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Antibacterial drugs Flashcards

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1
Q

Aminoglycosides

A

Protein synthesis inhibitor (Willey, et al., 2011, pp.832-838).
Contain a cyclohexane ring & amino sugars (Willey, et al., 2011, pp.832-838).

1) Bind to 30S ribosomal subunit & cause tRNA mismatching & therefore protein mistranslation (Willey, et al., 2011, pp.832-838).
2) Sec-dependant translocation system moves proteins into periplasm (Willey, et al., 2011, pp.832-838).
3) Some mistranslated proteins inserted into plasma membrane before they can be degraded (Willey, et al., 2011, pp.832-838).
4) Envelope stress-response system activated (Willey, et al., 2011, pp.832-838).
5) Changes in metabolic and respiratory pathways due to upregulation stress-response system forms hydroxyl radicals (Willey, et al., 2011, pp.832-838).
Radical formation causes cell death (Willey, et al., 2011, pp.832-838).

References: Willey, J.M., Sherwood, L.M., Woolverton, C.J. (2011) Prescott’s Microbiology. 8th edn. New York: McGraw-Hill.

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2
Q

Chloramphenicol

A

Protein synthesis inhibitor (Willey, et al., 2011, pp.832-838).
Synthesised chemically but first produced from Streptomyces venezuelae (Willey, et al., 2011, pp.832-838).
Inhibits peptidyl transferase reaction by binding to 23S rRNA on 50S subunit (Willey, et al., 2011, pp.832-838).
Broad spectrum of activity but is toxic (Willey, et al., 2011, pp.832-838).
Only used in life-threatening situations (Willey, et al., 2011, pp.832-838).
Side effects: depression of bone marrow function, leading to aplastic anaemia and decreased number of white blood cells (Willey, et al., 2011, pp.832-838).

References: Willey, J.M., Sherwood, L.M., Woolverton, C.J. (2011) Prescott’s Microbiology. 8th edn. New York: McGraw-Hill.

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3
Q

Tetracyclines

A

Protein synthesis inhibitor (Willey, et al., 2011, pp.832-838).
Four-ring structure with a variety of side chains attached (Willey, et al., 2011, pp.832-838).
Oxytetracycline & chlortetracycline are two examples of tetracycline antibiotics (Willey, et al., 2011, pp.832-838).
They are produced by Streptomyces (Willey, et al., 2011, pp.832-838).
They combine with 30S subunit of ribosome to inhibit binding of aminoacyl-tRNA molecules to A site of ribosome (Willey, et al., 2011, pp.832-838).
They are bacteriostatic and broad-spectrum antibiotics active against: rickettsias, chlamydiae, and mycoplasmas (Willey et al., 2011, pp.832-838).
Their use has decreased but sometimes used to treat acne (Willey, et al., 2011, pp.832-838).

References: Willey, J.M., Sherwood, L.M., Woolverton, C.J. (2011) Prescott’s Microbiology. 8th edn. New York: McGraw-Hill.

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4
Q

Macrolides

A

Protein synthesis inhibitors (Willey, et al., 2011, pp.832-838).
Contain 12-22 carbon lactone rings linked to one or more sugars (Willey, et al., 2011, pp.832-838).

Some examples of macrolides are erythromycin, clindamycin and azithromycin (Willey, et al., 2011, pp.832-838)

Erythromycin: inhibits peptide chain elongation during protein synthesis by binding to 23S rRNA of 50S ribosomal subunit (Willey, et al., 2011, pp.832-838).
Broad-spectrum antibiotic & bacteriostatic (Willey, et al., 2011, pp.832-838).
Treat patients allergic to penicillins (Willey, et al., 2011, pp.832-838).

References: Willey, J.M., Sherwood, L.M., Woolverton, C.J. (2011) Prescott’s Microbiology. 8th edn. New York: McGraw-Hill.

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5
Q

Sulfanomides / Sulfa drugs

A

Metabolic antagonists (Willey, et al., 2011, pp.832-838).
Structurally related to sulfanilamide which is an analog of PABA (used in folate synthesis) (Willey, et al., 2011, pp.832-838).
It decreases folate concentration by competing with PABA for active site of an enzyme (Willey, et al., 2011, pp.832-838).
Folic acid is precursor of purines and pyrimidines, causing inhibition of synthesis of purines and pyrimidines and termination of protein synthesis and DNA replication (Willey, et al., 2011, pp.832-838).

References: Willey, J.M., Sherwood, L.M., Woolverton, C.J. (2011) Prescott’s Microbiology. 8th edn. New York: McGraw-Hill.

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6
Q

Why do sulfa drugs have a high therapeutic index?

A

Sulfa drugs have a high therapeutic index because they are selectively toxic for many bacteria and protozoa as they produce their own folate and cannot take it up while humans don’t produce folate and instead intake it (Willey, et al., 2011, pp.832-838).

