Antimicrobial Therapies

Question 1

Prontosil?

Answer 1

Sulphonamide antibiotic that inihibts cell division by targeting folate biosynthesis Used to treat UTIs, RTIs and bacteraemia

Question 2

Antibiotic definition?

Answer 2

Antimicrobial agent produced by a microorganism that kills or inhibits other microorganisms

Question 3

Antiseptic?

Answer 3

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

Question 4

3 consequences of AB resistance?

Answer 4

Requirement for additional approaches e.g surgery Use of more toxic drugs Use of expensive therapy

Question 5

Aminoglycosides?

Answer 5

Bactericidal and target protein synthesis, RNA proofreading and cause damage to cell membrane. E.g gentamicin and streptomycin

Question 6

Rifampicin?

Answer 6

Bactericidal, targets RpoB subunit of RNA polymerase to stop transcription Spontaneous resistance common, patients’ secretions turn red/orange

Question 7

Vancomycin?

Answer 7

Bactericidal, targets Lipid II component of cell wall biosynthesis, as well as wall crosslinking via D-ala residues

Question 8

Linezolid?

Answer 8

Bacteriostatic- inhibits protein synthesis by binding to 50S rRNA subunit Gram-positive spectrum of activity

Question 9

Daptomycin?

Answer 9

Bactericidal- targets gram-positive cell membranes Quite toxic

Question 10

Beta lactams?

Answer 10

Bactericidal- interfere with synthesis of peptidoglycan component of cell wall by binding to penicllin-binding proteins

Question 11

Macrolides?

Answer 11

E.g erythromycin and azithromycin Can be bactericidal or bacteriostatic Mainly gram-positive Targets 50S ribosomal subunit preventing amino-acyl transfer and thus truncates polypetides

Question 12

Quinolones?

Answer 12

Broad-spectrum bactericidal- target DNA gyrase in GM-ve and topoisomerase IV in Gm +ve

Question 13

MIC?

Answer 13

Minimal inhibitory concentration- lowest concentration of AB required to inhibit growth

Question 14

4 mechanisms of AB resistance?

Answer 14

Altered target sites- e.g alternative penicillin binding proteins or 50S ribosomal subunits

Inactivation of antibiotic- e.g beta-lactamases

Altered metabolism- e.g imncreased production of enzyme substrate to out-compete AB or alternative metabolic pathways

Decreased drug accumulation- Reduced penetration of AB into cell (permeability) or increased efflux of AB out of cell

Question 15

Pseudomonas aeruginosa?

Answer 15

Gram negative, causes cystic fibrosis, burn wound infections and survives on abiotic surfaces

Question 16

E.Coli? (ESBL)

Answer 16

Gram negative- GI infection, neonatal meningitis

Question 17

Acinetobacter baumannii?

Answer 17

Gram negative- wounds, UTI, pneumonia and survives on abiotic surfaces

Question 18

Straphylococcus aureus?

Answer 18

Gram positive- wound and skin infections, pneumonia, septicaemia, infective endocarditis

Question 19

Clostridium difficile?

Answer 19

Pseudomembranous colitis, antibiotic-associated diarrhoea

Question 20

Enterococcus spp?

Question 21

3 sources of AB resistance genes?

Answer 21

Plasmids- often carry multiple resistanc genes

Transposons- allow transfer of genes from plasmids to chromosomes and vice versa

Naked DNA- DNA released from dead bacteria

Question 22

3 ways of AB resistance genes spread?

Answer 22

Transformation- uptake of extracellular DNA

Transduction- phage-mediated (virus) DNA transfer

Conjugation- pilus-mediated DNA transfer

Question 23

5 non-genetic mechanisms of AB resistance?

Answer 23

Biofilm- matrix encased communities of bacteria that are highly drug tolerant

Intracellular location

Slow growth

Spores

Persisters

Question 24

3 reasons for treatment failure other than AB resistance?

Answer 24

Inappropriate AB choice

Inappropriate dose and administration of AB

Poor penetration of AB into target site

Question 25

3 risk factors for hospital acquired infections?

Answer 25

Large number of ill people

Broken skin- surgical wound, IV, catheter

AB therapy may suppress natural flora

Question 26

3 ways of combatting AB resistance?

Answer 26

Prescribing strategies- tighter controls, temporary withdrawal of certain classes

Combination therapy

Quicker identifcation of infections caused by resistant strains

Question 27

3 responses to fungal infections?

Answer 27

Allergy

Mycotoxicoses- ingestion of fungi and their toxic products

Mycoses- superficial, cutaneous or subcutaneous invasion and colonisation of tissues

Question 28

3 targets for antifungal therapy?

Answer 28

Cell membrane- fungi use ergosterol instead of cholesterol

DNA synthesis- some compounds are selectively activated by fungi

Cell wall