Brainscape's Knowledge GenomeTM

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


See full index

immunology > antimicrobial therapies > Flashcards

antimicrobial therapies Flashcards

1
Q

what is prontosil?

A

synthetic bacteriostatic antibiotic

sulphonamide antibiotic

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

what is prontosil used to treat?

A

UTIs, RTIs, bacteraemia, prophylaxis for HIV+ people

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

How do beta-lactams work?

A

interfere with the synthesis of the peptidoglycan component of the bacterial cells wall

bind to penicillin-binding proteins (PBPs)

PBPs catalyse steps in the synthesis of peptidogylycan

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

examples of beta-lactams?

A

penicillin, methicillin

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

what are most modern naturally harvested antibiotics produced by?

A

soil-dwelling fungi, bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

antimicrobial meaning

A

chemical that selectively kills/ inhibits microbes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

antiseptic definition

A

chemical which kills or inhibits microbes that is usually used topically to prevent infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the breakpoint in antibiotics?

A

clinically-achievable concentration for bacteria to be killed by the antibiotics

i.e. the concentration of antibiotic where a bacterial infection will be eradicated successfully by the antibiotic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the minimal inhibitory concentration (MIC)

A

the lowest conc. of antibiotics required to inhibit growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

misconceptions about antibiotics at the start

A

resistance against more than one class of antibiotics wouldn’t occur at the same time

horizontal gene transfer wouldn’t occur

resistant organisms would be significantly less “fit” (varies)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

consequences of antibiotic resistance

A

increased time for effective therapy
requirement for additional approaches, like surgery
use of more expensive (newer drug) therapy
use of more toxic drugs like vancomycin
use of less effective second choice antibiotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

gram negative AB resistant bacteria

A

pseudomonas aeruginosa (cystic fibrosis/burn wound)
E. coli (ESBL) and E. coli, Klebsiella spp
Salmonella spp (MDR)
Acinetobacter baumannii (MDRAB) (wounds, UTI, pneumonia
Neisseria gonorrhoeae

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

gram positive AB resistant bacteria

A

MRSA/VISA
streptococcus pneumoniae
clostridium difficile (GI)
Enterococcus spp (VRE) (UTI, bacteraemia, infective endocarditis)

TB

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

what is an aminoglycoside

A

bactericidal antibiotic

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

mechanism of aminoglycosides

A

target 30S ribosomal subunit, RNA proofreading + can cause damage to cell membrane

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

what’s rifampicin

A

bactericidal antibiotic (frequent spontaneous resistance)

17
Q

mechanism of rifampicin?

A

targets RpoB subunit of RNA polymerase

18
Q

what is vancomycin

A

bactericidal antibiotic which targets Lipid II component of cell wall biosynthesis + wall cross linking via D-ala residues

toxic but used against MRSA etc

19
Q

everything abt linezolid u need to know

A

bacteriostatic

inhibits protein synthesis by binding to 50s rRNA subunit

only affects gram positive?

20
Q

daptomycin

A

bactericidal

targets cell membrane

gram positive

toxic

21
Q

4 mechanisms of antibiotic resistance

A

1- altered active site
2- inactivation of antibiotic
3- decreased drug accumulation
4- altered metabolism

22
Q

how does altered target site mechanism of resistance arise

A

acquisition of alternative gene/ gene which codes a target-modifying enzyme

23
Q

examples of altered target sites

A

MRSA encodes an alternative PBP (PBP2) with low affinity for beta-lactams

Streptococcus pneumoniae acquired the erm gene which encodes an enzyme which methylates the antibiotic target site in 50S ribosomal subunit

24
Q

inactivation of antibiotic

A

enzymatic degradation or alteration, rendering antibiotic ineffective.

Examples: beta-lactamase (bla) and chloramphenicol acetyl-transferase (cat).

ESBL and NDM-1 are examples of broad-spectrum beta-lactamases (can degrade a wide range of beta-lactams, including newest).

25
Q

what’s decreased drug accumulation?

A

reduced permeability of AB into bacterial cell and/or increased efflux of AB out of cell

drug does not reach conc required to be effective

26
Q

altered metabolism

A

increased production of enzyme substrate outcompetes antibiotic inhibitor (e.g. increased production of p-aminobenzoic acid confers resistance to sulphonamides)

or bacteria can switch to a diff metabolic pathway, reducing need for PABA

27
Q

what are macrolides

A

bacteriostatic gram-positive and sometimes gram negative

targets 50S ribosomal subunits, stops amino-acyl transfer, and truncation of polypeptides

e.g. erythromycin, azithromycin

28
Q

what are quinolones

A

Synthetic, broad spectrum, bactericidal.
Target DNA gyrase in gram neg and topoisomerase IV in gram pos

29
Q

sources of antibiotic resistance genes

A

plasmids (can carry multiple resistance genes)

transposons - integrate into chromosomal DNA + allows gene transfer from plasmid to chromosome and vice versa

naked DNA- from dead bacteria released into environment

30
Q

How can AB resistance genes be spread?

A

Transformation - uptake of extracellular DNA

Conjugation- pilus-mediated DNA transfer

Transduction - phage-mediated DNA transfer

31
Q

other reasons for resistance/ treatment failure

A

biofilm
intracellular location
slow growth
spores
persisters

inappropriate choice for organism
poor penetration into target site
inappropriate dose
inappropriate administration
presence of AB resistance within commensal flora (secretion of beta-lactamase)

32
Q

How do hospitals provide strong selective pressure for AB resistance?

A

large numbers of infected people require high doses of antibiotics- strong selective pressure for emergence/ maintenance of AB resistance

33
Q

examples of hospital acquired infections

A

MRSA
VISA
clostridium difficile
VRE
E. coli (ESBL/NDM-1)
P. aeruginosa
Acinebacter baumannii
Stenotrophomonas maltophilia

34
Q

Risk factors for hospital acquired infection

A

high number of people
crowded wards
presence of pathogens
broken skin (surgical wounds, IV catheter)
indwelling devices (intubation)
AB therapy can suppress normal flora
transmission by staff

35
Q

how to fix resistance

A

prescribing strategies
reduce use of broad-spectrum antibiotics
quicker identification of infections by resistant strains
combination therapy
knowledge of local strains/resistance patterns

36
Q

overcoming resistance

A

modify existing modifications e.g. prevent cleavage in beta-lactams or enhance efficacy

combine antibiotic + an inhibitor of e.g. beta lactamase

immunology (5 decks)

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