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IMMUNO my version > Antimicrobial Therapies > Flashcards

Antimicrobial Therapies Flashcards

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1
Q

Why are anti-bacterials safe for humans to use?

A

They target proteins found in bacterial cells but not found in humans

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2
Q

Describe the mechanism of action of beta-lactams?

A

Interfere with the synthesis of the peptidoglycan component of the bacterial cell wall by binding to penicillin-binding proteins (pops) which are needed for peptidoglycan synthesis. lack of cell wall=> cell lysis

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3
Q

What are some examples of beta-lactams?

A

Penicillin and Methicilin

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4
Q

What is the definition of an antibiotic?

A

An anti-microbial agent produced by microorganisms that kills or inhibits other microorganisms

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5
Q

What is an anti-microbial?

A

A chemical that selectively kills or inhibits microbes

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6
Q

What is the difference between bactericidal and bacteriostatic antibacterials?

A

Bactericidal kills the bacteria whereas bacteriostatic stops the bacteria from growing

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7
Q

What is an antiseptic?

A

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

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8
Q

What is the minimal inhibitory concentration?

A

The lowest concentration of antibacterial which is required to inhibit growth

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9
Q

what are some effects of antibacterial resistance?

A
  • Longer time needed for therapy to be effective
  • Require additional approaches
  • Use of expensive therapy (newer drugs)
  • Use of more toxic drugs
  • Use of less effective “second choice” antibiotics
  • icnreased mortality
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10
Q

How does antibiotic resistance emerge?

A

A population of bacteria will have some bacteria that are resistant and some that are not due to genetic variation

A selection pressure then acts on the population such as the antibiotic - those that are not resistant die, and patient starts to feel better

Patient then stops course of antibiotic but those that can survive still do not die - they live and proliferative meaning the entire population is now resistant

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11
Q

What are the 5 gram positive bacteria which are resistant to antibiotics?

A

Staphylococcus aureus
Streptococcus Pneumoniae
Mycobacterium tuberculosis
Clostriduim difficle
Enterococcus spp

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12
Q

What are the 6 gram negative bacteria which are resistant to antibiotics?

A

pseudonomas aeruginosa
E. Coli
E. Coli, Klebsiella
Salmonella
Acinetobacter baumannii
Neisseria gonorrhoeae

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13
Q

Which different processes do antibiotics target?

A

DNA replication
Cell wall synthesis
Plasma membrane damage
Protein synthesis
- Transcription
- Translation
Enzymatic activity/synthesis of metabolites

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14
Q

Why might you give a patient multiple different antibiotics?

A

They may act on different stages of bacterial growth and give a symbiotic effect.
e.g. sulfonamides and trimethoprim act on two different stages of bacterial development.

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15
Q

What type of antibiotic is prontosil?

A

A sulphonamide antibiotic ( broad spectrum)

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16
Q

What is prontosil used to treat?

A

UTIs and RTIs, bacteraemia and prophylaxis for HIV+ individuals

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17
Q

What bacteria does prontosil act on?

A

Gram positive bacteria

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18
Q

How do Aminoglycosides work?

A

bactericidal
Target protein synthesis, RNA proofreading and cause damage to cell membrane.

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19
Q

problem with aminoglycosides

A

toxic so has limited use

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20
Q

How does Rifampicin work?

A

It is a bactericidal antibiotic and targets the RpoB subunit of RNA polymerase - this blocks transcription meaning bacteria cannot replicate

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21
Q

What happens to secretions like urine and sweat when a person is on Rifampicin?

A

Makes them turn orange / red

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22
Q

How does vancomycin work?

A
  • bactericidal
  • targets lipid II component of cell wall biosynthesis & wall crosslinking via D-ala residues
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23
Q

How does daptomycin work?

A

It is a bacteriocidal antibiotic which targets bacterial cell membranes

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24
Q

What is the problem with daptomycin?

