Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Microbiology > antibiotics and virus > Flashcards

antibiotics and virus Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards
1
Q

Ampicillin - spectrum - advantage over earlier antibiotics?

A
  • G+; and G- -> rods and cocci - advantage: ow can treat G- rods -> increased the spectrum; became very popular ampicillin = amoxycillin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe HIV entry into host cell

A

HIV virus has gp160 protein - made up of gp41 (hydrophobic region) + gp120 - gp120 binds CD4 on T cells -> conformational change occurs; and gp41 hydrophobic region is exposed - CCR-5 is recruited - tighter binding - hydrophobic region of gp41 is unstable -> inserts into plasma membrane - membranes fuse; pore is formed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe the synthesis of peptidoglycan What enzyme is used Which antibiotics interfere with this process and how?

A
  • Precursor/building blocks synthesised in cytosol and on inside of plasma membrane - building blocks have a pentapeptide bridge and a peptide chain with terminal D-ala-D-ala residues - the terminal amino acid of the pentapeptide bridge (5 of same amino acid) joins between the D-alas; knocking the terminal one off enzyme: penicillin binding proteins (PBPs) beta-lactams: bind PBPs - stop cell wall synthesis [bacteriostatic] - the buildup of building blocks activates the cell’s autolytic system -> cell lysis [bacteriostatic] glycopeptides (eg vancomycin) - bind the D-ala residues -> don’t allow binding of PBPs to occur 46.jpg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

DNA viruses - where do they usually replicate? - do they bring in a polymerase? - exceptions

A
  • in nucleus - no - just use host’s - exceptions: hepadna; has a weird replication; carries polymerase; pox - replicates in cytoplasm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

DNA viruses: - capsid types - envelope types - genome types - examples

A
  • icosahedral or complex -> no helical - naked or enveloped - can be ss or ds - parvo; papova; adeno; hepadna; herpes; pox
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Features of penicillin V - spectrum - administration - advantage over penicillin G?

A
  • G+ (rod and cocci); G- cocci - acid stable; can be given orally - advantage: can be given orally
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Fluxloxacillin - spectrum - oral efficacy - toxicity

A
  • spectrum: GPC (Staphylococcus) - oral efficiacy: good - toxicity: low
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Glycopeptides (antibiotics) - give example - how does it work - when are they used - can they be used in combination with beta-lactams - how are they administered

A
  • vancomycin; teicoplain - bind to terminal D-ala -> block peptidoglycan synthesis - used in G+ rods/cocci that are resistant to beta-lactams -> MRSA; MRSE or in patients that are allergic to beta-lactams - no - they act at earlier stage than beta-lactams -> not useful in combo - administered by injection - not absorbed from GI tract
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How are enveloped viruses released from the host cell? (2)

A
  1. Bud out from the membrane - there are patches of viral glycoproteins in the plasma membrane (put there by ER and Golgi) - capsid proteins + nucleic acid condense directly adjacent to plasma membrane - membrane surrounding nucleocapsid bulges out and nips off 2. use secretory pathway - eg coronavirus - virus particles bud into Golgi-derived vesicles - released to outside of cell when vesicle fuses with membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How are non-enveloped viruses released from the host cell?

A
  • all non-enveloped are icosahedral capsids generally there is spontaneous assembly of capsid around genome (lock in in lowest energy state) - there might need to be proteolytic cleavage for final conformation - viruses accumulate in cytoplasm/nucleus and are released when cell lyses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How do aminoglycosides work? Which bacteria are they active against; which are they not active against? When are they used?

A
  • Bind to specific proteins in 30S ribosomal unit - interfere with formation of initiation scomplex with fmet-tRNA - cause misreading of mRNA codons Active against - G- (inc Pseud); Staph Not active: Streptococci; anaerobes Only use in severe life-threatening infections - because of resistace + toxicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How do beta-lactam antibiotics work?

A

Competitively bind penicillin binding proteins (transpeptidases) - beta-lactam ring mimics bond between D-ala-D-ala resides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How do DNA viruses amplify their genome?

A

just use the DNA-dependent RNA-polymerase found in human cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how do minus-sense RNA viruses amplify their genome?

A

bring in their own RNA-dependent RNA polymerase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How do plus-sense RNA viruses amplify their genome?

A

acts as mRNA - forces cell to make an RNA-dependent RNA-polymerase to copy its genome first is translated into a polyprotein - polyprotein is autocleaved (starts to fold; forms enzyme active site; cleaves itself) - further cleavage -> forms structural proteins; proteases; and an RNA polymerase - RNA polymerase can then copy the genome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how do retroviruses (plus-sense RNA) amplify their genome?

A

can use the DNA depedent RNA polymerase straight off - but bring in a reverse transcriptase (make DNA from RNA) -> does this because it replicates through integration into our genome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How do tetracycline antibiotics work?