References: Willey, J.M., Sherwood, L.M., Woolverton, C.J. (2011) Prescott’s Microbiology. 8th edn. New York: McGraw-Hill.

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7
Q

Metabolic antagonists

A

Act as structural analogs to metabolic intermediates and competitively inhibit the use of metabolites by key enzymes (Willey, et al., 2011, pp.832-838).
They are similar enough to compete with intermediates but different enough to prevent normal metabolism (Willey, et al., 2011, pp.832-838).

References: Willey, J.M., Sherwood, L.M., Woolverton, C.J. (2011) Prescott’s Microbiology. 8th edn. New York: McGraw-Hill.

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8
Q

Trimethoprim

A

Metabolic antagonist and a synthetic antibiotic (Willey, et al., 2011, pp.832-838).
Binds to dihydrofolate reductase, which converts dihydrofolic acid to tetrahydrofolic acid, and competes against dihydrofolic acid substrate (Willey, et al., 2011, pp.832-838).
Broad-spectrum antibiotic: can treat respiratory and middle-ear infections, urinary tract infections and travellers diarrhoea (Willey, et al., 2011, pp.832-838).
Combining with sulfanomides increases efficiency of treatment as it blocks two successive steps in folic acid pathway (Willey, et al., 2011, pp.832-838).

References: Willey, J.M., Sherwood, L.M., Woolverton, C.J. (2011) Prescott’s Microbiology. 8th edn. New York: McGraw-Hill.

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9
Q

Quinolones

A

Nucleic acid synthesis inhibitor (Willey, et al., 2011, pp.832-838).
Synthetic drugs that contain 4-quinolone ring (Willey, et al., 2011, pp.832-838).
Inhibits bacterial DNA gyrase, which is responsible for causing the negative twist in DNA and separates DNA strands (Willey, et al., 2011, pp.832-838).
Inhibition of DNA gyrase disrupts many processes such as DNA replication and repair, bacterial chromosome separation during division, and other processes (Willey, et al., 2011, pp.832-838).
Also inhibit topoisomerase II, which untangles DNA during replication (Willey, et al., 2011, pp.832-838).

References: Willey, J.M., Sherwood, L.M., Woolverton, C.J. (2011) Prescott’s Microbiology. 8th edn. New York: McGraw-Hill.

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10
Q

Nucleic acid synthesis inhibition

A

Inhibits DNA polymerase and DNA helicase, which blocks replication, or RNA polymerase, which blocks transcription (Willey, et al., 2011, pp.832-838).
Bacterial and eukaryotic nucleic acid synthesis doesn’t differ, and thus is not as selectively toxic (Willey, et al., 2011, pp.832-838).

References: Willey, J.M., Sherwood, L.M., Woolverton, C.J. (2011) Prescott’s Microbiology. 8th edn. New York: McGraw-Hill.

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11
Q

Describe the structure and function of penicillins.

A

Cell wall synthesis inhibitors (Willey, et al., 2011, pp.832-838).
Derivatives of 6-aminopenicillanic acid, and contain a B-lactam ring (Willey, et al., 2011, pp.832-838).
Their structure is similar to D-alanyl-D-alanine on peptidoglycan peptide side chains (Willey, et al., 2011, pp.832-838).
Blocks cell wall formation by blocking enzyme which catalyses transpeptidation reaction to form peptidoglycan cross-links, causing osmotic lysis (Willey, et al., 2011, pp.832-838).
Can also activate bacteria’s autolytic enzymes by binding to periplasmic proteins (Willey, et al., 2011, pp.832-838).

Can cause membrane leakage and death by activating bacterial holins, which form holes in plasma membrane (Willey, et al., 2011, pp.832-838).
Murein hydrolases can move through holes, disrupt peptidoglycan and lyse cell (Willey, et al., 2011, pp.832-838).

References: Willey, J.M., Sherwood, L.M., Woolverton, C.J. (2011) Prescott’s Microbiology. 8th edn. New York: McGraw-Hill.

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12
Q

Cephalosporins

A

Cell wall synthesis inhibitors (Willey, et al., 2011, pp.832-838).
They are isolated from the fungus Cephalosporium (Willey, et al., 2011, pp.832-838).
Have a B-lactam structure (Willey, et al., 2011, pp.832-838).
They inhibit transpeptidation reaction during synthesis of peptidoglycan, similar to penicillins (Willey, et al., 2011, pp. 832-838).
They are broad-spectrum drugs given to patients who are allergic to penicillins (Willey, et al., 2011, pp.832-838).

References: Willey, J.M., Sherwood, L.M., Woolverton, C.J. (2011) Prescott’s Microbiology. 8th edn. New York: McGraw-Hill.

