Ch 20 Antimicrobial Drugs Flashcards

1
Q

What is an antibiotic?

A

A substance produced by microbes that inhibits other microbes.

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2
Q

What’s the name for synthetic sulfa drugs?

A

Antimicrobial

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3
Q

What is antibiotic resistance?

A

Formerly effective medications have less impact on bacteria

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4
Q

Is it easy to find drugs against prokaryotic cells that don’t affect eukaryotes?

A

Yes

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5
Q

Are fungi, protozoan or helminths difficult to treat?

A

Yes because their cellular structure is alike human cells.

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6
Q

What is a superinfection?

A

When the pathogen develops resistance to antibiotics.

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7
Q

What are the five major action modes of antibacterial drugs?
CONCEPT QUESTION
Clue: qps

A
Inhibition of:
Cell wall processes - penicillin
Protein synthesis - tetracycline
Nucleic acid replication - rifampin
Plasma membrane processes - polyxin B
Metabolism - sulfanilamide
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8
Q

How could a magic bullet work?

A

Not affecting host cells

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9
Q

What is another name for chemotherapy?

A

Selective toxicity.

Finds and destroys pathogens but not harm the host.

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10
Q

How is the Disk Diffusion Test run?

A

An agar plate is uniformly inoculated
Chemotherapeutic disks are placed
Zones of inhibitions form
Largest zone, best performing drug

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11
Q

What is the E test?

A

The minimal inhibitory concentration, MIC, of a drug is found. The epsilometer shows the lowest concentration that blocks bacterial growth.

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12
Q

What is a broth dilution test?

A

The minimal bactericidal concentration, MBC, of an antimicrobial drug is found.

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13
Q

What are the four mechanisms of microbial resistance to antimicrobial drugs?
Concept question
Draw Fig. 20.20

A

Blocking entry
Inactivation by enzymes
Alteration of target molecule
Effluent of antibiotic drug

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14
Q

Which are more resistant to antibiotics, Gram negative or Gram positive?

A

Gram negative are more resistant because of their less permeable cell walls and porins.

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15
Q

What is the therapeutic index?

A

Measuring risk vs. benefit

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16
Q

What is a bacteriophage?

A

A virus that attacks bacteria.

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17
Q

What are bacteriocins?

A

Bacterial toxins produced to inhibit the growth of similar bacteria.

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18
Q

What is a persister cell?

A

A surviving bacteria that has resistant characteristics.

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19
Q

Who discovered penicillin?

A

1928 Fleming

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20
Q

What is the difference between narrow and broad antibiotics?

A

Broad kill the infection and many other desirable bacteria; narrow only kill the intended target.

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21
Q

What is a beta-lactam ring, what drugs use it, and what does it do?

A

The β-lactam ring is named because the nitrogen atom is attached to the β-carbon atom relative to the carbonyl. It is the core structure of penicillins. Nearly all of these antibiotics work by inhibiting bacterial cell wall biosynthesis.

22
Q

What are macrolides?

A

lactose ring
Erythromycin 50 S
Remember Christmas decoration

23
Q

What is an abscess and how do they relate to microbiology?

A

An accumulation of pus.
Bacterial accumulation infection.
S. aureaus and S. pyrogenes

24
Q

What is meningitis?

A

Inflammation of the meninges caused by viral or bacterial infection

25
Q

What are protease inhibitors?

A

Protesase is an enzyme that breaks down proteins, so the protease inhibitor stops viruses like HIV.

26
Q

What are integrase inhibitors?

A

Antiretroviral drug designed to block the action of integrase, a viral enzyme that inserts the viral genome into the DNA of the host cell.

27
Q

What is a virus?

A

DNA or RNA in a protein coat. Very small.

28
Q

What are inferons and name a drug that promotes interferon production?

A

Used against viruses that inhibits warts.

Imiquimod

29
Q

What type of drug is used to treat malaria and what is a specific example?

A

Antiprotozoan - mosquitoes

Choloroquine - from tree bark

30
Q

What is acyclovir used for?