A

Bind to 30S of ribosome - inhibit recognition phase of protein sythesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How do you overcome beta-lactamases clinically?

A

Administer them with a beta-lactamase inhibitor - eg clavulonic acid + ampicillin = comoxyclav - molecules: have beta-lactam ring and bind to beta-lactamases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Jawetz’s laws

A

bacteriostatic + bacteriostatic = additive or indifferent bacteriostatic + bactericidal = antagonistic bactericidal + bactericidal = synergistic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Methicillin - spectrum - why was it developed - administration - toxicity - what is the problem with its administration - what is resistance to methicillin a marker for?

A

Methicillin - spectrum - G+ cocci - Staphylococcus - why was it developed - because resistant Staph was selected for by penicillin - administration - injected - toxicity - moderate - problem: toxicity - resistance is a marker for resistance towards all beta-lactams

21
Q

Penicillin G - origin - spectrum - administration - toxicity - problems?

A
  • bacterial origin - G+ (rods and cocci); G- cocci - acid labile - must be given as injection - v low toxicity problem: can’t be given orally
22
Q

RNA viruses - where do they replicate - do they carry RNA polymerase? - exceptions?

A
  • replicate in cytoplase (exception - retrovirus) - plus-sense; don’t carry; form polyprotein; minus-sense must carry - exceptions: retrovirus (makes reverse transcriptase); reo (carries polymerase; because replicates inside its capsid)
23
Q

RNA viruses: - capsid types - envelope types - genome types - examples

A
  • icosahedral or helical - icosahedral - naked or env; helical - always enveloped - genomes: ss or ds; plus or minus-sense eg - reo; picorna; flavi; toga; retro; corona; rhabdo; orthomyxo
24
Q

What are 2 ways that viruses penetrate cell?

A
  1. Fusion with host cell membrane (eg HIV) - coat fuses with membrane 2. Endocytosis (eg togavirus) - cell membrane invaginates to form vesicle in cytoplasm - in cytoplasm - lysis of endosome; low pH of vesicle triggers conformational change in viral proteins and exposure of fusion region
25
Q

What are 3 ways that the viral genome can change?

A
  1. mutation - error in copying the nucleic acid (esp in RNA viruses - no “proofreading” 2. recombination - exchange of stretches of nucleic acid 3. reassortment - swap segments (in viruses with segmented genomes)
26
Q

What are 4 major ways of antibiotic resistance in bacteria

A
  1. drug inactivation - betalactamase; covalent modification of aminoglycosides 2. Alter drug target - alter penicillin binding protein (beta-lactam - MRSA); alter terminal D-ala (vancomycin - VRE); overproduce target (VISA) 3. Reduce access of drug to target - reduce entry into cell (aminoglycosides - modify outer membrane); increase efflux from cell (aminoglycosides; tetracycline) 4. Failure to activate inactive precursor
27
Q

What are all G- bacteria intrinsically resistant to

A

Vancomycin - too large to fit through outer membrane

28
Q

What are all mycoplasma resistant to?

A

beta-lactams + vancomycin -> no peptidoglycan

29
Q

What are all P. aeruginosa intrinsically resistant to

A

Ampicillin/amoxicillin - have chromosome-encoded beta-lactamase

30
Q

What are multiresistance plasmids?

A

Plasmids that encode multiple resistances Can be selected for in commensals - because they are constantly being impacted by antibiotics -> in one go; transfer resistance to many antibiotics

31
Q

What are some post-processing changes that virus proteins undergo?

A
  • post-translational cleavage of polyproteins/trimming of structural proteins by virus-coded proteases - glycosylation of glycoproteins in RER and Golgi -> results in their deposition on cell surface
32
Q

What are some reasons for using combinations of antibiotics? (5)

A
  • temporary measure to cover all possibilities - delay emergence of resistance (eg in TB) - treat mixed infections - reduce toxicity - achieve synergy
33
Q

What are the 3 methods of gene transfer? How do they work What do they require

A

Transformation - donor DNA is chopped up by restriction enzymes; competent cell takes up fragments and inserts them into its DNA through homologous recombination Requires: - naturally competent bacteria - pneumococci - some homology between DNA -> related species Phage-mediated transduction - bacteriophage has enzymes that digest cell wall and pump DNA into new bacterium - phage also contains integrases - integrate DNA into bacteria nucleic acid -> usualyl does this wiht own DNA; and then package up own DNA to make new phage -> but can also make mistakes and transfer bacterial DNA between cells Plasmid-mediated conjugation - cytoplasmic bridge forms between bacteria - sex pillus - transfers plasmids between thm Requires: cell-cell contact but bacteria don’t have to be related

34
Q

what are the components of a virus; what are they made of

A

genome - DNA/RNA capsid - with/out nucleocapsid - protein subunits envelope - maybe with matrix connecting to capsid - lipids; with surface glycoproteins

35
Q

What are the main methods for testing antibiotic susceptibility?

