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Drugs And Disease > Treatment of bacterial infections > Flashcards

Treatment of bacterial infections Flashcards

1
Q

What is an antibiotic?

A

Derived from microorganisms.

Can be broad or narrow spectrum.

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2
Q

Semisynthetic?

A

Chemical modification of antibiotics.

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3
Q

Synthetic?

A

Chemically synthesised in the lab (antibacterical).

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4
Q

What are the 4 key mechanisms of antibiotic action?

A

Inhibit bacterial cell well.
Inhibit bacterial DNA synthesis.
Inhibit bacterial protein synthesis.
Act as antimetabolites.

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5
Q

Staphylococcal aureus?

A

Gram +ve.
Grow in grape like clusters on skin and responsible for wound infections.
MRSA.

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6
Q

Streptococcal pneumoniae.

A

Gram +ve.
Grow in chain like clusters.
Cause pneumonia and meningitis.

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7
Q

Escherichia coli

A

Gram -ve.
Rod like
Many urinary tract infections.

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8
Q

Haemophilus influenzeae

A

Gram -ve.

Vaccination about HiB but other forms cause respiratory tract/ear infections.

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9
Q

Explain gram positive bacteria.

A

Peptidoglycan cell wall ~ 30nm
= thick, interacts with gram stain.
Plasma membrane.

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10
Q

Explain gram negative bacteria.

A 
Outer membrane (protective) with water filled 'porin' channels.
Proteins joining outer membrance to peptidoglycan (~3nm) across periplasmic space.
Inner plasma membrane.

Stains poorly - thick outer membrane where stain can’t get through and then very thin peptidoglycan therefore takes up little stain.

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11
Q

Explain the bacterial peptidoglycan cell wall.

A

N-acetylmuramic acid (NAMA) and N-acetylglucosamine (NAG) are linked via sugar residues.

NAMA and NAMA peptide side chains are linked by amide linkage.

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12
Q

Explain the formation of the peptidoglycan cell wall.

A

NAMA, NAG and amide linkage (building blocks) are formed inside the cell and transported across the plasma membrane attached to a lipid transporter.

Released and linked to each other by TRANSGLYCOSYLASE enzyme into a linear strand.

Linear strand are crossed linked by TRANSPEPTIDASE.

Lipid transporter returns to the cell interior.

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13
Q

Explain the general inhibition of the cell wall production.

A

B-lactam antibiotics (bacteriocidal)
- penicillins, cephalosporins, carbapenems, monobactams.

They prevent the amide bonds forming between NAMA peptide side chains by inhibiting transpeptidase and transglycosylase.

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14
Q

Explain the structure of B lactam.

A

4 ring structure - highly reactive and interacts with transglycosylase and transpeptidase…therefore NO CELL WALL FORMATION.

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15
Q

What is the effect of changing th side chains of B lactam?

A

Alter…
…oral bioavailability (stability in stomach acid/interactions with food)
…susceptibility to B-lactamase
…spectrum of activity.

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16
Q

What is clavulanic acid?

A

Inhibits many forms of B-lactamase.

17
Q

What is B-lactamase?

A

Destroys the B-lactam rings - doesn’t interact with and inhibit enzymes - cell wall is still produced.

18
Q

Benzyl penicillin?

A

Pencillin antibiotic.
Pen G.
Broad spectrum, gram -ve, not orally active, susceptible to B-lactamase.

19
Q

Methicillin?

A

Penicillin antibiotic - resistant to Blactamase but by other methods. Not orally active. nephrotoxic.

20
Q

Axmocillin.

A

Penicillin antibiotic - administered with clavulanic acid - co-amoxiclav.

21
Q

Name a cephalosporin antibiotic.

A

Cefalexin. Good for gram +ve not -ve, susceptible to B-lactamase.

22
Q

Side effects of b-lactams?

A

Upset the gut flora - GI disturbances
Hypersensitivity reactions; rash - anaphylatic shock.
Convulsions if given intrathecally.

23
Q

Name 3 other antibacterials that interfere with the cell wall production.

A

Cycloserine - prevent NAMA side chain formation
Vancomycin - inhibit release of cell wall building block from lipid transporter (good for +ve).
Bacitracin - prevent recycling of lipid transporter.

24
Q

Explain the inhibition of DNA synthesis.

A

By Fluroquinolones eg ciprofloxacin.
Inhibit the folding of DNA by DNA gyrase
Good for +ve and -ve, orally active
BUT - doesn’t cross BBB, antacids prevent absorption from gut.

25
Q

Explain how you would inhibit protein synthesis.

A

The structure and size of ribosomes are different.
Human: 40S and 60S.
Bacteria: 50S (where transpeptidation occurs) and 30S (3 binding sites for DNA).

26
Q

Explain aminoglycosides.

A

Streptomycin.
Bacteriocidal.
Causes misreading of the 30S sunbunit
Good against aerobic gram -ve bacteria. Transported across the cell wall by an O2 dependent transporter (which can be blocked by chloromephenicol).

Causes nephro and ototoxicity.

27
Q

Explain tetracyclines?

A

Doxycycline.
Compete with tRNA for codon on mRNA 30S.
Broad spectrum - bacteriostatic - resistance is a problem.
Orally active but forms insoluble complexes with Ca++ and iron.
GI upset.

28
Q

Explain chloramphenicol

A

Inhibits transpeptidation.
Broad spectrum, bacteriostatic, resistance is problem
Idiosyncratic bone marrow supression
Used in eye drops to treat bacterial conjunctivitis,

29
Q

Explain macrolides.

A

Erythromycin. Inhibits translocation of the risbosome along the mRNA.
Bacteriostatic.

30
Q

What are antimetabolites?

A

Chemicals that inhibit the use of a metabolite.

31
Q

How do bacteria synthesis folate and then use it for DNA synthesis?

A

PABA –dihydropteroate synthase–>folate–dihydrofolate reductase–>tetrahydrofolate… DNA synthesis.

32
Q

Explain sulfonamides.

A

Sulfanilamide
Analogues of PABA - compeitive inhbitor of dihydropteroate synthase.
Bacteriostatic
Orally active - corss the BB, metabolised in the liver.

33
Q

Trimethoprim?

A

Inhibit DHFR

1000x more potent in bacteria.

34
Q

Explain the drug treatment of TB caused by mycobacterium tuberculosis.

A

Thick lipid rich, waxy cell wall (not g+/-ve).

Rifampicin - combinations, for a long time.

35
Q

Explain resistance.

A

Resistance occurs to spontaneous mutations that anable the bacteria to withstand the deletrious effects of the drugs…and bacteria have high replication rates, mutations occur more frequently

Resistant genes = plasmids - easily passed between bacteria.
Plasmid genes can act as transposons - jump from plasmid DNA to chromosomal DNA and back…spread resistance.

36
Q

What are the 6 main ways that resistance occurs?

A

1) Metabolic bypass - alternative means of producing folic acid.
2) Target overproduction - excessive production of PBPs - outcompete penicillin.
3) Active excretion of antibacterial from inside bacteria - resistance to tetracyclines and erythromycin.
4) Reduced entry of antibacterial across cell wall - mutation in porins?
5) Destruction or inactivation of the antibacterial (B-lactamase)
6) Mutations in target molecules to make them less sensitive to anitbiotics - vancomycin resistance

37
Q

How can you decrease the development of resistant strains?

A

1) Decrease inaapropriate use of antibiotics
2) Limit key antibiotics
3) Use antibiotics in rotations/combinations
4) Avoid prophylaxis in animal feed stuff.

Drugs And Disease (22 decks)

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