Chapter 20 SB Questions

Two drawbacks to ticarcillin and piperacillin are:

- have less activity against gram positive bacteria - destroyed by beta-lacamases

Like the macrolides, streptogramins, lincosamides, and chloramphenicol, the oxazolidinones bind to the ______ of bacteria. 50S ribosomal subunit 30S ribosomal subunit DNA polymerase RNA polymerase

50S ribosomal subunit

The pleuromutilins bind to the bacterial _______ thereby inhibiting _______. cross-linking enzymes; peptidoglycan formation 50S ribosomal subunit; translation RNA polymerase; transcription DNA polymerase; replication

50S ribosomal subunit; translation

antibiotics that irreversibly bind to the 30S ribosomal subunit, causing it to distort and malfunction. This blocks translation initiation and causes misreading of mRNA by ribosomes. Polymyxins Carbapenems Fluoroquinolones Aminoglycosides Oxazolidinones

Aminoglycosides

Why is metronidazole effective only against anaerobic microorganisms? The drug is quickly oxidized by O2, which destroys its function. Anaerobic metabolism is required to convert the medication to its active form. The medication targets a protein found only in the electron transport chain of anaerobic organisms. Aerobic organisms possess enzymes that rapidly degrade the drug.

Anaerobic metabolism is required to convert the medication to its active form.

Surveys indicate that far too many people believe that antibiotics are effective against viruses, often seeking prescriptions to "cure" viral infections. Why should antibiotics never be taken for viral infections? Multiple select question. Antibiotics are not effective against viruses. Misuse of antibiotics only selects for antibiotic-resistant bacteria in the normal microbiota. Use of antibiotics weakens the immune system by not letting it deal with the infection. Antibiotics will make the viral infections last longer.

Antibiotics are not effective against viruses. Misuse of antibiotics only selects for antibiotic-resistant bacteria in the normal microbiota.

Explain how drug resistance develops in bacteria and ultimately limits the usefulness of all known antimicrobials. Antimicrobials cause microbes to mutate their DNA to develop resistance; this advantage allows them to flourish. Antimicrobials kill or inhibit sensitive organisms, providing a selective advantage to resistant strains; these strains spread in the population. Microbes develop resistance in response to exposure to antimicrobials in order to survive; they then do better than those that do not. Antimicrobials create resistant strains of bacteria that grow much better than susceptible strains and come to dominate the population.

Antimicrobials kill or inhibit sensitive organisms, providing a selective advantage to resistant strains; these strains spread in the population.

What is the function of penicillin-binding proteins (PBPs)? Bind to penicillin and enzymatically degrade it; bacteria that produce PBPs are resistant to penicillin and related β-lactam drugs. Catalyze the formation of peptide bridges between adjacent glycan strands in the final stages of peptidoglycan synthesis. Catalyze the formation of penicillin; molds of the genus Penicillium, discovered by Alexander Fleming, produce these. Bind to penicillin to prevent it from entering the cell; this gives bacteria resistance to the β-lactam class of drugs.

Catalyze the formation of peptide bridges between adjacent glycan strands in the final stages of peptidoglycan synthesis.

Fidaxomincin is a relatively new bactericidal antibiotic that passes through the intestinal tract without being absorbed. It is particularly useful for treating infections cause by what bacterium? Clostridium botulinum Staphylococcus aureus Shigella dysenteriae Escherichia coli Clostridioides difficile

Clostridioides difficile

Select all that apply Which steps must be taken to prevent the spread of antimicrobial resistance? Countries around the world must make important policy decisions about the appropriate uses of the medications The general public must take responsibility for the appropriate use of the medications. Physicians must take responsibility for the appropriate use of the medications. Antibiotic use must stop altogether because resistance is a global problem.

Countries around the world must make important policy decisions about the appropriate uses of the medications The general public must take responsibility for the appropriate use of the medications. Physicians must take responsibility for the appropriate use of the medications.

Which of the following antimicrobials inhibit nucleic acid synthesis? β-lactams, chloramphenicol and tetracyclines Fluoroquinolones, rifamycins, and metronidazole

Fluoroquinolones, rifamycins, and metronidazole

______ are functionally and structurally related to the tetracyclines, but they have a wider spectrum of activity and are effective against many bacteria that have acquired resistance to the tetracyclines. Tigecycline is the only example currently approved. Macrolides Aminoglycosides Glycylcyclines

Glycylcyclines

The pleuromutilins are active against many types of ______. parasitic worms dimorphic fungi Gram-negative bacteria Gram-positive bacteria

Gram-positive bacteria

The antifungal drug griseofulvin interferes with the action of tubulin, the protein that polymerizes to form microtubules and a factor necessary in nuclear division. Tubulin is found in all eukaryotic cells. How can the selective toxicity of griseofulvin be explained? Inability of fungal cells to break down the drug Selective excretion by human cells Greater uptake by fungal cells Better detoxification by human cells Poorer resistance of fungal cells

Greater uptake by fungal cells

Select all that apply Because of its activity against members of the genus Mycobacterium, rifampin is primarily used to treat ______. cholera Hansen's disease (leprosy) tuberculosis shigellosis whooping cough walking pneumonia

Hansen's disease (leprosy) tuberculosis

Sulfa drugs have a high therapeutic index, meaning they have low toxicity. Why is this? The drug is unable to cross over the plasma membrane of eukaryotic cells. Human cells have lysosomes, which rapidly degrade the drug, preventing harm. Human cells use a different pathway to synthesize folate. The human liver is very effective at detoxifying these drugs. Human cells lack the enzyme that binds these medications.