A

Determine MIC - through dilution Disc susceptibility test - then measure zone of inhibition E-test strip - more sophisticated diffusion

36
Q

What are the major mechanisms of resistance to aminoglycosides?

A
  1. Production of aminoglycoside-modifying enzyme (plasmid) -> reduces entry of drug 2. Modifying outer membrane -> reduced entry (only in G- bacteria) 3. Efflux - pump drug out of cell (more importat in tetracycline) 4. Ribosomal mutation - can’t bind
37
Q

What are the mechanisms for resistance against beta-lactams? (3) Give example of bacteria for each

A
  1. Altering target site - make new PBP (MRSA; MRSE; Strep. pneumoniae; N. gonorrhoeae; H. influenzae) 2. Altering access to target site (G- bacteria -> have outer membrane; so beta-lactams must diffuse in through porins -> mutate the porins) 3. Produce beta-lactamases - catalyse hydrolysis of beta-lactam ring -> now ineffective In G+ - release these into extracellular enviromet In G- they stay in the periplasm (Pseudomonas)
38
Q

What are the mechanisms of antagonism in antibiotics?

A
  • inhibition of bactericidal activity by bacteriostatic agent (eg tetracycline = bacteriostatic; stops growth but bactericidal penicillin only attacks growing bacteria) - induction of enzymatic degradation - some drugs induce beta-lactamase - competition for binding of same target - inhibition of target
39
Q

What are the mechanisms of resistance to glycopeptides (3) Examples

A
  1. Intrinsic resistance - G- bacteria - have outer membrane -> antibiotic can’t enter - altered target - no terminal D-ala-D-ala 2. Acquired resistance - encode a ligase - produces pentapeptides terminating in D-ala-D-lac VRE - vacomycin resistant enterococcus - scary because may share plasmids with MRSA VISA - vancomycin inermediate staph aureus - soaks up the vancomycin because it increases its peptidoglycans
40
Q

What are the mechanisms of synergy in bacteria? (3)

A
  • Block sequential steps in a pathway - Inhibit enzymatic degradation (clavulonic acid + beta-lactams) - Enhance antimicrobial uptake by bacteria (penicillin messes with wall -> aminoglycoside can get in)
41
Q

What are the stages of viral replication?

A
  1. Attachment 2. Penetration 3. Uncoating 4. Genome replication; RNA synthesis; Protein synthesis 5. Assembly 6. Release
42
Q

What are the two types of beta-lactamases and what implications does this have on antibiotic treatment?

A

they are either plasmid-encoded; or chromosomally encoded -> different beta-lactamase inhibitors work for each eg. clavulonic acid - only acts on plasmid-encoded -> won’t work on Pseudomonas (has chromosomally-encoded beta-lactamase) ticarcilin -> isn’t broken down by chromosomally-encoded (but when use this - use with clavulonic acid; in case it has inherited a plasmid) Timentim = combo of ticarcilin + clavulonic acid

43
Q

What are the types of viral capsids?

A

Icosahedral - made up of 20 triangular faces; composed of capsomeres Helical - wraps around nucleic acid; always has an envelope; always RNA Complex symmetry - pox viruses

44
Q

What defines/limits the host species or type of cell a virus infects? What is notable about HIV?

A

Which receptors it uses to bind attach to cell HIV - uses 2 different receptors on same host cell - first for initial attachment; then closer attachment

45
Q

What is antigenic drift? How does it arise? What is the difference in antigenic drift in HIV and influenza?

A

Change in antigenic structure of a virus - eg change in structure of glycoprotein Arises through point mutations - selective advantage if mutation is in antibody bindig site Influenza - occurs on population scale HIV - diversity of strains within a single patient (because is persistent infection)

46
Q

What is the structure of beta-lactam

A

“house with garage and car” house = chimney may be S; N; C; may or may not have double bond on right edge house can be pentagon or hexagon paste-11991548690433.jpg

47
Q

What specific considerations must be made regarding choice of antibiotic? (7)

A

Antimicrobial spectrum Clinical efficacy Route of administration Route of excretion Pharmacokinetics/dynamics Availability Cost

48
Q

Which bacteria are susceptible to beta-lactams

A

Only those that have a cell wall - G+ - some are active against G- rods - more recent: active against resistant organisms; like Pseudomonas Not active agaist - Mycoplasma (no cell wall) - mycobacteria (very impenetrable wall) - intracellular pathogens - Brucella; Legionella; Chlamydia

49
Q

Why does the beta-lactam antibiotic spectrum vary? (3)

A
  • different PBPs (broad spectrum antibiotic - binds more of these) - different accessibility of antibiotic to PBP (eg solubility in outer membrane) - susceptibility to beta-lactamase varies

Microbiology (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions