, more rapid, irreversible damage to bugs
9.     What is a disadvantages of –cidal drugs?
9.     cytotoxic storm
10.  What do –static drugs prevent that give them an advantage?
10.  inhibition of bacterial toxins and inflammatory mediators
11.  T/F Two static drugs can be used in combination to kill a pathogen.
11.  T – if mechanism is in different part or completely different pathways
12.  T/F The same antibiotic may be cidal or static against different bacteria.
12.  T – Ex. Penicillin – cidal a pneumococci, static a enterococci
13.  What is the lowest concentration of drug that inhibits the growth of the organism called?
13.  Minimal Inhibitory Concentration (MIC)
14.  What are the 2 options for MIC testing?
14.  Turbidity and Viability
15.  How is Turbidity used to determine the MIC?
15.  Determined by growing organism in tubes then adding various concentrations of drugs, lowest concentration tube where broth is clear.
16.  How is Viability used to determine the MIC?
16.  Preinoculate blood agar plate then place antibiotic discs, allow to grow then determine zone of inhibition, diameter is compared to standards to determine sensitivity of the organism to that drug.
17.  What is the Minimal Bactericidal Concentration (MBC)?
17.  Concentration of drug that actually kills the organism rather than the concentration that merely inhibits growth
18.  How is the MBC determined?
18.  transfer clear broth tube to blood agar plate, MBC is the plate without growth
19.  What type of drugs have an MBC equal or very similar to the MIC?
19.  Bacteriocidal
20.  What is the relationship of MBC to MIC in Bacteriostatic drugs?
20.  The MBC is significantly higher than MIC
21.  T/F MIC and MBC concentrations can be used to compare effectiveness of an antibiotic.
21.  F – Effectiveness is based on how much of the drug you can actually administer to the patient
22.  What 5 differences can antibiotics target in bacterial cells?
22.  Cell wall synthesis, Cell membrane, DNA replication + Nucleotide Biosynthesis, Topoisomerases, Protein Synthesis
23.  What type of antibiotics target the crosslinking in bacterial cell walls?
23.  Penicillin, Cephalosporins, Carbapenems, Monobactams
24.  What do Peptide antibiotics target? what are 2 examples?
24.  Cell membrane; Polymyxins, Daptomycin
25.  What drugs target DNA replication and Nucleotide Biosynthesis?
25.  Metronidazole, Sulfonamides, TMP-SMX
26.  What do Quinolones target?
26.  Topoisomerase
27.  What drug targets DNA-directed RNA polymerase?
27.  Rifampin
28.  What causes an overgrowth of drug resistant strains of Clostridium difficile? What is this called?
28.  complication of antibiotics due to suppression of the normal flora of the bowel; Pseudomembranous Colitis
29.  What are the normal cell wall hydrolyzing enzymes?
29.  autolysins
30.  How do autolysins participate in killing the cell when peptidoglycan synthesis is inhibited?
30.  autolysins activity continues without a new unit to insert and cell will eventually lyse in hypotonic environment.
31.  What type of enzyme is Penicillin Binding Proteins?
31.  transpeptidase
32.  What does transpeptidase do?
32.  catalyzes the final crosslinking step in the synthesis of peptidoglycan
33.  What does Penicillin do?
33.  Irreversibly binds at the active site of the transpeptidase enzyme that cross-links the peptidoglycan strands. inhibiting cross-linking
34.  What are 3 ways resistance may develop?
34.  1. Production of penicillinases or ?-lactamases; 2. Mutated PBP, so penicillin can’t bind 3. develop tolerance – inactivation of autolysin
35.  What are ?-lactam antibiotics structural analogs of?
35.  D-Ala-D-Ala end of peptidoglycan pentapeptide
36.  What are 4 problems with Penicillin G?
36.  1. Hydrolysis by gastric acid; 2. Penicillinase sensitivity; 3. Allergic response; 4. Ineffective against gram neg. enterics
37.  What is the breakdown product of penicillin that can be used to elicit different drug properties?
37.  6 aminopenicillanic acid (6-APA)
38.  Which Penicillin has the highest activity against G+ cocci and bacilli?
38.  Narrow spectrum penicillins
39.  What are examples of Narrow spectrum penicillins?
39.  G and V
40.  What are Broader Spectrum Penicillins affective against?
40.  G+ and G- enteric bacilli
41.  What are some examples of Broader Spectrum Penicillins?
41.  Ampicillin, Amoxicillin, Cyclacillin, Carbenicillin, Ticarcillin.
42.  What drugs are considered the Antistaphylocococcal Penicillins? Examples?
42.  Narrow Spectrum/Penicillinase Resistant Drugs; Methacillin, Nafcillin, Oxacillin, closacillin, dicloxacillin
43.  What drug has a similar structure and mechanism of action identical to penicillin?
43.  Cephalosporins
44.  How do cephalosporins differ from penicillins?
44.  acid stability, penicillinase resistance, antigenically dissimilar
45.  What is the progression of 1st to 4th generation cephalosporins?
45.  broadening in G- susceptibility; diminution of activity against G+; increased ?-lactamase resistance; increased capability to enter CSF
46.  What oral cephalosporin is affective against Gram + cocci (staph & strep)?
46.  Cephalexin (Keflex)
47.  What has rendered many 2nd and 3rd generation cephalosporins inaffective?
47.  Extended Spectrum ?-Lactamases
48.  What type of antibiotic crosses the blood brain barrier and is effective against Enteric G- bacteria?
48.  3rd Generation – Ceftriaxone
49.  What antibiotic is effective against E. Coli?
49.  4th Generation – Cefepime
50.  What in Carbapenems allows movement through the outer membrane of G- bacteria?
50.  small hydroxyethyl side chain
51.  What is the structure of the Carbapenems?
51.  ?-lactam ring attached to five-membered cyclic ring with carbon
52.  What are Carbapenems highly resistant to?
52.  ?-lactamases
53.  What are 3 examples of Carbapenemases?
53.  KPC, OXA, Metallo-?-lactamases
54.  How do the carbapenems create Resistance?
54.  altered porin channes decreasing permeability
55.  What type of antibiotic can be used in penicillin allergic patients?
55.  Monobactams
56.  What is the drug of choice for MRSA?
56.  Vancomycin
57.  What was the first strain to show resistance to Vancomycin?
57.  Enterococcus faecalis
58.  What is Vancomycin restricted to?
58.  Gram + organisms
59.  What kind of antibiotic is Streptomycin and what kind of action does it have?
59.  aminoglycoside antibiotic, Bactericidal
60.  What is an Aminoglycosides?
60.  aminosugars linked by a glycosidic bond to an aminocyclitol
61.  What kind of damage can Amionoglycosides cause to the human body?
61.  Kidney and/or 8th cranial nerve damage
62.  How do Aminoglycosides produce a –cidal mechanism?
62.  1. few streptomycin molecules enter the cell through imperfections in the growing membrane; 2. Binds to 30S ribosomal protein, distorts and causes misreading; 3. Misreading causes “bad” proteins to be made, more membrane leakiness, more streptomycin enters;
63.  How does Daptomycin (peptide antibiotic) target bacteria?
63.  Cell membrane
64.  How does it irreversibly bind to the bacterial cell membrane?
64.  calcium-dependent membrane insertion of molecule
65.  What is the mechanism of action of Daptomycin?
65.  Irreversibly binds to bacterial cell membrane, rapidly depolarizes the cell membrane, Efflux of K+, Cell death by multiple failures in biosystems.