A

Viral infections, like chickenpox

31
Q
  1. Distinguish between the term antibiotic and disinfectant:
A
  • ANTIBIOTIC: substance produced by microorganisms that in small amounts inhibits another microorganism (selective toxicity); 1928 Fleming → Penicillium & Staph aureus
  • DISINFECTANT: chemical used to kill microorganisms
32
Q
  1. Give examples of bacteria and fungi that produce antibiotics:
A

-BACTERIA THAT PRODUCE ABX:
Bacillus subtilis → bacitracin
-FUNGI THAT PRODUCE ABX:
Penicillium chrysogenum → Penicillin

33
Q

3.Explain what is meant by the term broad-spectrum antibiotic:

A
  • BROAD-SPECTRUM ANTIBIOTIC: antibiotics that affect a broad range of gram+ or gram- bacteria
  • (can destroy normal flora which competes with and checks growth of pathogen → leaves open to superinfection)
  • Superinfection → growth of target organism that has developed resistance to the ABX, replaces original sensitive strain and infection continues
  • Bactericidal → KILLS
  • Bacteriostatic: uses host own defence mechanism to kill bacteria (maybe afraid of toxic results…)
34
Q
  1. Identify the cellular targets of antibiotics:
A
  • ABX CELLULAR TARGETS: (fives modes of action)
  • inhibition of cell wall synthesis, penicillin
  • inhibition of protein synthesis: (Erythromycin, Tetracycline)
  • inhibition of nucleic acid replication and transcription
  • injury to plasma membrane
  • inhibition of synthesis of essential metabolites
35
Q
) For the following classes of antibiotics identify the site and mechanism (if known) of action and type of bacteria typically affected. (This is not a list that you need to memorize, but you should be aware of the cellular targets for antibiotics): 
A. Penicillins
B. Monobactams
C. Cephalosporins
D. Carbapenems
E. Bacitracin
F. Vancomycin
G. Isoniazid
H.  Ethambutol
I. Aniino
J. Tetracyclines
I. Chloramphenicol
K.  Macrolides
M. Polymyxin B
N. Rifamycin
O. Quinolones
P. Sulfonamides
Q. Oolyenes
R. Azoles
S. Nucleoside analogs
A

?

36
Q

6) Discuss the advantages of using more than one antibiotic in treating an infection:

A
  • synergism: ex: PCN & streptomycin to treat bacterial endocarditis
  • damage to cell walls by PCN makes it easier for streptomycin to enter
37
Q

7) Identify the major problem in the use antifungal and antiprotozoal drugs:

A
  • Eukaryotes, such as fungi, use the same mech to synth proteins and nucleic acids as higher animals → more difficult to find a point of selective toxicity in eukaryotes than in prokaryotes
  • Quinacrine: tx for giardiasis→ optic nerve damage if dosage not controlled
    ANTIFUNGAL TARGETS:
    Membrane sterols → Amphotericin B, miconazole → combine with sterols in PM, ergosterol vs cholesterol, KIDNEY TOXICITY
    Cell wall → B-glucan, echinocandins, Aspergillus, Candida, Pneumocystis
    Inhibit nucleic acids → flucytocine - converted into cytosine analog
    Block microtubule assembly → griseofulvin
    ANTIPROTOZOAN:
    Chloroquine → inhibits DNA synthesis (malaria)
    Diiodohydroxyquin → unknown mode of action, amoebic diseases
    Metronidazole → damages DNA → Entamoeba, Trichomonas
    Nitazoxanide → interferes with metabolism of anaerobes

NOTE: ANTIVIRALS:
-In the developed world- 60% viral, 15% bacteria → infrastructure (water, sewers, etc.) / (pretty much opposite in the underdeveloped world)
-attachment / penetration / uncoating / DNA, RNA synthesis / assembly
→ protease inhibitors (Indinavir: HIV)
→ Integrase inhibitors (HIV)
→ Inhibit attachment (Zanamivir: influenza / block CCR5: HIV)
→ inhibit uncoating (Amantadine: influenza)
→ enzyme inhibitors: fusion inhibitors (enfuvirtide:HIV), inhibit attachment(zanamivir:influenza), inhibit uncoating(amantadine:influenza)
→ interferons: prevent spread of viruses to new cells (alpha interferon:viral hepatitis), imiquimod (promotes interferon production)
*HIV: cocktails are the key! (stats - hit with 3… statistically super low that mutation can escape…)
AZT, acyclovir→ looks similar… gets in there and screws things up. (analogue)
Nucleoside analogues are nucleosides which contain a nucleic acid analogue and a sugar. Nucleotide analogs are nucleotides which contain a nucleic acid analogue, a sugar and one to three phosphate groups.Nucleoside and nucleotide analogues can be used in therapeutic drugs, include a range of antiviral products used to prevent viral replication in infected cells. The most commonly used is acyclovir, although its inclusion in this category is uncertain, because it acts as a nucleoside but contains no actual sugar, as the sugar ring is replaced by an open-chain structure.