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A

its toxic, so need to limit dose and give intravenously

25
How does linezolid work?
- inhibits the initiation of protein synthesis by binding to the 50s ribosomal RNA subunit - bacteriostatic
26
what is meant by the term selective toxicity in terms of anitbiotics?
when the antibiotics only act in bacterial cells, due to the large differences between mammals and prokaryotes
27
What are the four main mechanisms of antibiotic resistance? AIMeD
Altered target site Inactivation of antibiotic Metabolism - altered metabolism Drug accumulation
28
Describe with an example of how antibiotics can become resistant through altering the target site
can arise from acquisition of alternative gene or a gene that encodes a target-modifiying enzyme Eg MRSA encodes a different penicillin binding site with a low affinity ( binds less strongly) for the antibiotic
29
How is Streptococcus pneumoniae resistant to erythromycin?
 occurs via the getting the erm gene, which encodes an enzyme that methylates the AB target site in the 50S ribosomal subunit.​
30
Give an example of how a bacteria can inactivate an antibiotic (this is a mechanism of antibiotic resistance)
Beta-lactamases and chloramphenicol can degrade a wide range of beta lactam rings meaning they cannot bind to the penicillin binding protein on the bacteria
31
Give an example of how bacteria can be resistant to an antibiotic through altered metabolism?
This is where the bacteria produce another enzyme substrate which can outcompete antibiotic inhibitor eg increased production of PABA confers resistance to sulfonamides
32
Describe how bacteria can show antibiotic resistance through decreased drug accumulation?
Reduced penetration of antibiotic into the bacterial cell due to increased efflux of antibiotic out of the cell - this means the drug does not reach the concentration required to be effective
33
How do bacteria efflux the drug out in order to confer antibiotic resistance?
efflux pumps
34
What are two examples of macrolide antibiotics?
Erythromycin and azithromycin
35
How do macrolides work?
Targets 50s ribosomal subunit preventing amino-acyl transfer and thus truncation of polypeptides
36
What types of bacteria do macrolides work on?
gram positive and some grapm negative
37
How do quinolones work?
Target DNA gyrase in gram negative and topoisomerase IV in gram positive bacteria
38
What are three sources of antibiotic resistance genes?
Plasmids, Transposons and Naked DNA
39
Describe how plasmids act as a source of antibiotic resistance?
Plasmids are extra-chromosomal circular DNA which often carry extra multiple antibiotic resistant genes - selection for one maintains resistance to all
40
What are transposons and how can they help to facilitate antibiotic resistance?
They are sections of DNA that have the capacity to move from one location to another in the genome - they can then integrate into chromosomal DNA, allowing the transfer of plasmid genes to the chromosomal DNA and vice versa
41
What is naked DNA?
DNA that has been released into the surrounding environment from dead bacteria
42
What are the three mechanisms for horizontal (between bacteria) spread of AB resistance in bacteria?
Transformation, conjugation and transduction
43
What is transduction?
Phage mediated DNA transfer
44
What is conjugation?
Pilus mediated DNA transfer
45
What are the five non-genetic sources of antibiotic resistance?
Biofilm Intracellular location Slow growth Spores Persisters
46
What are the 5 given reasons for treatment failure aside from AB resistance? DOPe AC
Inappropriate Dose (half life) Inappropriate choice for Organism Poor PEnetration of AB into target site Inappropriate Administration (oral vs IV) Presence of AB resistance within Commensal flora e.g. secretion of beta-lactamase
47
What has to be taken into consideration when measuring resistance using agar plates and zones of inhibition?
Measureents make in vitro may not fully reflect the situation in vivo
48
What do hospitals prodivde for antibiotic resistance?
They provide a strong selection pressure
49
What are the risk factors associated with Hospitals Acquired Infections
Risk factors for HAIs CAB DIPS Crowded wards Antibiotic therapy Broken skin Devices (indwelling) Ill and immunosuppressed patients Pathogens present Staff in contact with multiple patients
50
Describe how antibiotic therapy can impair commensal flora?
Normally, commensal organisms can out-compete pathogen WRT adhesion, metabolism, growth. Pathogen cannot colonise at levels sufficient for infection. After AB therapy => pathogen has no competition which can lead to overgrowth.  When a pathogen then produces toxins which damages the host, it becomes a symptomatic infection, and can spread to other patients
51
How can we prevent the emergence of drug resistant bacteria and nosocomial infections?
Tighter controls on prescribing such antibiotics Reduce use of broad-spectrum antibiotics Combination therapy Identify infections quickly KNowledge of local strains Restricting use for serious infections only
52
What are the three broad classes of conditions that fungi can cause in humans? d
Allergy - allergic reactions to fungal products Mycoses - superficial, subcutaneous or systemic colonisation, invasion and destruction of human tissue Mycotoxicoses - ingestion of fungi and their toxic products
53
What gram-negative organisms causes HA pneumonia, burn wounds and particularly effects the immunocompromised hosts and survives on abiotic surfaces?
Pseudomonas aeruginosa
54
What gram negative organism causes ITU infections, and survives on abotioc surfaces?
Acinetobacter baumannii
55
What gram-positive organism colonises the nasopharynx and causes blood stream infections and shows disseminated spread?
Staphylococcus aureus
56
What gram positive organism is a commensal or gastrointestinal tract, but can also cause blood stream infections and UTIs?
Enterococcus
57
What gram positive organism is a major cause of antibiotic associated diarrhoea and mortality?
Clostridium
58
What are the major Gram Positive antibiotic resistant bacterial pathgens?
Clostridium difficle Enterococcus Streptococcus Pneumoniae
59
What are the major gram negative antibiotic resistant bacterial pathogens?
Pseudomonas aeruginosa E. Coli Salmonella

IMMUNO my version (14 decks)

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