66.  What is Daptomycin active against?
66.  G+ infections; MRSA, VRE, S. pyogenes
67.  T/F Resistance to Daptomycin is rare.
67.  T
68.  In the Lungs, what does Daptomycin bind avidly with making it ineffective against pneumonia?
68.  Pulmonary Surfactant
69.  What is an example of an antibiotic that has Nucleotide Biosynthesis activity?
69.  Sulfonamide
70.  What is the mechanism of action of sulfonamide?
70.  Blocks dihydropteroate synthetase;
71.  At what point in the synthesis of folic acid synthesis does trimethoprim inhibit?
71.  dihydrofolate reductase; DHF –Xa THF
72.  How can bacteria become resistant to Trimethoprim?
72.  mutations in DHFR
73.  How does resistance develop to Sulfonamides?
73.  slowly and stepwise
74.  What does the mixture of Trimethoprim-Sulfamethoxazole have activity against?
74.  broad spectrum activity against aerobic bacteria and pheumocystis
75.  What is a way that bacteria can thymidine to get around the inhibition of folic acid?
75.  from DNA released from dead cells in the pus of a cyst or abscess
76.  What Bacterial enzymes are a target for quinolones?
76.  DNA gyrase, Topoisomerase IV
77.  What Quinolone is most active against Gram – aerobic bacteria?
77.  Ciprofloxacin
78.  What spectrum or bacteria are Quinolones active against?
78.  G- aerobic, G- enteric rods or cocci, G+ and anaerobic
79.  How can drugs be used to attenuate protein synthesis in Bacteria while not affecting us?
79.  Bacteria have 70S R with 30S and 50S subunits, while we have 80S R with 40S and 60 S subunits
80.  What drugs are active against 30S?
80.  Aminoglycosides, Tetracyclins
81.  What does Neosporin contain?
81.  Polymyxin B Sulfate (Gram – rods, alters cell membranes), Bacitracin Zinc (Gram+), Neomycin Sulfate (broad spectrum)
82.  What is the Mechanism of Tetracycline?
82.  Inhibition of protein synthesis by binding 30S ribosome, block acceptor site, inhibiting aminoacyl-tRNA binding.
83.  What is Tetracyclin active against?
83.  gram + and gram –
84.  Why should Tetracyclin be avoided during the latter half of pregnancy and in children under 8 years?
84.  can cause permanent discoloration of the teeth and enamel
85.  What is a side effect of Chloramphenicol?
85.  penetrates human mitochondreia and inhibits mitochondrial protein synthesis, causing bone marrow depression
86.  What is a type of Macrolide Antibiotic?
86.  Erythromycin
87.  How do Macrolides terminate the peptide linking?
87.  binds reversibly at 2 sites on the 50S ribosome causing dissociation of the tRNA
88.  Which drug is one of the least toxic drugs?
88.  Erythromycin
89.  What drug was the first ketolide antibiotic and is active against most respiratory tract pathogens?
89.  Telithromycin
90.  What is a serious side effect of clindamycin?
90.  pseudomembranous colitis
91.  What antibiotic is active against Vancomycin-resistant enterococci and MRSA?
91.  Quinupristin/Dalfopristin (Synercid)
92.  What are 5 ways to reduce antimicrobial resistance to antibiotics?
92.  1. Rapid diagnosis to reduce inappropriate use
93.  What is Innate resistance?
93.  a trait of bacterial species that was present before the introduction of antimicrobial agents
94.  What is Acquired (Emergent) resistance?
94.  antimicrobial agent USE-DRIVEN selection and accumulation of resistant bacterial strains
95.  What are 2 origins of acquired resistance?
95.  New Single Mutation, Acquisition of DNA from other bacteria (Horizontal Gene Transfer)
96.  T/F Once resistant strains of bacteria are present in a population, exposure to antimicrobial drugs favors their survival.
96.  T
97.  What are the 5 principles of Antimicrobial Resistance?
97.  1. Resistance is likely to emerge
98.  Can integrons contain simultaneous resistance to several classes of antibiotics?
98.  Yes
99.  T/F the use of one antibiotic can activate the expression of a whole gene cassette.
99.  T
100.       How does antibiotic selective pressure create resistance?
100.        Cells that have an integron for resistance of a particular antibiotic will survive. Removal of that antibiotic can cause the integron to be lost because its not necessary.
101.       What is an example of an enzyme used by bacteria for drug inactivation?
101.        ?-lactamases
102.       How do altered porins in G- bacteria create resistance?
102.        decreased access to target
103.       How do altered PBP’s create resistance?
103.        Penicillin cannot bind to the cell’s altered PBP’s allowing cross-linking to occur.
104.       What other proteins can be involved in bacterial resistance to drugs?
104.        Outer membrane Proteins (OMP); Porins; PBP
105.       T/F Virtually all G- express a gene for a ?-lactamase.
105.        T – occurs at least in low levels in the periplasmic space
106.       What is the mechanism that bacteria use for tetracycline resistance?
106.        altered Efflux pumps, protection of ribosomal target sites
107.       T/F Penicillin resistance due to ?-lactamase production occurs in S. pneumonia
107.        F
108.       What do ?-lactamases target?
108.        penicillins and cephalosporins
109.       What will bind to ?-lactamases to inhibit them?
109.        Clauvanic Acid and Sulbactam
110.       What are persisters? What protects them?
110.        small number of dormant survivor bacterial without antibioticresistance mechanism; Biofilms
111.       T/F You intend on being attacked by an Octopus after Assessment 3.
111.        T – Great I’ll help you defend it

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