Infection Session 2

Question 1

Why is physiological state relevant in gestational diabetes?

Answer 1

During pregnancy bacteria in the large bowel can cause gestational diabetes

Question 2

What is the difference in calendar and relative time when considering a patient with a suspected infection?

Answer 2

Calendar time considers seasonal diseases e.g. Flu or chickenpox
Relative considers time since a potential exposure

Question 3

By what 7 mechanisms can infection occur?

Answer 3

Contiguous spread
Inoculation
Haematogenous
Ingestion
Inhalation
Vector
Vertical transmission

Question 4

How do aerosols form?

Answer 4

Around a ‘seed’ e.g. a dust particle

Question 5

Why is chickenpox so contagious?

Answer 5

Virus rapidly multiplies in lungs and is transmitted via inhalation

Question 6

What sequence does management of infection usually take?

Answer 6

History –> examination –> diagnosis –> specific+/- supportive Tx –> infection prevention in hospital and community

Question 7

How are the vast majority of infection diagnoses made?

Answer 7

History alone

Question 8

Why is debridement of tissue sometimes used to treat infection?

Answer 8

Dead tissue has a low redox potential and bloodflow so is a perfect environment for anaerobic bacteria

Question 9

Why does the dead space left following debridement often need packing?

Answer 9

Blood/serosa can accumulate here and promote microbial growth

Question 10

What outcomes are possible following an infection?

Answer 10

Resolution
Chronic infection –> potential disability
Death

Question 11

What is an antibiotic?

Answer 11

Antimicrobial produced by a living organism

Question 12

What are the four main types of antimicrobials?

Answer 12

Antibacterial
Antiviral
Antiprotozoal
Antifungal

Question 13

What is the difference between a bactericidal and bacteriostatic antibacterial agent?

Answer 13

Bactericidals kill, bacteriostatics inhibit

Question 14

What are the ideal features of antimicrobial agents?

Answer 14

Selectively toxic
Few adverse effects
Reach site of infection
Oral/IV formulation
Long half-life for infrequent dosing
No interference w/other drugs

Question 15

How do beta-lactams act as antibacterials?

Answer 15

Inhibit cell wall regeneration by binding to penicillin binding protein so new X-links cannot be formed

Question 16

How do glycopeptides act as antibacterials?

Answer 16

Bind to peptidoglycan thus blocking cell wall X-linking enzyme

Question 17

What mechanisms can bacteria use to be resistant to beta-lactams?

Answer 17

Decrease their permeability to them
Express beta-lactamases to inactivate drug
Alter target enzyme so it has a lower affinity

Question 18

Which classes of antibacterials inhibit protein synthesis by blocking a variety of enzymes?

Answer 18

Tetracyclines
Aminoglycosides
Macrolides

Question 19

How can bacteria be resistant to tetracyclines?

Answer 19

Increase efflux to actively pump out before it takes effect

Alter target enzyme

Question 20

Which class of antibacterials do trimethoprim and rifampicin belong to and how do they act?

Answer 20

Quinolones (floroquinolones clinically)

Bind to DNA gyrase to interfere with DNA supercoiling

Question 21

What are polymixins?

Answer 21

Antibacterials that inhibit cell membrane function

Question 22

Will a bacterium only ever have one mechanism of resistance to one particular drug?

Answer 22

No, might have different mechanisms for same class as well as multiple mechanisms for different classes

Question 23

Does there need to be a high level of antibiotic exposure for a chromosomal gene mutation resulting in antibiotic resistance to occur?

Answer 23

No

Question 24

What two methods form the basis of antibiotic resistance?

Answer 24

Chromosomal gene mutation

Horizontal gene transfer

Question 25

What is the qualitative method of measuring antibiotic activity?

Answer 25

Disc sensitivity to examine zone of inhibition around disc

Question 26

What is the quantitative measure of antibiotic sensitivity?

Answer 26

Minimum inhibitory concentration

Question 27

How is minimum inhibitory concentration measured?

Answer 27

Bacterial broth is cultured in a serial dilution of antibiotic

Question 28

Are carbapenems broad or narrow spectrum?

Answer 28

Broad - including anaerobes and most G-ve

Question 29

What are penicillins mainly active against?

Answer 29

Streptococci

Question 30

What is flucoxacillin active against?

Answer 30

Staph and streptococci

Question 31

Give an example of a commonly used beta-lactamase inhibitor combination therapy.

Answer 31

Co-amoxiclav

Question 32

How do new generation of cephalosporins compare to old generations?

Answer 32

Increased G-ve spectrum and decreased G+ve activity

Question 33

Are cephalosporins active against anaerobes?

Answer 33

No

Question 34

What is the relevance of cephalosporins to C.diff infection?

Answer 34

Broad spectrum so widespread use --> resistant C.diff strains

Question 35

How does the activity of vancomycin against G+ve bacteria compare to its activity against G-ve?

Answer 35

Active against most G+ve but not G-ve

Question 36

Why is vancomycin given orally for intestinal infections?

Answer 36

Not normally absorbed into the blood

Question 37

Why must care be taken with vancomycin use?

Answer 37

It has a narrow therapeutic window

Question 38

What class of antimicrobials does vancomycin belong to?

Answer 38

Glycopeptides

Question 39

Why are tetracyclines not widely used in hospitals?

Answer 39

Broad spectrum

Question 40

In what common situation might carbapenems, tetracyclines or macrolides be used?

Answer 40

Penicillin allergy

Question 41

What are tetracyclines active against?

Answer 41

Chlamydia Some protozoa Atypical pneumonia pathogens

Question 42

Why are tetracyclines not given to children under 12 y.o.?

Answer 42

Stain bones and teeth yellow

Question 43

Which antimicrobial is reserved for severe G-ve sepsis?

Answer 43

Gentamicin

Question 44

Why is gentamicin reserved as a last resort for severe G-ve sepsis?

Answer 44

Profound activity against G-ve but is potentially nephrotoxic

Question 45

What is used in primary care as an alternative to penicillin for mild G+ve infections?

Answer 45

Macrolides

Question 46

Why are macrolides used in combination with drugs for typical respiratory pathogens?

Answer 46

They are active against atypical respiratory pathogens

Question 47

Name two macrolides.

Answer 47

Erythromycin | Clarithromycin

Question 48

What activity do quinolones have?

Answer 48

Very active against G-ve and atypical pathogens

Question 49

Why is there a concern with quinolones and C.diff infection?

Answer 49

Rapidly increasing resistance

Question 50

What action do trimethoprim and sulphonamides have?

Answer 50

Inhibit folic acid synthesis

Question 51

What is trimethoprim most commonly used for in the UK?

Answer 51

UTI

Question 52

When might you use a combination of trimethoprim and sulphonamides?

Answer 52

In a specific and unusual infection

Question 53

What class of antifungals acts by inhibiting cell-membrane synthesis?

Answer 53

Azoles

Question 54

What is an over-the-counter antifungal used to treat Candida?

Answer 54

Fluconazole

Question 55

How does the activity of Azoles and Polyenes differ even though their mechanism of action is the same?

Answer 55

Azoles active against yeasts +/- moulds | Polyenes active against more complicated moulds

Question 56

Why can aciclovir be used against Herpes simplex and Varicella Zoster viruses?

Answer 56

Upon phosphorylation it inhibits viral DNA polymerase

Question 57

How does Tamiflu work?

Answer 57

Inhibits viral neuraminidase

Question 58

What is metronidazole active against?

Answer 58

Anaerobic bacteria and several protozoa

Question 59

What are the 7 patient factors which can affect disease?

Answer 59

``` Age Gender Physiological state Pathological state Social factors Time Place ```