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Medical And Microbiology > Unit 3 B > Flashcards

Unit 3 B Flashcards

1
Q

List 5 characteristics of an ideal antimicrobial drug.

A

Toxic to the microbe but nontoxic to the host

Microbicidal rather than microbiostatic

Does not lead to the development of antimicrobial resistance.

Reasonably priced

Does not disrupt the host’s health by causing allergies or predisposing the host to other infections.

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2
Q

Chemotherapeutic drug

A

Any chemical used in the treatment, relief, or prophylaxis of a disease.

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3
Q

Prophylaxis

A

Use of a drug to prevent imminent infection of a person at risk.

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4
Q

Antimicrobial chemotherapy

A

The use of drugs to control infection.

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5
Q

Antimicrobials

A

All-inclusive term for any antimicrobial drug, regardless of what type of microorganism it targets

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6
Q

Antibiotics

A

Substances produced by the natural metabolic processes of some microorganisms – or created by scientists – that can inhibit or destroy microorganisms; generally, the term is used for drugs targeting bacteria & not other types of microbes.

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7
Q

Naturally derived antibiotics come from many sources, but most come from 2 genera of bacteria & 2 genera of fungi. What are these genera?

A

Bacteria: Streptomyces & Bacillus

Fungi: Penicillium & Cephalosporium

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8
Q

Semisynthetic antibiotics

A

new drugs are created by chemically altering the structure of naturally occurring antibiotics.

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9
Q

Synthetic antibiotics

A

Some natural compounds cannot be obtained without the destruction of a habitat or organismal population. Drugs created in the laboratory mimic the action of these natural compounds. (fully made in lab)

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10
Q

What 3 factors must be taken into account when choosing an antimicrobial drug for treatment?

A

Identity (the identity of the microorganism causing the infection)

Sensitivity (the degree of the microorganism’s susceptibility (sensitivity) to various drugs)

Condition (the overall medical condition of the patient)

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11
Q

Kirby-Bauer

A

Process: take a petri plate and cover with the bacteria, place on the plate antibiotic disc.

Read the results: How close can the bacteria grow to the antibiotic disc. (closer to the disc more resistant.

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12
Q

Etest

A

Process: paper strip with antibiotic with concentration variation, tells up what dose the antibiotic is effective.

Read the results: bottom of the tear drop tells us what concentration of antibiotic is needed to stop growth of bacteria

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13
Q

MIC test

A

Process: Each row gets its own antibiotic, across the row the concentration of antibiotic increases. You can use this test to see if the bacteria is cidal or static.

Read the results: go across and at the x is the smallest effective dosage of drug, and you can take it and put it on a petri plate to see if colonies grow.

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14
Q

Be able to calculate & compare TI values to choose the appropriate drug in a scenario.

A

Toxic dose to person divided by toxic dose to infectious agent. (higher number better)

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15
Q

What aspects of patient history may play a role in choosing an antibiotic?

A

Preexisting medical conditions

Allergies

Underlying liver or kidney disease

Age like infants and elderly

pregnancy

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16
Q

What factors could lead to an antibiotic working in vitro (in lab tests), but failing during patient treatment?

A

Inability of the drug to diffuse into that body compartment (brain, joints, skin)

Resistant microbes in the infection that didn’t make it into the sample collected for testing.

An infection caused by more than one pathogen (mixed), some of which are resistant to the drug.

The patient did not take the antimicrobials correctly.

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17
Q

Define selective toxicity.

A

Antimicrobial drugs should kill or inhibit microbial cells without simultaneously damaging host tissues.

The best drugs in current use block the actions or synthesis of molecules in microorganisms but not vertebrate cells.

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18
Q

Critical thinking: Why are pathogens like viruses harder to design effective drug therapies for?

A

Viruses use our machinery to replicate, so it is harder to develop an effective drug without harming us.

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19
Q

Broad-spectrum

A

effective against more than one group of bacteria (ex. Tetracyclines)

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20
Q

Narrow-spectrum

A

Only target a specific group (ex. Polymaxin & Penicillins)

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21
Q

What are the 5 metabolic targets of antibiotics.

A

Inhibition of cell wall synthesis

Inhibition of nucleic acid (DNA & RNA) structure & function

Inhibition of protein synthesis

Interference with cell membrane structure of function

Inhibition of folic acid synthesis

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22
Q

Penicillins

A

MOA- This class blocks the peptide crosslinking of peptidoglycan by inhibiting penicillin binding proteins (PBPs), making cell wall synthesis impossible.

Ex.- Ampicillin, Amoxicillin, Penicillin, and Methicillin.

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23
Q

Cephalosporins

A

MOA- This class blocks the peptide crosslinking of peptidoglycan by inhibiting penicillin binding proteins (PBPs), making cell wall synthesis impossible.

Ex.- Ceftriaxone, Cefalexin

24
Q

Tetracyclines

A

MOA- Binds to the 30S ribosomal subunit, preventing tRNA attachment.

Ex.- Tetracycline, Doxycycline.

25
Q

Macrolides

A

MOA- Binds to the 50S ribosomal subunit, preventing translocation of the ribosome.

Ex.- Erythromycin, Clarithromycin, and Azithromycin.

26
Q

Sulfonamides

A

MOA- Structural analogs of PABA, serving as competitive inhibitor to folic acid synthesis (needed for purine/pyrimidine production)

Ex.- Sulfadiazine, Sulfamethoxazole

27
Q

Fluoroquinolones

A

MOA- Inhibit gyrase & topoisomerase, blocking the ability of these enzymes to prevent supercoiling.

Ex.- Ciprofloxacin, Levofloxacin

28
Q

Polymyxins

A

MOA- interacts with membrane phospholipids of bacterial membranes, altering their permeability.

Ex.- Polymyxin B, Colistin

29
Q

What are the proposed methods for treating biofilm infections?

A

Interrupting quorum sensing pathways. Adding DNase to antibiotics. Pretreatment.
Impregnating implanted devices like urinary catheters with antibiotics prior to insertion.

30
Q

Allylamines

A

membrane sterol synthesis inhibition

31
Q

Azoles

A

membrane sterol synthesis inhibition

32
Q

Echinocandins

A

wall synthesis inhibition

33
Q

Macrolide polyene

A

(antibiotics) membrane disruption

34
Q

What is the MOA of praziquantel & what type of organism does it target?

A

MOA: target the þ subunits of voltage-gated Ca2+ channels. It is anti-parasitic it treats infections caused by worms (liver flukes) or Schistosoma (blood flukes).

35
Q

What are the three most common modes of action for antivirals & provide an example of each.

A

Barring penetration of the virus into the host cell (inhibition of virus entry): Enfuvirtide, Amantadine (Zanamivir, Oseltamivir)

Inhibition of Nucleic Acid Synthesis (Blocking the transcription & translation of viral molecules): Acyclovir, Ribavirin, Zidovudine, Lamivudine, Didanosine, Zalcitabine, Stavudine, Nevirapine, Efavirenz, Delavirdine

Inhibition of Viral Assembly/Release (Preventing maturation of viral particles): Indinavir, Saquinavir

36
Q

Intrinsic

A

bacteria must be resistant to any antibiotic that they themselves produce.

37
Q

Acquired resistance

A

bacterial resistance to a drug to which they were previously sensitive.

38
Q

While antibiotic resistance can be found in secluded natural systems, why does extensive antibiotic use in medicine increase the amount of antibiotic resistance in pathogens?

A

Because when they are exposed to the antibiotic they are more likely to evolve resistance to antibiotics (this is to survive)

39
Q

What are the 2 major ways that antibiotic resistance emerges in bacteria?

A

Resistance through spontaneous mutation.
Resistance through horizontal transfer. (Resistance (R) factors: Virulence genes that are transferred through conjugation, transformation or transduction.

40
Q

5 mechanisms of antibiotic resistance were discussed. You should be able to describe all 5 ways. 1

A

New enzymes are synthesized, inactivating the drug

41
Q

5 mechanisms of antibiotic resistance were discussed. You should be able to describe all 5 ways. 2

A

Permeability or uptake of the drug into the bacterium is decreased.

42
Q

5 mechanisms of antibiotic resistance were discussed. You should be able to describe all 5 ways.

A

Drug is immediately eliminated.

43
Q

5 mechanisms of antibiotic resistance were discussed. You should be able to describe all 5 ways. 4

A

Binding sites for drugs are decreased in number and/or affinity

44
Q

5 mechanisms of antibiotic resistance were discussed. You should be able to describe all 5 ways. 5

A

An affected metabolic pathway is shut down, or an alternative pathway is used.

45
Q

How does antibiotic treatment encourage the formation of antibiotic-resistant cells?

A

When the population of bacteria is exposed to the antibiotics it kills the sensitive individuals so the ones who live will keep replicating this is how we slowly create an antibiotic resistant bacteria.

46
Q

What percentage of cases where antibiotics are prescribed for ear, nose, & throat infections is likely viral?

A

75%

47
Q

Define what a superinfection is.

A

When a nonproblem pathogen is left with no competition (due to antibiotic) and can replicate and become a problem/infection.

48
Q

Why is a potential post-antibiotic era alarming?

A

If we run out of effective antibiotics, then bacterial infections will be more likely to kill us like in the past.

49
Q

Provide an example of a new approach to antibiotic therapy.

A

Novel approach: disabling host molecules that the invaders use to enhance their position.

Bacteriophage solutions: Using bacteriophages in Eastern European countries. Incorporating phage into wound dressings. Phages are extremely specific & only infecting one species of bacteria, leaving normal microbiota alone.

50
Q

Define the function of probiotics.

A

Preparations of live microorganisms fed to animals & humans to improve intestinal bio. Replace microbes lost during antimicrobial therapy. (contains bacteria)

51
Q

Define the function of prebiotics.

A

Nutrients that encourage the growth of beneficial microbes in the intestine. (feed bacteria)

52
Q

Define the function of repoopulation (fecal transplant) therapies.

A

Involves transfer of feces, containing beneficial normal biota, from healthy to affected patients via colonoscopy.

53
Q

What are the three categories to major antimicrobial drug side effects?

A

Direct damage to tissues through toxicity

Allergic reactions

Disruption in the balance of normal microbial biota

54
Q

Why should pregnant women not be prescribed tetracycline?

A

It binds to the enamel of teeth and causes permanent gray to brown discoloration permanently in babes. (can cause live damage in pregnant individuals)

55
Q

Is black hairy tongue actually hairy? If not, what is it?

A

It is not actually hairy, it is deposits of red blood cells.

56
Q

What is the most common side effect complain of oral antibiotics? What is the likely cause of this symptom?

A

Diarrhea: direct irritation of the intestinal lining and cause disruption of the intestinal microbiota

57
Q

Describe what an antigen is & how this may sometimes lead to allergy.

A

Drugs acts as an antigen that stimulates the allergic response.

Medical And Microbiology (16 decks)

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