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Antibiotics Flashcards

(56 cards)

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1
Q

Define differential toxicity?

A

It is a concept that the drug is more toxic to the infecting organism than to the host.

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2
Q

Define Antibiotics?

A

Substance produced by microroganism, which in small amounts inhibit or kill the bacteria
Majority are based on naturally occurring compounds.
May be natural or synthetic
Used to treat infections inside the body or outside using creams

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3
Q

Before the discovery of antibiotic penicillin, which treatments were used?

A

Silver nitrate and Arsenic
Both were extremely cytotoxic

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4
Q

Who discovered antibiotics and the first antibiotic produced?

A

Alexander Flemming-
Peniciliin produced from penicillium fungus

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5
Q

What are the socio-economic and healthcare advances related to antibiotics discovery?

A

Low morbidity and mortality rates
Increased survival rates with co-morbidities
Increased surgical survival rates
More complex surgical procedures can be performed
Fewer healthcare admissions
Lower economic burden
Fewer lost working hours
Increased productivity

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6
Q

Give examples of gram positive bacillus which can produce antibiotics

A

Bacillus subtilis
Bacillus polymyxa

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7
Q

What antibiotic does bacillus polymyxa produce?

A

Polymyxin

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8
Q

What antibiotic does bacillus subtillus produce?

A

Bacitracin

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9
Q

Give an exmaple of fungi and the antibody it produces

A

Penicillium notatum - penicillin

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10
Q

What Are Actinomycetes?

A

Actinomycetes are a group of Gram-positive, filamentous bacteria that are kind of a hybrid between bacteria and fungi in behavior and appearance.
They can also produce antibiotics

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11
Q

What makes an ideal antibiotic

A

🧫 Appropriate spectrum- Targets the right type of bacteria (narrow when possible, broad when needed).
❤️ Non-toxic to host- No damage to human cells; minimal side effects.
🔒 Low resistance potential- Less likely to create resistant strains (big win in long-term effectiveness).
⚠️ No hypersensitivity- Doesn’t trigger allergic reactions or immune overdrive.
🫀 Good tissue penetration- Reaches the site of infection effectively.
⏳ Long half-life (means that the antibiotic stays longer in the body, which reduces dosage frequency)
💊 No drug interactions Safe to use with other medications.
🧃 Easy to administer
💸 Affordable- Accessible to patients and healthcare systems

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12
Q

Define broad spectrum

A

drug is effective against a wide range of antibiotics (both gram + and - bacteria) like tetracycline

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13
Q

Define narrow spectrum

A

Drugs are effective against a limited number of species ( either gram + or -)

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14
Q

Define minimum inhibitory concentration

A

Minimum concentration of antibiotic required to inhibit the growth of microorganism

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15
Q

Define minimum bactericidal concentration?

A

Minimum concentration required to kill the microorganisms

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16
Q

Define bacteriostatic

A

Stops the bacteria from growing

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17
Q

Define bactericidal

A

Kills the bacteria

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18
Q

Define time dependent killing

A

Time-dependent killing means that the antibiotic works best when it stays in the body at a certain level for a longer period of time.
Longer exposure- more effective at killing

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19
Q

Define concentration dependent killing

A

Concentration-dependent killing means that the higher the concentration of the antibiotic, the more effective it is at killing bacteria.

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20
Q

Define prophlaxis

A

Antimicrobial agents are administrered to prevent infection

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21
Q

Define treatment

A

Antimicrobial agents are administred to cure existing or suspected infection

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22
Q

List some features of bacterial cell

A

Cell wall, cell membrane, capsules, pilli or fimbriae, cytoplasm, bacterial dna and nucleic acids, ribosomes, flagella, spores

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23
Q

What are the 5 antibacterial target sites?

Study These Flashcards
A

Cell wall
Cell membrane
Protein synthesis
Nucleid acid synthesis (DNA)
Antimetabolites

24
Q

What are 2 classes of antibiotics which inhibit cell wall synthesis. Give example of antibody from each class