Human cells lack the enzyme that binds these medications.

Why might it not be possible to successfully treat an infection with a given medication even if the minimum inhibitory concentration (MIC) of the drug for the causative bacterial strain is known? The tests for the MIC are often unreliable. The patient's immune system may clear the drug before it is able to impact the infection. It is not always possible to achieve that concentration in vivo. The drug may target the normal microbiota before clearing the infection. There may be too many bacteria in the infection for the drug to work effectively.

It is not always possible to achieve that concentration in vivo.

Because nucleic acid synthesis is a common feature of all eukaryotic cells, it is generally a poor target for antifungal drugs. How is the drug flucytosine able to effectively target this process in yeast versus human cells? It mimics a common nutrient used by the yeast cell and so fits effectively through porins in its membrane. It is taken up by yeast and converted by yeast enzymes to an active, inhibitory form. It is unable to cross the human cell membrane, whereas it exploits receptors on the yeast surface that initiate uptake. It is rapidly degraded by enzymes produced only in human cells.Because nucleic acid synthesis is a common feature of all eukaryotic cells, it is generally a poor target for antifungal drugs.

It is taken up by yeast and converted by yeast enzymes to an active, inhibitory form.

Why is bacitracin limited to use in topical applications such as non-prescription first-aid ointments? It is too expensive to be taken orally. It is not transported well in the bloodstream. It cannot be formulated into a pill form. It is poorly absorbed in the intestine. It is too toxic for other uses.

It is too toxic for other uses.

In terms of treating infections in humans, why is the bacterial cell wall such a good drug target for antimicrobials? The cell wall offers numerous sites for drugs to target, making it relatively more susceptible to degradation than a smaller, less complex structure. Its structure is inherently weak, so it is relatively easy for antimicrobials to break it apart. The antimicrobials do not have to be taken up, since the cell wall is on the outside of the bacterial cell. It is unique in containing peptidoglycan; antimicrobials that interfere solely with peptidoglycan synthesis do not affect eukaryotic cells.

It is unique in containing peptidoglycan; antimicrobials that interfere solely with peptidoglycan synthesis do not affect eukaryotic cells.

Antibacterials like daptomycin and polymyxin B essentially make holes in the bacterial membrane. Why, in terms of the function of the membrane, is this deadly to bacteria? It makes the membranes no longer selectively permeable. It decreases the permeability of the membranes. It prevents the membranes from allowing substances across. It makes the membranes more selectively permeable. It forces the membranes to maintain a gradient of concentrations on either side.

It makes the membranes no longer selectively permeable.

Resistance can result from structural changes in efflux pumps, changing the range of drugs that can be pumped out. Why is resistance that develops by this mechanism particularly worrisome? It might enable an organism to pump an antimicrobial inside the cell, sequestering it away and reducing the overall concentration outside the cell. It might allow an organism to selectively pump out one antimicrobial but not another. It might allow an organism to become resistant to several drugs simultaneously. It might enable an organism to enzymatically modify the antimicrobial. It might allow an organism to pump out the drug faster.

It might allow an organism to become resistant to several drugs simultaneously.

Compared with antibacterial, antifungal, and antiviral drugs, why does relatively little research and development go into antiprotozoan and antihelminthic drugs? Diseases caused by protozoa and helminths were not recognized as early as those caused by bacteria and viruses. Most parasitic diseases are concentrated in the poorer areas of the world where people simply cannot afford to spend money on expensive medications. Diseases caused by protozoa and helminths are much more benign, resulting in very small numbers of deaths globally each year. There are so few protozoan or helminthic diseases in humans.

Most parasitic diseases are concentrated in the poorer areas of the world where people simply cannot afford to spend money on expensive medications.

Select all that apply Unfortunately, the aminoglycosides are generally quite toxic to humans. Which of the following are examples of how these drugs can be effectively used to minimize their toxicity? Neomycin used in non-prescription topical ointments. Neomycin administered orally in large doses for a short time. Tobramycin injected intravenously over a long period of time to treat an infection. Tobramycin administered through inhalation to treat Pseudomonas aeruginosa lung infections in cystic fibrosis patients.

Neomycin used in non-prescription topical ointments. Tobramycin administered through inhalation to treat Pseudomonas aeruginosa lung infections in cystic fibrosis patients.

An antimicrobial medication is added to a culture of bacteria. The medication weakens the cell wall of the microbes, causing them to swell and burst due to osmotic pressure changes. Which of the following antimicrobials was most likely used? Tetracycline Rifamycin Penicillin Polymyxin B Sulfonamide

Penicillin

How can changes in the porin proteins in the outer membrane of Gram-negative bacteria result in resistance to antimicrobials? Porins bind specifically to certain substrates; modifications can allow them to bind irreversibly to antimicrobials instead. Porins enzymatically modify molecules on the outside of the cell; changes can allow them to target antimicrobial drugs. Porin proteins play an important role in detoxifying materials to which the cell is exposed. Porins selectively permit small molecules to enter the periplasm; changes in these porins can prevent certain drugs from entering.

Porins selectively permit small molecules to enter the periplasm; changes in these porins can prevent certain drugs from entering.

aminoglycosides

Protein synthesis inhibitor

tetracyclines

Protein synthesis inhibitor

Genes encoding resistance to antimicrobial drugs can spread to different strains, species, and even genera, most commonly through conjugative transfer of ______________ _________________.

R plasmids

Rifamycins are antibiotics that bind to _______ of bacteria thus preventing _______. the 50S ribosomal subunit; translation DNA polymerase; replication RNA polymerase; transcription the cross-linking enzymes; peptidoglycan formation

RNA polymerase; transcription

What is the primary benefit of the newer aminoglycosides binding to several sites on the ribosome? They bind the ribosomes much more than earlier versions, better interrupting protein synthesis. Eukaryotic ribosomes are less likely to be targeted by the drug. Resistance due to spontaneous mutation is unlikely. They can target a much greater variety of structure in ribosomes, increasing the range of species affected. Bacteria are less likely to enzymatically degrade them.

Resistance due to spontaneous mutation is unlikely.

_______, an inhibitor of transcription, is primarily used to treat tuberculosis and to prevent meningitis in people exposed to Neisseria meningitidis. Bacitracin Streptomycin Metronidazole Tetracycline Rifampin

Rifampin

Select all that apply What are two ways that changes in efflux pumps can lead to resistance to an antimicrobial? Structural changes in the pumps can influence the range of drugs that can be pumped out. Efflux pumps can be altered to enzymatically degrade materials that pass through them, including antimicrobials. Efflux pumps can produce antibodies that bind to antimicrobials in the environment, protecting the cell from their actions. The efflux pump can sequester the antimicrobial inside the cell, reducing the external concentration to safe levels. A cell can increase production of the efflux pumps, thereby ejecting the drug faster.

Structural changes in the pumps can influence the range of drugs that can be pumped out. A cell can increase production of the efflux pumps, thereby ejecting the drug faster.

T/F eukaryotic pathogens such as fungi more closely resemble human cells than do bacteria

TRUE

Isoniazid, ethambutol, and pyrazinamide are first-line drugs that are useful for treating the bacterial disease

TUBERCULOSIS

Why are Gram-negative bacteria intrinsically resistant to glycopeptide antibiotics such as vancomycin? The antibiotics do not cross their outer membrane. Gram-negative bacteria produce enzymes that degrade the antibiotics. Gram-negative bacteria lack the peptide side chain of NAM molecules to which glycopeptide antibiotics bind. The antibiotics bind to the lipopolysaccharide layer (LPS), preventing the medications from reaching their NAM target.

The antibiotics do not cross their outer membrane.

Why is combination therapy effective in preventing the rise of mutants resistant to antibiotics? The synergistic combination of multiple drugs kills bacteria much more effectively than just a single drug. Because they are under attack from multiple fronts, the bacteria are unable to mutate their DNA in time to survive. By treating the patient not just with antibiotics but other curative approaches, he or she is much more likely to get healthy faster. The chance of a cell simultaneously developing mutational resistance to multiple drugs is extremely low.

The chance of a cell simultaneously developing mutational resistance to multiple drugs is extremely low.

hy are vancomycin-resistant enterococci (VRE) of special concern? Enterococci are a particularly deadly strain of pathogens. The resistance in these strains is encoded on a plasmid, so it is transferable to other organisms. Vancomycin is usually reserved as a last resort for treating life-threatening infections caused by Gram-positives resistant to all β-lactam drugs. Enterococci are a common cause of health-care associated infections. They are the only bacteria that have demonstrated resistance to vancomycin.

The resistance in these strains is encoded on a plasmid, so it is transferable to other organisms. Vancomycin is usually reserved as a last resort for treating life-threatening infections caused by Gram-positives resistant to all β-lactam drugs. Enterococci are a common cause of health-care associated infections.

Select all that apply Compared to conventional methods, commercial modifications of antimicrobial susceptibility testing offer what advantages? They can test for microbes that cannot be tested via the other methods. The results can be obtained more quickly. They are less labor-intensive. They are more effective at testing for anaerobic microorganisms.

The results can be obtained more quickly. They are less labor-intensive.

Considering that all cells synthesize proteins, how is it possible to selectively target prokaryotic protein synthesis with antibacterials? Unlike prokaryotic cells that lack membrane transporters, eukaryotic cells have transporters that actively remove the antibacterial drugs. The structure of the prokaryotic 70S ribosome is sufficiently different from the eukaryotic 80S ribosome. Antibacterials are unable to cross the plasma membrane of eukaryotic cells. Unlike in prokaryotic cells, protein synthesis in eukaryotic cells takes place in the nucleus, where it is protected from the drugs. Prokaryotic ribosomes function in a completely different manner than those in eukaryotic cells, so their function can be selectively blocked.

The structure of the prokaryotic 70S ribosome is sufficiently different from the eukaryotic 80S ribosome.

The glycylcyclines are a new class of antibacterial drug related to the tetracyclines. How do they compare to the tetracyclines? Select all that apply They reversibly bind to the 30S ribosomal subunit, whereas the tetracyclines bind to the 50S subunit. They have a different mechanism of action. They are effective against many bacteria that have acquired resistance to the tetracyclines. They have a wider spectrum of activity.

They are effective against many bacteria that have acquired resistance to the tetracyclines. They have a wider spectrum of activity.

Consider the group of enzymes that catalyze the formation of peptide bridges between adjacent glycan strands, an essential step in the final stages of peptidoglycan synthesis. Why are these enzymes commonly called penicillin-binding proteins (PBPs)? They are enzymes that produce penicillin for the cell. Their function is to bind penicillin and enzymatically degrade it, protecting the cell from the effects of the antibiotic. They bind penicillin and were initially discovered during experiments to study the effects of the medication. They attach to penicillin and block its entry into the cell, thereby protecting the cell from the toxic actions of the drug.

They bind penicillin and were initially discovered during experiments to study the effects of the medication.`

How do the polyenes work at controlling fungal pathogens? They embed themselves in the cytoplasmic membrane, forming protein channels that serve as pores to release the contents of the cell. They serve as phospholipases, removing the polar phosphate groups from the phosopholipids of the plasma membrane. They bind to ergosterol, disrupting the fungal membrane and causing leakage of the cytoplasmic contents that leads to cell death. They block cell wall formation by inhibiting the synthesis of chitin subunits.

They bind to ergosterol, disrupting the fungal membrane and causing leakage of the cytoplasmic contents that leads to cell death.

Which of the following correctly describe how R plasmids contribute to resistance in microbial populations? They can spread to different strains, species, or even genera via conjugative transfer. They enzymatically degrade a wide range of antimicrobial medications. They are secreted into the environment, where they protect the cells by interfering with antimicrobial medications. They often carry several different resistance genes, each one encoding resistance to a specific antimicrobial drug.

They can spread to different strains, species, or even genera via conjugative transfer. They often carry several different resistance genes, each one encoding resistance to a specific antimicrobial drug.

There are a few antibacterial medications that interfere with cell membrane integrity. How do they lead to bacterial cell death? They cause the cells to leak. They cause the phospholipids to reverse their orientation so that the polar head groups orient inward and the lipid tails point outward. They prevent the assembly of the phospholipid bilayer. They degrade proteins embedded in the cell membrane. They prevent the cell from synthesizing new lipid membrane.

They cause the cells to leak.

Why are so few antibiotics effective against Mycobacterium tuberculosis? They grow too quickly for the drugs to be effective. They grow slowly. Most drugs target items specific to either Gram-negatives or Gram-positives. They rapidly metabolize any drugs given. Their waxy cell wall prevents the entry of many drugs.

They grow slowly. Their waxy cell wall prevents the entry of many drugs.

What characteristic of Mycoplasma species gives them intrinsic (innate) resistance to penicillin and other antimicrobials with the same target?

They lack a cell wall and are therefore resistant to drugs that interfere with peptidoglycan synthesis.

Why is it so difficult to selectively target viruses with drugs? They rely almost exclusively on the host cell's metabolic machinery for their replication, so there are few targets for selective toxicity. They are too small be be impacted by most antimicrobials. Unlike bacteria, they are able to avoid antimicrobials by hiding inside the nucleus of the host cell. Their metabolism is too slow; most antimicrobials require actively metabolizing pathogens in order to work. Their protein capsid blocks the action of the drugs.

They rely almost exclusively on the host cell's metabolic machinery for their replication, so there are few targets for selective toxicity.

What best explains why the first-line drugs are generally given in combination of two or more to patients who have active tuberculosis, caused by Mycobacterium tuberculosis? To reduce the chance that resistant mutants will develop. This avoids the need to determine whether or not the bacteria are resistant to the drug being used. The drugs are relatively ineffective on their own, but together their action is synergistic. Mycobacterium are so resistant to antibacterials that it takes targeting at least two different processes to kill them.

To reduce the chance that resistant mutants will develop.

True or false: Compared to conventional methods of antimicrobial susceptibility testing, commercial modifications are less labor-intensive.

True

Select all that apply What two reasons explain the selective toxicity of nucleoside and nucleotide analogs? The host cells chemically modify the nucleotide analogs, preventing their action on the host genome. Virally encoded enzymes are more likely than the host cell polymerases to incorporate a nucleotide analog. Host cell polymerase detects the incorrect nucleotide analogs and alters their structure back to that of the correct nucleotide. With increased incorporation of nucleotide analogs, more damage is done to the rapidly replicating viral genome than to the host.

Virally encoded enzymes are more likely than the host cell polymerases to incorporate a nucleotide analog. With increased incorporation of nucleotide analogs, more damage is done to the rapidly replicating viral genome than to the host.

What two reasons explain the selective toxicity of nucleoside and nucleotide analogs? The host cells chemically modify the nucleotide analogs, preventing their action on the host genome. Host cell polymerase detects the incorrect nucleotide analogs and alters their structure back to that of the correct nucleotide. With increased incorporation of nucleotide analogs, more damage is done to the rapidly replicating viral genome than to the host. Virally encoded enzymes are more likely than the host cell polymerases to incorporate a nucleotide analog.

With increased incorporation of nucleotide analogs, more damage is done to the rapidly replicating viral genome than to the host. Virally encoded enzymes are more likely than the host cell polymerases to incorporate a nucleotide analog.

Acquired resistance to vancomycin is typically due to ______. the production of active transporters in the plasma membrane that pump the vancomycin back out of the cell the production of vancomycin-degrading enzymes a change in the peptide side chain of the NAM molecule that prevents vancomycin from binding the gain of the ability to produce extracellular binding proteins that competitively bind to vancomycin and inactivate it

a change in the peptide side chain of the NAM molecule that prevents vancomycin from binding

The lincosamides are bacteriostatic; they prevent the continuation of translation by binding to ______. a ribosomal subunit DNA polymerase tRNA the mRNA transcript RNA polymerase

a ribosomal subunit

Examples of acquired resistance include ______. the lack of a cell wall of Mycoplasma species the outer membrane of many Gram-negative bacteria a spontaneous mutation resulting in resistance resistance resulting from horizontal gene transfer

a spontaneous mutation resulting in resistance resistance resulting from horizontal gene transfer

