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POM 4 Immunology > 4.3 Antimicrobial Therapies > Flashcards

4.3 Antimicrobial Therapies Flashcards

1
Q

Why are anti-bacterials safe for humans to use?

A

Selective toxicity

Target processes in bacteria but not mammals

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2
Q

Describe the mechanism of action of beta-lactams?

A

They have a beta-lactam ring that binds the serine residue on penicillin binding protein, inactivating it

Thus the cross bridges between peptidoglycan molecules can’t form, so the bacterial cell wall doesn’t form

Thus water enters 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
Bacteriostatic stops the bacteria from growing

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7
Q

What is an antiseptic?

A

Chemical that kills/inhibits microbes, used topically

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8
Q

What is the minimal inhibitory concentration?

A

The lowest concentration of antibiotic 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 difficile
Enterococcus spp

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12
Q

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

A

E.coli
Salmonella
Pseudomonas aeruginosa

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13
Q

Which different bacterial processes do antibiotics target?

A

DNA replication
Cell wall synthesis
Plasma membrane damage
Protein synthesis (translation, transcription)
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

Sulphonamide

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16
Q

What is prontosil used to treat?

A

UTIs and RTIs
Bacteraemia
Prophylaxis for HIV+ individuals

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17
Q

What is the mechanism of protonsil?

A

Bacteriostatic and synthetic

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18
Q

What bacteria does prontosil act on?

A

Gram positive bacteria

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19
Q

How does rifampicin work?

A

Bactericidal antibiotic

Targets the RpoB subunit of RNA polymerase, blocking transcription so the bacteria cannot replicate

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20
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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21
Q

How does vancomycin work?

A

Bactericidal, targets lipid II component of cell wall biosynthesis and wall crosslinking via D-ala residues

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22
Q

How does daptomycin work?

A

Bactericidal, targets cell membrane

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23
Q

What is the problem with daptomycin?

A

Toxicity limits the dose

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24
Q

How does linezolid work?

A

Bacteriostatic, binds 50S subunit of rRNA to inhibit protein synthesis

25
Q

Why is linezolid effective against gram positive mainly?

A

Due to lipopolysaccharides present in gram positive outer membrane

26
Q

What are the four main mechanisms of antibiotic resistance? AIMeD

A

Altered target site
Inactivation of antibiotic
Metabolism is altered
Drug accumulation

27
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 modifying enzyme

E.g. MRSA encodes a different penicillin binding site with a low affinity for the antibiotic

28
Q

How is Streptococcus pneumoniae resistant to erythromycin?

A

Acquires the erm gene

Gene encodes for an enzyme that methylates the antibiotic target site in the 50S ribosomal subunit

29
Q

Give an example of how a bacteria can inactivate an antibiotic

A

Beta-lactamases and chloramphenicol can degrade beta lactam rings, preventing binding to penicillin binding proteins on bacteria

30
Q

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

A

Bacteria can produce another enzyme substrate which outcompetes antibiotics

E.g. increased production of PABA confers resistance to sulfonamides

31
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

Thus the drug does not reach the concentration required to be effective

32
Q

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

A

Efflux pumps

33
Q

What are two examples of macrolide antibiotics?

A

Erythromycin and azithromycin

34
Q

How do macrolides work?

A

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

35
Q

What types of bacteria do macrolides work on?

A

Gram positive and some gram negative

36
Q

How do quinolones work?

A

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

37
Q

What are three sources of antibiotic resistance?

A

Plasmids, transposons and naked DNA

38
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

39
Q

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

A

Sections of DNA that can move from one location to another in the genome

They can integrate into chromosomal DNA, allowing transfer of plasmid genes to chromosomal DNA and vice versa

40
Q

What is naked DNA?

A

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

41
Q

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

A

Transformation, conjugation and transduction

42
Q

What is transformation?

A

Uptake of extracellular DNA

43
Q

What is transduction?

A

Phage mediated DNA transfer

44
Q

What is conjugation?

A

Pilus mediated DNA transfer

45
Q

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

A

Biofilm
Intracellular location
Slow growth
Spores
Persisters

46
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)
AB resistance within Commensal flora (e.g. secretion of beta-lactamase)

47
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

48
Q

What do hospitals prodivde for antibiotic resistance?

A

They provide a strong selection pressure

49
Q

What are the risk factors associated with Hospitals Acquired Infections? CAB DIPS

A

Crowded wards
Antibiotic therapy
Broken skin

Devices (indwelling)
Ill and immunosuppressed patients
Pathogens
Staff in contact with multiple patients

50
Q

Describe how antibiotic therapy can impair commensal flora?

A

Normally commensal organisms can outcompete pathogens for adhesion, metabolism and growth

After antibiotic therapy, the pathogen has no competition, leading to overgrowth

When the pathogen produces toxins damaging the host, this causes a symptomatic infection

51
Q

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

A

Broad spectrum reduction
Existing medication alteration

Strategies of prescription
Identifying infections quickly
Combinations of antibiotics and inhibitors
Knowledge of local strains

52
Q

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

A

Allergy - allergic reactions to fungal products
Mycoses
Mycotoxicoses

53
Q

What are mycoses?

A

Superficial, subcutaneous or systemic colonisation, invasion and destruction of human tissue

54
Q

What are mycotoxicoses?

A

Ingestion of fungi and their toxic products

55
Q

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

A

Pseudomonas aeruginosa

56
Q

What gram negative organism causes UTIs, and survives on abotic surfaces?

A

Acinetobacter baumannii

57
Q

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

A

Staphylococcus aureus

58
Q

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

A

Enterococcus

59
Q

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

A

Clostridium

POM 4 Immunology (14 decks)

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