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immuno bac Flashcards

1
Q

whats prontosil

A

the first example of a sulphonamide antibiotic

only effetcive with gp bacteria

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2
Q

charateritics

A

Bacteriostatic.- doesnt kill only stop repliccating

Synthetic

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3
Q

what is it sometimes used with

A 
Trimethoprim called  (co-trimoxazole).
both have some function
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4
Q

treat

A

UTIs, RTIs, bacteraemia and prophylaxis for HIV+ individuals.

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5
Q

Bactericidal

A

kills bacteria.

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6
Q

Bacteriostatic

A

stops bacteria growing

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7
Q

Antimicrobial

A

hemical that selectively kills or inhibits microbes (bacteria, fungi, viruses).

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8
Q

Antiseptic

A

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

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9
Q

what does ab resistance lead to

A

AB resistance leads to increased mortality, morbidity and cost
Increased time to effective therapy.
Requirement for additional approaches – e.g. surgery.
Use of expensive therapy (newer drugs).
Use of more toxic drugs e.g. vancomycin.
Use of less effective ‘second choice’ antibiotics.

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10
Q

where are Aminoglycosides

A

Bactericidal.
Target protein synthesis (30S ribosomaml subunit), RNA proofreading and cause damage to cell membrane.
Toxicity has limited use, but resistance to other antibiotics has led to increasing use.

can cause hearing loss

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11
Q

what is Rifampicin

A

Bactericidal.
Targets RpoB subunit of RNA polymerase.
Spontaneous resistance is frequent.
Makes secretions go orange/red – affects compliance taking long causes

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12
Q

what is Vancomycin

A

Bactericidal.
Targets Lipid II component of cell wall biosynthesis, as well as wall crosslinking via D-ala residues
Toxicity has limited use, but resistance to other antibiotics has led to increasing use e.g. against MRSA
given intravenously

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13
Q

what is Linezolid

A

Bacteriostatic.
Inhibits the initiation of protein synthesis by binding to the 50S rRNA subunit.
Gram-positive spectrum of activity.
doesn’t effect gn

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14
Q

Daptomycin

A 
Bactericidal.
Targets bacterial cell membrane.
Gram-positive spectrum of activity.
Toxicity limits dose. 
can't target lps on gn
given intervenosly
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15
Q

Beta-lactams

A

Interfere with the synthesis of the peptidoglycan component of the bacterial cell wall.
Examples include Penicillin and methicillin.
Bind to penicillin-binding proteins.
PBPs catalyse a number of steps in the synthesis of peptidoglycan.
inhibite biosythesis of cell wall

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16
Q

Antibiotics target many different bacterial processes and are selectively toxic 


A

they inhibit process in bacterial cell not in human cells
The large number of differences between mammals and bacteria result in multiple targets for antibiotic therapy – selective toxicity

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17
Q

What is unique to bcteira

A

peptidoglycan wall

lpa

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18
Q

Macrolides

A

treats gonococal
Gram-positive and some Gram-negative infections.
Targets 50S ribosomal subunit preventing amino-acyl transfer and thus truncation of polypeptides.
preventing growth

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19
Q

Quinolones

A

Synthetic, broad spectrum, bactericidal.
Target DNA gyrase in Gm-ve and topoisomerase IV in Gm+ve. dna damage and death of organism
against gonnocal and lung

20
Q

Breakpoint

A

(clinically-achievable concentration)

if bacteria can grow at that point or higher than reistant, if less that suseptible

21
Q

what does routine use of penicllin provide

A

Routine use of penicillin provided selective pressure for the acquisition and maintenance of resistance genes.

22
Q

how does antiboitic resistance occur

A

Altered target site.
Inactivation of antibiotic.
Altered metabolism.
Decreased drug accumulation.

23
Q

what is altered target site

A

Can arise via acquisition of alternative gene or a gene that encodes a target-modifying enzyme.
Methicillin-resistant Staphylococcus aureus (MRSA) encodes an alternative PBP (PBP2a) with low affinity for beta-lactams.
Streptococcus pneumoniae resistance to erythromycin occurs via the acquisition of the erm gene, which encodes an enzyme that methylates the AB target site in the 50S ribosomal subunit.