38
Q

8) Define zone of inhibition:

A

-ZONE OF INHIBITION: In a Kirby-Bauer test, the size of the zone of inhibition indicates the degree of sensitivity of bacteria to a drug. In general, a bigger area of bacteria-free media surrounding an antibiotic disk means the bacteria are more sensitive to the drug the disk contains.

39
Q

9) Define minimal inhibitory concentration: (MIC)

A
  • the lowest antibiotic concentration that prevents visible bacterial growth
  • plastic-coated strip contains a gradient of antibiotic concentrations, & the MIC can be read from a scale printed on the strip
  • E-test
  • determines of drug is bacteriostatic
40
Q
  1. Describe the advantage of the broth dilution test: (MBC)
A
  • lowest concentration of a chemotherapeutic agent that kills bacteria
  • minimal bactericidal concentration
  • determined by making a sequence of decreasing concentrations of the drug in a broth; then inoculated w/ test bacteria; the wells that don’t show growth can be cultured in broth or on plates free of the drug; if growth occurs the drug was not bactericidal & MBC can be determined
41
Q

11) Distinguish between nosocomial infections and those infections found in the general population:

A
  • nosocomial infections are hospital acquired
42
Q

12) Identify and discuss several advances of the last 100 years that have contributed to reducing the incidence of disease:

A

?

43
Q
  1. State the three mechanisms by which bacteria can inactivate antibiotics:
A

?

44
Q

14) Discuss the genetic mechanisms by which bacteria develop (acquire) resistance to antibiotics: CONCEPT QUESTION

A
  • enzymatic destruction or inactivation of the drug
    → mainly affects PCN & cephalosporins
    → MRSA
    → destruction or inactivation by enzymes mainly affects antibiotics that are natural products
  • prevention of penetration to the target site w/in the microbe
    → Gram - (more resistant to ABX because of cell wall that restricts absorption of many molecules to mvmnts through openings called porins)
    → mutants modify porin so ABX are unable to enter the periplasmic space
    → B-lactamases are present in periplasmic space, ABX enter & get degraded before entering the cell
  • alteration of the drug’s target site
    → (seen in viruses… reverse transcriptase → things change so no longer affected by drugs)
  • rapid efflux (ejection) of the antibiotic
    → (pseudomonas → great “pumping system” to get rid of “toxic” agents)
45
Q

15) Discuss the bacterial mechanisms by which resistance can be spread throughout a clinical environment and human behaviors that contribute to the spread of resistance:

A
  • ex: microbe could become resistant to trimethoprim by synthesizing large amounts of enzyme against drug that’s targeted
  • polyene ABX can become less effective when resistant organisms produce smaller amounts of the sterols against which the drug is effective
46
Q

16) Define MRSA & discuss the problem with MRSA in the clinical setting & Identify methods that can be employed to reduce the spread of MRSA in the clinical setting:

A
  • methicillin resistant staphylococcus aureus
  • resistant to bacteria; spreads in hospital
  • super bug
  • hand washing
  • isolation
47
Q

17) Identify and discuss both bacteria and human factors that contribute to the emergence and transmission of bacterial resistance to antibiotics:

A
  • taking ABX in home can affect one person’s flora
  • social drug
  • missue
  • costly
  • use old ABX
  • use someone elses
  • injection→ clear air bubble; don’t inhale;
48
Q

18) Discuss methods to control the appearance of drug resistance in bacteria:

A
  • finish regiment
  • never use old
  • never use someone else’s
  • dosage
  • most specific ABX prescribed
  • hand washing
  • isolation
49
Q

What is beta-lactam ring, beta-lactamase, and beta-lactamase inhibitors?

A
  • chemical structure in antibiotics;
  • bacterial enzyme that increases resistance to beta-lactam ring antibiotics;
  • drug inhibitors to fight beta-lactamase
50
Q

What is a side affect of taking tetracycline?

A

Green teeth