What groups of bacteria are generally not sensitive to aminoglycosides? Gram-negative bacteria Gram-positive bacteria obligate anaerobes that undergo fermentation exclusively anaerobes, enterococci, and streptococci that lack respiratory metabolism

anaerobes, enterococci, and streptococci that lack respiratory metabolism

Metronidazole interferes with DNA synthesis and function, but only in ______ microorganisms. anaerobic aerobic

anaerobic

By binding to the 50S ribosomal subunit, chloramphenicol prevents peptide bonds from being formed and, consequently, blocks translation; the effect is ______. bacteriostatic bactericidal

bacteriostatic

A synergistic combination of two streptogramins, quinupristin and dalfopristin, is effective against a variety of Gram-positive bacteria. Individually, each drug is ______, but together they are ______. useless; effective bacteriostatic; bactericidal

bacteriostatic; bactericidal

Methicillin-resistant Staphylococcus aureus (MRSA) are resistant to methicillin as well as nearly all other ___________ - ______________ drugs

beta-lactam

Which of the following is the most likely target for antiprotozoan drugs? cell wall synthesis cell membrane integrity nucleic acid synthesis catabolic pathways biosynthetic pathways

biosynthetic pathways

rifamycin

blocks initiation of transcription by binding to RNA polymerase

Antibiotics that are most likely to disrupt the normal microbiota are termed broad-spectrum. narrow-spectrum. targeted spectrum. semi-synthetic. therapeutic.

broad-spectrum.

How does one determine whether a bacterial strain is resistant, susceptible, or intermediate via the Kirby-Bauer disc diffusion method? by measuring clearing zone size and comparing that to a chart that correlates size of zone of inhibition to susceptibility of bacteria to the drug by measuring and comparing each clearing zone; the smallest one is the drug to which the bacterial strain is most susceptible by comparing each clearing zone with a second plate inoculated with a different known strain of bacteria by measuring and comparing each clearing zone; the largest one is the drug to which the bacterial strain is most susceptible

by measuring clearing zone size and comparing that to a chart that correlates size of zone of inhibition to susceptibility of bacteria to the drug

Select all that apply Which of the following statements about antiviral drugs are true? viral resistance to them is not possible because viruses are not alive cannot eliminate latent viral infections are generally effective against only a specific type of virus target the metabolic machinery of the virus

cannot eliminate latent viral infections are generally effective against only a specific type of virus

Select all that apply Which four of the following are β-lactam antibiotics? carbapenems sulfonamides quinolones monobactams cephalosporins penicillins polymyxins tetracyclines

carbapenems monobactams cephalosporins penicillins

daptomycin

cell membrane integrity

β-lactam drugs

cell wall (peptidoglycan) synthesis

vancomycin

cell wall inhibitor

Protease inhibitors are used to treat HIV infections by inhibiting the HIV-encoded protease, preventing it from ______. assembling the protein coat and packaging the viral genome inside cleaving the translated polyprotein into individual proteins degrading complement system proteins involved in innate immunity cutting apart host cell proteins involved in protecting the cell from the virus

cleaving the translated polyprotein into individual proteins

Drugs such as streptomycin for which a single point mutation causes resistance are sometimes used in combination with one or more other drugs. This way, if any cell spontaneously develops resistance to one drug, another drug will still kill it. This approach is called __________________ _____________________

combination therapy

There are two categories of MRSA strains. The one called CA-MRSA refers to __________________ acquired methicillin-resistant Staphylococcus aureus.

community

All of the following are examples of mechanisms of acquired antimicrobial drug resistance EXCEPT ______. an alteration in the target molecule, preventing the drug from binding an efflux pump increasing the rate of elimination of a drug from a cell development of a mutation in response to an antimicrobial porin proteins preventing or reducing uptake of the drug into the cell production of an enzyme that modifies the drug, inactivating it

development of a mutation in response to an antimicrobial

The following are all reasons that different β-lactam antibiotics vary in their spectrum of activity EXCEPT ______. differences in the β-lactam ring structure influence how well the antimicrobial binds to the penicillin-binding proteins different penicillin-binding proteins have different affinities for the β-lactam antibiotics penicillin-binding proteins of obligate anaerobes differ from those of aerobes the outer membrane of Gram-negatives prevents the antibiotics from accessing the penicillin-binding proteins the peptidoglycan of Gram-positives is exposed to the outside environment, so the antibiotics can directly contact the enzymes that synthesize it penicillin-binding proteins of Gram-positives differ somewhat from those of Gram-negatives

differences in the β-lactam ring structure influence how well the antimicrobial binds to the penicillin-binding proteins

The following are all reasons that different β-lactam antibiotics vary in their spectrum of activity EXCEPT ______. penicillin-binding proteins of obligate anaerobes differ from those of aerobes differences in the β-lactam ring structure influence how well the antimicrobial binds to the penicillin-binding proteins different penicillin-binding proteins have different affinities for the β-lactam antibiotics the peptidoglycan of Gram-positives is exposed to the outside environment, so the antibiotics can directly contact the enzymes that synthesize it the outer membrane of Gram-negatives prevents the antibiotics from accessing the penicillin-binding proteins penicillin-binding proteins of Gram-positives differ somewhat from those of Gram-negatives

differences in the β-lactam ring structure influence how well the antimicrobial binds to the penicillin-binding proteins

The aminoglycosides are generally not effective against anaerobes, enterococci, and streptococci because they ______. bind irreversibly to the cell wall of these Gram-positive bacteria are blocked by the outer membrane of these bacteria are degraded by an an enzyme produced by these organisms enter bacterial cells by an active transport process that requires respiratory metabolism

enter bacterial cells by an active transport process that requires respiratory metabolism