24
Q

Inactivation of antibiotic

A

Enzymatic degradation or alteration, rendering antibiotic ineffective.

25
Q

Altered metabolism

A

Increased production of enzyme substrate can out-compete antibiotic inhibitor (e.g. increased production of PABA confers resistance to sulfonamides).
Alternatively, bacteria switch to other metabolic pathways, reducing requirement for PABA.

26
Q

Decreased drug accumulation

A

Reduced penetration of AB into bacterial cell (permeability) and/or increased efflux of AB out of the cell – drug does not reach concentration required to be effective.

27
Q

Sources of antibiotic resistance genes

A

Plasmids – extra-chromosomal circular DNA, often multiple copy. Often carry mutliple AB res genes – selection for one maintains resistance to all.
Transposons. Integrate into chromosomal DNA. Allow transfer of genes from plasmid to chromosome and vice versa.
Naked DNA. DNA from dead bacteria released into environment.

28
Q

what is transformation

A

allow bacteria to take up dna from their environment

plasmid or chromosomes

29
Q

Transduction

A

phage-mediated DNA transfer)

30
Q

Conjugation

A

pilus-mediated DNA transfer)

31
Q

Biofilm

A

matrix encased community of bacteria that are highly drug tolerant

32
Q

intracellular location

A

in human cells shielding them

33
Q

Slow growth

A

if they not using lots of process to replicate then antiboitics can’t inhibit them

34
Q

Spores

A

VERY RESISTANT TO HEAT SNTISEPTIC AND ANTIBOITIC

35
Q

Persisters

A

dormant

not using any process that are inhibited by antibiotics

36
Q

Non-genetic mechanisms of resistance/treatment failure

A 
Biofilm
Intracellular location
Slow growth
Spores
Persisters
37
Q

why may treatment fail

A

Inappropriate choice for organism
Poor penetration of AB into target site
Inappropriate dose (half life)
Inappropriate administration (oral vs IV)
Presence of AB resistance within commensal flora e.g. secretion of beta-lactamase

38
Q

can Genes encoding resistance can be shared between bacteria via horizontal gene transfer

A

yep

39
Q

why do hospitals provide strong selective pressure for AB resistance

A

Large numbers of infected people receiving high doses of antibiotics - strong selective pressure for emergence/maintenance of AB resistance

40
Q

Risk-factors for HAI

A

High number of ill people! (immunosuppression)
Crowded wards
Presence of pathogens
Broken skin – surgical wound/IV catheter
Indwelling devices - intubation
AB therapy may suppress normal flora
Transmission by staff – contact with multiple patients

41
Q

why is bacteria killing gut and microbiota dangerous

A

Pathogen has no competition - overgrowth

42
Q

Addressing resistance

A

Prescribing strategies – tighter controls, temporary withdrawal of certain classes. Restriction of ABs for certain serious infections
Reduce use of broad-spectrum antibiotics- damage microbiota
Quicker identification of infections caused by resistant strains
Combination therapy 2 or more ab tohether
Knowledge of local strains/resistance patterns

43
Q

Overcoming resistance

A

Modification of existing medications to e.g. Prevent cleavage (beta-lactams) or enhance efficacy. E.g. Methicillin.
Combinations of antibiotic + inhibitor of e.g. Beta-lactamase. E.g. Augmentin.

44
Q

how to fungi eat

A

ukaryote organisms that digest their food outside of the cell by secreting hydrolytic enzymes which can break down biopolymers to be absorbed for nutrition

45
Q

what do fungi cause

A

Allergy – allergic reactions to fungal products e.g. allergic bronchopulmonary aspergillosis (ABPA)
Mycotoxicoses – ingestion of fungi and their toxic products e. g. aflatoxin
Mycoses – superficial, subcutaneous or systemic colonisation, invasion and destruction of human tissue.

46
Q

what are the targets for antifungal therapy

A

cell membrane
dna sythesis
cell wall

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