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Flashcards in Ch 20 Antimicrobial Drugs Deck (50)

What is an antibiotic?

A substance produced by microbes that inhibits other microbes.


What's the name for synthetic sulfa drugs?



What is antibiotic resistance?

Formerly effective medications have less impact on bacteria


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



Are fungi, protozoan or helminths difficult to treat?

Yes because their cellular structure is alike human cells.


What is a superinfection?

When the pathogen develops resistance to antibiotics.


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

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


How could a magic bullet work?

Not affecting host cells


What is another name for chemotherapy?

Selective toxicity.
Finds and destroys pathogens but not harm the host.


How is the Disk Diffusion Test run?

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


What is the E test?

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


What is a broth dilution test?

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


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

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


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

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


What is the therapeutic index?

Measuring risk vs. benefit


What is a bacteriophage?

A virus that attacks bacteria.


What are bacteriocins?

Bacterial toxins produced to inhibit the growth of similar bacteria.


What is a persister cell?

A surviving bacteria that has resistant characteristics.


Who discovered penicillin?

1928 Fleming


What is the difference between narrow and broad antibiotics?

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


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

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.


What are macrolides?

lactose ring
Erythromycin 50 S
Remember Christmas decoration


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

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


What is meningitis?

Inflammation of the meninges caused by viral or bacterial infection


What are protease inhibitors?

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


What are integrase inhibitors?

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


What is a virus?

DNA or RNA in a protein coat. Very small.


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

Used against viruses that inhibits warts.


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

Antiprotozoan - mosquitoes
Choloroquine - from tree bark


What is acyclovir used for?

Viral infections, like chickenpox


1. Distinguish between the term antibiotic and disinfectant:

-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


2. Give examples of bacteria and fungi that produce antibiotics:

Bacillus subtilis → bacitracin
Penicillium chrysogenum → Penicillin


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

-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…)


4. Identify the cellular targets of antibiotics:

-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


) 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



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

- synergism: ex: PCN & streptomycin to treat bacterial endocarditis
- damage to cell walls by PCN makes it easier for streptomycin to enter


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

- 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
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
Chloroquine → inhibits DNA synthesis (malaria)
Diiodohydroxyquin → unknown mode of action, amoebic diseases
Metronidazole → damages DNA → Entamoeba, Trichomonas
Nitazoxanide → interferes with metabolism of anaerobes

-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.


8) Define zone of inhibition:

-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.


9) Define minimal inhibitory concentration: (MIC)

- 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


10. Describe the advantage of the broth dilution test: (MBC)

- 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


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

- nosocomial infections are hospital acquired


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



13. State the three mechanisms by which bacteria can inactivate antibiotics:



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

- enzymatic destruction or inactivation of the drug
→ mainly affects PCN & cephalosporins
→ 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)


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:

- 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


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:

- methicillin resistant staphylococcus aureus
- resistant to bacteria; spreads in hospital
- super bug
- hand washing
- isolation


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

- 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;


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

- finish regiment
- never use old
- never use someone else’s
- dosage
- most specific ABX prescribed
- hand washing
- isolation


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

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


What is a side affect of taking tetracycline?

Green teeth