Penicillinase and chloramphenicol acetyltransferase are both examples of ______. enzymes produced by bacteria that chemically modify a specific drug, interfering with its function newer antimicrobials produced in bioreactors by bacteria for use against resistant microorganisms newer versions of penicillin and chloramphenicol produced by chemical modification enzymes found in the metabolic pathways involved in the production of antibiotics by microorganisms

enzymes produced by bacteria that chemically modify a specific drug, interfering with its function

Compared with bacteria, there are relatively few drugs available for use against fungal pathogens because ______. fungi have many more mechanisms for resisting drugs than do bacteria very little research has been conducted on fungal pathogens eukaryotic pathogens such as fungi more closely resemble human cells than do bacteria fungi mutate and evolve resistance to drugs more rapidly than bacteria

eukaryotic pathogens such as fungi more closely resemble human cells than do bacteria

True or false: A Gram-negative rod that does not produce an ESBL (extended-spectrum β-lactamase) would likely be treated with a carbapenem.

false

True or false: Most antibacterial medications interfere with metabolic pathways.

false

True or false: Susceptibility of a pathogen to a specific antimicrobial drug is almost always predictable.

false

True or false: There are no useful antimicrobials that inhibit nucleic acid synthesis because the processes are essentially the same in both eukaryotic and prokaryotic cells, making the drugs too toxic to humans.

false

Which of the following is an antibiotic that interferes with bacterial transcription by binding to the RNA polymerase? fidaxomincin polymyxin clindamycin bacitracin pleuromutilin

fidaxomincin

The minimum bactericidal concentration is determined by ______. taking the inverse of the MIC for a given medication for a given organism finding out how many live bacterial cells remain in tubes from the MIC test that showed no growth finding out the concentration of a medication that causes the largest zone of inhibition in a Kirby-Bauer test finding out which antibiotic used in a MIC test inhibits all bacterial growth

finding out how many live bacterial cells remain in tubes from the MIC test that showed no growth

The minimum bactericidal concentration is determined by ______. taking the inverse of the MIC for a given medication for a given organism finding out which antibiotic used in a MIC test inhibits all bacterial growth finding out the concentration of a medication that causes the largest zone of inhibition in a Kirby-Bauer test finding out how many live bacterial cells remain in tubes from the MIC test that showed no growth

finding out how many live bacterial cells remain in tubes from the MIC test that showed no growth

Among the most useful antibacterial medications that interfere with metabolic pathways are the_____________ biosynthesis inhibitors: sulfonamides and trimethoprim.

folate

Like the sulfonamides, trimethoprim inhibits an enzyme in the pathway for synthesis of ________________; when used together, the two drugs have a synergistic effect.

folate

The rate of elimination of an antimicrobial is expressed as its

half-life

NS5A inhibitors offer a relatively new option for treating ______ infections, acting by inhibiting a protein required for replication of the viral genome. human papillomavirus (HPV) common cold virus human immunodeficiency virus (HIV) hepatitis C virus (HCV)

hepatitis C virus (HCV)

Because neomycin is too toxic for systemic use, it is best used ______. occasionally, intravenously internally during surgical procedures in topical ointments orally, but only once a year orally in combination with another drug that counteracts its effects

in topical ointments

What are four common mechanisms of acquired resistance to antimicrobial medications? alteration of the DNA in response to the drug increased elimination of the drug decreased uptake of the drug alteration in the target molecule production of a drug-inactivating enzyme

increased elimination of the drug decreased uptake of the drug alteration in the target molecule production of a drug-inactivating enzyme

Flucytosine is taken up by yeast cells and then converted by yeast enzymes to a form that interferes with nucleic acid synthesis by ______. inhibiting an enzyme required for nucleic acid synthesis cutting the genome in multiple locations, much like a restriction enzyme inserting itself into the genome at multiple points, leading to irreparable mutations binding to the yeast DNA and blocking replication

inhibiting an enzyme required for nucleic acid synthesis

Aztreonam is a monobactam antibiotic that ______. blocks protein synthesis disrupts cell membrane integrity inhibits cell wall synthesis prevents nucleic acids synthesis interferes with folic acid metabolism

inhibits cell wall synthesis

Ethambutol

inhibits incorporation of mycolic acid into the cell wall

Isoniazid

inhibits mycolic acid synthesis

rifampin

inhibits transcription (RNA polymerase inhibitor)

polymyxin B

injury to plasma membrane

Tavaborole is one of the more recently developed antifungal medications. It inhibits protein synthesis by ______. binding to and blocking the action of 80S ribosomes interfering with an enzyme that "charges" a tRNA molecule by attaching the correct amino acid binding to the AUG start codon of mRNA and preventing the attachment of ribosomes

interfering with an enzyme that "charges" a tRNA molecule by attaching the correct amino acid

For most infections, vancomycin, the most widely used glycopeptide used in the United States, must be administered intravenously because it ______. does not survive the pH of the small intestine is poorly absorbed from the intestinal tract is too toxic to be consumed orally is digested in the intestinal tract by the normal microbiota is rapidly broken down by stomach acid

is poorly absorbed from the intestinal tract

second-line drugs are generally

less effective than first line drugs

Erythromycin and clarithromycin are _______ antibiotics that inhibit _______ synthesis. macrolide; peptidoglycan macrolide; protein glycopeptide; protein glycopeptide; peptidoglycan

macrolide; protein

The macrolides are not effective against members of the family Enterobacteriaceae because _______. the cell walls of these bacteria is thinner than those of other bacteria macrolides are rapidly degraded by enzymes in the fermentation pathway of these bacteria macrolides do not pass through the outer membrane of these bacteria macrolides do not survive passage into the intestinal tract where these bacteria are found

