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PSYCH > 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

They have a beta-lactam ring which binds to the serine residue on penicillin binding protein, which inactivates the enzyme. This means that the cross bridges between peptidoglycan molecules that form the outer layer of the bacteria cannot form so the cell wall doesn’t form. This means that water enters into the bacteria and it dies

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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
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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 three gram positive bacteria which are resistant to antibiotics?

A

Streptococcus Pneumoniae
Clostriduim difficle
Enterococcus spp

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12
Q

What are three gram negative bacteria which are resistant to antibiotics?

A

E.coli
Salmonella
Pseudomonas Aruginosa

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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

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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 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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19
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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20
Q

How does vancomycin work?

A

targets lipid II component of cell wall biosynthesis & wall crosslinking via D-ala residues

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21
Q

How does daptomycin work?

A

It is a bacteriocidal antibiotic which ragets bacterial cell membranes

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22
Q

What is the problem with daptomycin?

A

toxicity limits the dose

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23
Q

How does linezolid work?

A

inhibits the initiation of protein synthesis by binding to the 50s ribosomal RNA subunit

24
Q

Why is linezolid effective against gram positive mainly?

A

due to the lipopolysaccharides present in gram positive bacterias outer membrane

25
Q

What are the four main mechanisms of antibiotic resistance? AIMeD

A

Altered target site
Inactivation of antibiotic
Metabolism - altered metabolism
Drug accumulation

26
Q

Describe with an example of how antibiotics can become resistant through altering the target site

A

Acquision of an alternative gene that encodes for a target-sit modifying enzyme

Eg MRSA encodes a different penicillin binding site with a low affinity for the antibiotic

27
Q

How is Streptococcus pneumoniaeresistant to erythromycin?

A

occurs via the acquisition of theermgene, whichencodes an enzyme that methylates the AB target sitein the 50S ribosomal subunit.​

28
Q

Give an example of how a bacteria can inactivate an antibiotic (this is a mechanism of antibiotic resistance)

A

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

29
Q

Give an example of how bacteria can be resistant to an antibiotic through altered metabolism?

A

This is where the bacteria produce another enzyme substrate which can outcompete antibiotic inhibitor eg increased production of PABA confers resistance to sulfonamides

30
Q

Describe how bacteria can show antibiotic resistance through decreased drug accumulation?

A

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

31
Q

How do bacteria efflux the drug out in order to confer antibiotic resistance?

A

efflux pumps

32
Q

What are two examples of macrolide antibiotics?

A

Erythromycin and azithromycin

33
Q

How do macrolides work?

A

Targets 50s ribosomal subunit preventing amino-acyl transfer and thus truncation of polypeptides

34
Q

What types of bacteria do macrolides work on?

A

gram positive and some grapm negative

35
Q

How do quinolones work?

A

Target DNA gyrase in gram negative and topoisomerase IV in gram positive bacteria

36
Q

What are three sources of antibiotic resistance?

A

Plasmids, Transposons and Naked DNA

37
Q

Describe how plasmids act as a source of antibiotic resistance?

A

Plasmids are extra-chromosomal circular DNA which often carry extra multiple antibiotic resistant genes - selection for one maintains resistance to all

38
Q

What are transposons and how can they help to facilitate antibiotic resistance?

A

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

39
Q

What is naked DNA?

A

DNA that has been released into the surrounding environment from dead bacteria

40
Q

What are the three mechanisms for horizontal spread of AB resistance in bacteria?

A

Transformation, conjugation and transduction

41
Q

What is transduction?

A

Phage mediated DNA transfer

42
Q

What is conjugation?

A

Pilus mediated DNA transfer

43
Q

What are the five non-genetic sources of antibiotic resistance?

A 
Biofilm
Intracellular location
Slow growth
Spores
Persisters
44
Q

What are the 5 given reasons for treatment failure aside from AB resistance? DOPe AC

A

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

45
Q

What has to be taken into consideration when measuring resistance using agar plates and zones of inhibition?

A

Measureents make in vitro may not fully reflect the situation in vivo

46
Q

What do hospitals prodivde for antibiotic resistance?

A

They provide a strong selection pressure

47
Q

What are the risk factors associated with Hospitals Acquired Infections

A

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

48
Q

Describe how antibiotic therapy can impair commensal flora?

A

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

49
Q

How can we prevent the emergence of drug resistant bacteria and nosocomial infections?

A

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

50
Q

What are the three broad classes of conditions that fungi can cause in humans?

A

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

51
Q

What gram-negative organisms causes HA pneumonia, burn wounds and particularly effects the immunocompromised hosts and survives on abiotic surfaces?

A

Pseudomonas aeruginosa

52
Q

What gram negative organism causes ITU infections, and survives on abotioc surfaces?

A

Acinetobacter baumannii

53
Q

What gram-positive organism colonises the nasopharynx and causes blood stream infections and shows disseminated spread?

A

Staphylococcus aureus

54
Q

What gram positive organism is a commensal or gastrointestinal tract, but can also cause blood stream infections and UTIs?

A

Enterococcus

55
Q

What gram positive organism is a major cause of antibiotic associated diarrhoea and mortality?

A

Clostridium

56
Q

What are the major Gram Positive antibiotic resistant bacterial pathgens?

A

Clostridium difficle
Enterococcus
Streptococcus Pneumoniae

57
Q

What are the major gram negative antibiotic resistant bacterial pathogens?

A

Pseudomonas aeruginosa
E. Coli
Salmonella

PSYCH (78 decks)

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