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A

Beta-lactams - penicillin
Glycopeptides- vancomycin

25
What are 2 classes of antibiotics which target nucleic acid synthesis
Quinolones/ floroquinolones Rifamycins
26
Give an example of quinolones class antibiotic
ciprofloxacin
27
Give an example of rifamycins class antibiotic
Rifampicin
28
What are 4 classes of antibiotics which inhibit protein synthesis?
Macrolides Lincosamides Aminoglycosides Chloramphenicol
29
Give an example of macrolides class antibiotic
Eryhtromycin
30
Examples of lincosamides
clidamycin
31
Example of aminoglycosides
gentamicin/ streptomysin
32
Example of chloramphenicol
chloramphenicol
33
Give example of antibiotics which target cell membrane
Polymyxins B
34
Which classes of antibiotics act as antimetabolites?
Trimethroprim Sulfonamides
35
Examples of trimethrophrin and sulfonamides
SMX and TMP
36
What are safety issues associated with antimicrobial use?
Hypersensitivity reactions Antibiotic resistance Toxicity Interactions with other medications Fetal damage/ risk to pregnant women
37
Define antimicrobial resistance
Ability of an organism to resist the effects of chemotherapeutic drugs to which it is normally susceptible Resistance could be natural or genetically encoded by plasmids
38
Give an example of critical, high and medium bacteria to which we urgently need antibiotics?
Critical- Pseudomonas aureginosa High- Staphylococcus aureus (MRSA, VRSA) Medium- Streptococcus pneumoniae
39
What are some consequences of antibiotic resistance?
Treatment failure Increase in morbidity and mortality rates Surgical complications Increased demands on healthcare Lost working hours Lack of effective alternatives
40
Define multi-resistance and give an example of bacteria-
Multi-resistance is when bacteria is resistant to many antibiotics. E.g. Pseudomonas aeruginosa is resistant to B-lactams, quinolones and chloramphenicol (Inherent resistance) S. aureus- resistant to many antibiotics (Acquired)
41
Define cross-resistance
Occurs within the same class of antibiotics- E.g if bacteria is resistant to penicillin, it may also be resistant to cephalosporins and amoxicillin as these are alse beta-lactam antibiotics.
42
What should we do about antimicrobial resistance?
Promote responsible prescribing Improve infection prevention controls in humans and animals Raise awareness of the problem Development of new drugs Improve strnghtening of surveillance
43
The antibiotics which target cell wall are
bactericidal and time-dependent killing
44
Properties of antiviral drugs
must be able to enter infected cells must be able to interfere with viral nucleic acid synthesis. must be able to prevent the virus from attaching to host cell stimulate host immune response
45
What is HAART?
highly active antiviral therapy currently used against influenza, herpes, respiratory synctial virus
46
What does HAART consist of
3 medications including: Protease inhibitors - prevent viral replication Reverse transcriptase inhibitors - prevent production of DNA from RNA Fusion inhibitors- inhibit viral fusion to host cells preventing its entry and replication
47
what are 2 types of resistance
natural acquired
48
What are examples natural (inherent) resistant?
when bacteria lacks the target of antibiotic (e.g., membrane) when bacteria lacks the transport system for enzyme gram- bacteria have outer wall which establishes permeability against the antibiotics
49
Example of acquired resistance
1- modification of existing genetic materia i.e. mutation occurs in their DNA 2- acquisition of new genetic materia via vertical (from parents to offspring) or horizontal (from one microbe to another)
50
Why has antibitoic emergence occured
Due to overuse of antibiotics - exposes harmless bacteria to develop resistance Due to veterinary use - Antibiotics are commonly used in livestock to prevent infection but to also promote faster growth. this has lead to resistant bacterias like salmonella which can be passed from animals to humans via direct contact with animals or through food.
51
Provide2 examples of antibiotic resistance mechanisms
1- B-lactamse enzymes - break down beta lactam antibiotics by cleaving them e.g. penicillinases destroy penicillin 2- Altered PBP. bacteria mutates the target which B-lactams bind to e,g, MRSA has altered PBP site and is resistant to methicillin.
52
What is extended - spectrum B-lactamases?
These are enzymes produced by some bacteria. Their job is to break down β-lactam antibiotics, such as penicillins and cephalosporins, making the drugs ineffective. They can destriy wide range of B-lactam antibiotics.
53
The genes which code for extended spectrum beta lactamse are found where
plasmids these can be shared easily between bacteria through conjugation This means that even unrelated bacteria can "catch" resistance genes quickly.
54
How does bacteria become resistant to vancomycin
precursors change vancomycin can no longer bind
55
what should we done to stop antibiotic resistance
Promote responsible Prescribing 2. Improve infection prevention controls in human and animal systems 3. Raise awareness of the problem 4. Improve research to inform understanding 5. Development of new drugs, vaccines…. 6. Improve strengthening of surveillance….. 7. Strengthen UK & international collaborations
56
Alternative therapies to antibiotics
bacteriocins- proteins produced by bacteria to kill other bacteria often competitors Anti-virulence agents such as kinase inhibitors - stop viral replications eseential oils antimicrobial peptides predatory bacteria

Infection Science (18 decks)

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