macrolides do not pass through the outer membrane of these bacteria

A bacterial enzyme that adds a methyl group to an rRNA molecule of the 50S ribosome confers resistance to ______. macrolides, lincosamides, and streptogramins quinolones, rifampins, and sulfonamides penicillins, cephalosporins, and vancomycin

macrolides, lincosamides, and streptogramins

Multiple select Enterococci are one of the most dramatic examples of antimicrobial resistance because ______. many strains have R plasmids their penicillin-binding proteins have low affinity for certain β-lactam antibiotics their outer membrane limits the entry of antibiotics some strains are even resistant to vancomycin the mycolic acids in their cell walls block the entry of many drugs they are intrinsically less susceptible to many common antimicrobials

many strains have R plasmids their penicillin-binding proteins have low affinity for certain β-lactam antibiotics some strains are even resistant to vancomycin they are intrinsically less susceptible to many common antimicrobials

Pyrazinamide

mechanism unknown

trimethoprim

metabolic inhibitor

sulfonamides

metabolic pathways (folate biosynthesis)

In the case of changes to the target that result in drug resistance, they would most commonly arise from ______. replacement of the structure with an analogous one that provides the same function the complete removal of the structure as a result of a mutation minor structural changes in the target, which prevent the drug from binding major structural changes in the target, which prevent the drug from binding

minor structural changes in the target, which prevent the drug from binding

If a bacterium is resistant to the macrolides, lincosamides, and streptogramins, it most likely produces an enzyme that ______. cleaves those three types of antibiotics modifies an rRNA molecule of the 50S ribosomal subunit blocks the import of drugs into the cell catalyzes the efflux of the drugs out of the cell

modifies an rRNA molecule of the 50S ribosomal subunit

In general, the later generations of cephalosporins are _____ effective against Gram-negative bacteria and _____ susceptible to destruction by some β-lactamases. more; more less; more more; less less; less

more; less

Most antiparasitic drugs targeting worms probably interfere with _______. neuromuscular function respiration reproduction gastrointestinal function

neuromuscular function

fluoroquinolones

nucleic acid synthesis

rifamycins

nucleic acid synthesis

Entry inhibitors are a new group of drugs effective against HIV that ______. block the uptake of nutrients by the virus prevent the virus from penetrating the host cells prevent the transmission of the virus from one host to another prevent the viral genome from being packaged inside the protein capsid

prevent the virus from penetrating the host cells

Antivirals that interfere with viral uncoating ______. block the exit of the virion from the lipid envelope block the assembly of the nucleic acids and protein coat into a finished virion prevent viral replication by preventing the nucleic acid from separating from the protein coat prevent the packaging of viral genome into the protein coat

prevent viral replication by preventing the nucleic acid from separating from the protein coat

Integrase inhibitors offer a new option for treating HIV infections by ______. stopping the virus from assembling its nucleic acids and proteins to form new virions preventing the virus from the immune system inside the cell nucleus preventing the virus from inserting the DNA copy of its genome into that of the host cell blocking the virus from attaching to the receptors in the cell membrane that initiate uptake of the virus

preventing the virus from inserting the DNA copy of its genome into that of the host cell

The purpose of combining penicillin with a β-lactamase inhibitor is to ______. block the central metabolism of the bacteria to stop growth so that the penicillin is more effective synergistically enhance the impact of the penicillin by targeting a second component of the bacteria increase the binding affinity of penicillin to the penicillin-binding proteins protect the penicillin from enzymatic destruction

protect the penicillin from enzymatic destruction

Neuraminidase inhibitors inhibit neuraminidase, an enzyme instrumental for the ______ of influenza viral particles. synthesis assembly uptake release replication

release

Azoles inhibit ergosterol synthesis. This ______. prevents ergosterol from cross-linking in the fungal cell wall, weakening it so that changes in osmotic pressure result in lysis blocks the proper segregation of chromosomes during cell division results in defective fungal membranes that leak cytoplasmic contents inhibits the cell from properly synthesizing proteins

results in defective fungal membranes that leak cytoplasmic contents

When treating Mycobacterium tuberculosis, second-line drugs may be used because they ______. are more effective than the first-line drugs work most effectively when used with the first-line drugs prevent strains from becoming resistant to the first-line drugs are generally less toxic than the first-line drugs serve as an alternative when strains are resistant to the first-line drugs

serve as an alternative when strains are resistant to the first-line drugs

Select all that apply When a nucleotide analog is incorporated into a growing nucleotide chain, it ______. sometimes prevents additional nucleotides from being added can block the action of RNA polymerase, preventing transcription sometimes binds to DNA polymerase, preventing replication can result in a defective strand with altered base-pairing properties can selectively delete other nucleotides from the strand

sometimes prevents additional nucleotides from being added can result in a defective strand with altered base-pairing properties

Just a single specific base-pair change in the gene encoding a ribosomal protein alters the target enough to make the cell resistant to the antibiotic ______. streptomycin methicillin penicillin

streptomycin

Antibacterials that are structurally similar to para-aminobenzoic acid (PABA) and therefore competitively inhibit folic acid synthesis are the sulfonamides and related compounds, collectively referred to as ______________ drugs

sulfa

Drugs that are more effective when taken together are

synergistic.

Efflux pumps are ______. important in setting up the proton motive force responsible for ATP synthesis in respiring cells systems that bacteria use to transport compounds into the cell for storage systems that bacteria use to transport damaging compounds out of a cell involved in energy production for the cell by utilizing the proton motive force to generate ATP used by the cell to passively transport substances into the cell

systems that bacteria use to transport damaging compounds out of a cell

The macrolides prevent the continuation of translation by reversibly binding to ______. the 50S ribosomal subunit the incoming tRNA molecule the mRNA being translated the 30S ribosomal subunit

the 50S ribosomal subunit

Select all that apply In the Kirby-Bauer disc diffusion test, what are factors that influence the size of a clearing zone of inhibition around a microbial disc? the number of discs tested at the same time the degree of susceptibility of the organism to the drug the amount of the drug on the disc the stability of the drug the presence of other drugs on the other discs the molecular weight of the drug

the degree of susceptibility of the organism to the drug the amount of the drug on the disc the stability of the drug the molecular weight of the drug

Enzymes required for nucleic acid synthesis are the targets of some groups of antimicrobial drugs. Those that target topoisomerases in particular are ______. β-lactams the rifamycins metronidazoles the fluoroquinolones

the fluoroquinolones

Drugs in a family called echinocandins interfere with synthesis of β-1,3 glucan. As a result, ______. the fungal cell wall will be weakened and the cell will burst fungal cells do not attach properly to surfaces fungal cells are unable to divide the cytoplasmic membrane does not anchor properly to the cell wall regular uptake of nutrients is inhibited

the fungal cell wall will be weakened and the cell will burst

A gene codes for an enzyme that chemically modifies an aminoglycoside, rendering the drug inactive. The gene encoding that enzyme is thought to have originally come from ______. an R plasmid acquired from a strain of E. coli the same species of Streptomyces that produces the drug a mutation in a gene in the central metabolic pathway of a bacterium spontaneous mutation of bacterial gene coding for a degradative enzyme

the same species of Streptomyces that produces the drug

All of the following statements regarding broad-spectrum penicillins are true EXCEPT ______. they are active against Gram-negatives they include ampicillin and amoxicillin their additional side chain gives them a broad spectrum of activity they can be inactivated by many β-lactamases they are active against penicillin-sensitive Gram-positives

their additional side chain gives them a broad spectrum of activity

An advantage of the cephalosporins is ______. they are especially effective against Gram-positive bacteria their chemical structure makes them resistant to inactivation by certain β-lactamases earlier generations in particular are more effective against Gram-negative bacteria they have a very high binding affinity for penicillin-binding proteins of Gram-positivestheir chemical structure makes them resistant to inactivation by certain β-lactamases

their chemical structure makes them resistant to inactivation by certain β-lactamases

All of the following correctly describe the lincosamides EXCEPT ______. they are particularly useful for treating infections resulting from intestinal perforation because they inhibit Bacteroides fragilis they can increase the risk of developing Clostridium difficile-associated disease because most C. difficile strains are resistant to the lincosamides they inhibit a variety of Gram-negative and Gram-positive bacteria they act by preventing the formation of peptide bonds between glycan chains of peptidoglycans they are bacteriostatic

they act by preventing the formation of peptide bonds between glycan chains of peptidoglycans

All of the following correctly describe the aminoglycosides EXCEPT ______. they are bacteriostatic, inhibiting the growth of bacteria but not killing them their binding causes misreading of mRNA by ribosomes that have already passed the initiation step their binding blocks initiation of translation they irreversibly bind to the 30S ribosomal subunit, causing it to distort and malfunction

they are bacteriostatic, inhibiting the growth of bacteria but not killing them

All of the following are true statements regarding the natural penicillins EXCEPT _______. penicillin V is more stable in acid and, therefore, better absorbed than penicillin G when taken orally bacteria that produce penicillinase are resistant to the natural penicillins they are the original penicillins produced naturally by the mold Penicillium chrysogenum they are broad-spectrum antibiotics, effective against a wide range of both Gram-positives and Gram-negatives

they are broad-spectrum antibiotics, effective against a wide range of both Gram-positives and Gram-negatives

All of the following accurately describe the tetracyclines EXCEPT ______. they block attachment of tRNA and prevent translation from continuing they are actively transported into prokaryotic but not animal cells they are equally toxic to eukaryotic and prokaryotic cells and so must be used only as a last resort they are bacteriostatic they reversibly bind to the 30S ribosomal subunit

they are equally toxic to eukaryotic and prokaryotic cells and so must be used only as a last resort

The selective toxicity of the tetracyclines is because ______. animal cells actively oxidize them via glycolysis, using the energy to fuel the cell they bind to the prokaryotic 30S ribosomal subunit eukaryotic cells possess lysosomes that actively degrade these drugs

they bind to the prokaryotic 30S ribosomal subunit

The selective toxicity of the tetracyclines is because ______. they bind to the prokaryotic 30S ribosomal subunit animal cells actively oxidize them via glycolysis, using the energy to fuel the cell eukaryotic cells possess lysosomes that actively degrade these drugs

they bind to the prokaryotic 30S ribosomal subunit

The fluoroquinolones are synthetic drugs that inhibit one or more of a group of enzymes called ___________, which maintain the supercoiling of DNA within the bacterial cel

topoisomerases

Two streptogramins (quinupristin and dalfopristin) act synergistically when administered together, with each binding to a different site on the 50S ribosomal subunit and inhibiting distinct steps of ______. transcription translation cell wall synthesis DNA replication

translation

Antiviral drugs that interfere with nucleic acid synthesis target ______. viral genes for the synthesis of nucleic acids from precursors host cell enzymes that replicate viral nucleic acid host cell genes involved in metabolism virally encoded genes involved in metabolism virally encoded enzymes that replicate viral nucleic acid

virally encoded enzymes that replicate viral nucleic acid