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13
Q

Vancomycin

A

Cell wall synthesis inhibitor produced by Streptomyces orientalis (Willey, et al., 2011, pp.832-838).
It is a glycopeptide antibiotic composed of a peptide joined to a disaccharide (Willey, et al., 2011, pp.832-838).
Peptide binds to D-alanyl-D-alanine sequence and blocks transpeptidase reaction (Willey, et al., 2011, pp.832-838).
Bactericidal for Staphylococcus, Clostridium, Bacillus, Streptococcus and Enterococcus (Willey, et al., 2011, pp.832-838).
Enterococcus and Staphylococcus aureus have developed resistance by changing D-alanine to D-lactate or a D-serine residue (Willey, et al., 2011, pp.832-838).

References: Willey, J.M., Sherwood, L.M., Woolverton, C.J. (2011) Prescott’s Microbiology. 8th edn. New York: McGraw-Hill.

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14
Q

Teicoplanin

A

Cell wall synthesis inhibitor produced by Actinoplanes teichomyceticus (Willey, et al., 2011, pp.832-838).
Similar to vancomycin but has less side effects (Willey, et al., 2011, pp.832-838).
Effective against staphylococci, clostridia, streptococci, enterococci, Listeria, and many gram positive pathogens (Willey, et al., 2011, pp.832-838).

References: Willey, J.M., Sherwood, L.M., Woolverton, C.J. (2011) Prescott’s Microbiology. 8th edn. New York: McGraw-Hill.

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15
Q

What are some ways bacteria can gain resistance to drugs?

A

Prevent drug from entering cell (Willey, et al., 2011, pp.832-838).
Pump drug out of cell after it has entered (Willey, et al., 2011, pp.832-838).
Inactivate drug by chemical modification (Willey, et al., 2011, pp.832-838).
Modify the target of the antibiotic, so that it cannot function (Willey, et al., 2011, pp.832-838).
Find an alternate pathway to bypass the sequence which is inhibited, or by increasing target metabolite production (Willey, et al., 2011, pp.832-838).

References: Willey, J.M., Sherwood, L.M., Woolverton, C.J. (2011) Prescott’s Microbiology. 8th edn. New York: McGraw-Hill.

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16
Q

Give some examples of how bacteria prevent drugs from entering the cell, allowing it to gain resistance to the drug.

A

Penicillin G doesn’t affect many gram negative bacteria as it cannot cross the bacterial outer membrane (Willey, et al., 2011, pp.832-838).

Sulfanomide resistance can be achieved by decreasing permeability (Willey, et al., 2011, pp.832-838).

Myobacteria have a high content of mycolic acids in a complex lipid layer outside peptidoglycan which is impermeable to most water-soluble drugs (Willey, et al., 2011, pp.832-838).
This allows them to resist many drugs (Willey, et al., 2011, pp.832-838).

References: Willey, J.M., Sherwood, L.M., Woolverton, C.J. (2011) Prescott’s Microbiology. 8th edn. New York: McGraw-Hill.

17
Q

Explain how bacteria pump drugs out of the cell after it has entered to gain resistance to the drug.

A

They contain efflux pumps which are transport proteins that expel drugs (Willey, et al., 2011, pp.832-838).

They contain multidrug-resistance pumps which are nonspecific (Willey, et al., 2011, pp.832-838).

Contain drug/proton antiporters which allow protons to enter the cell while the drug leaves (Willey, et al., 2011, pp.832-838).
These are present in E. coli, P. aeruginosa and S. aureus (Willey, et al., 2011, pp.832-838).

References: Willey, J.M., Sherwood, L.M., Woolverton, C.J. (2011) Prescott’s Microbiology. 8th edn. New York: McGraw-Hill.

18
Q

Give some examples to describe how bacteria inactivate drugs by chemical modification to develop drug resistance.

A

Penicillin can be modified by hydrolysis of the B-lactam ring by penicillinase (Willey, et al., 2011, pp.832-838).

Chemical groups can be added to drugs in order to inactivate them (Willey, et al., 2011, pp.832-838).
For example, chloramphenicol acetyltransferase adds acetyl-CoA to the two hydroxyl groups on chloramphenicol which inactivates it (Willey, et al., 2011, pp.832-838).

References: Willey, J.M., Sherwood, L.M., Woolverton, C.J. (2011) Prescott’s Microbiology. 8th edn. New York: McGraw-Hill.

19
Q

Explain how target modification can help bacteria to gain antibiotic resistance.

A

Antibiotics have a specific target which they use to kill the bacteria (Willey, et al., 2011, pp.832-838).
These targets can be changed by the bacteria so that the antibiotic cannot function (Willey, et al., 2011, pp.832-838).
For example, erythromycin and chloramphenicol are antibiotics that are protein synthesis inhibitors, and they bind to the 23S rRNA of the 50S ribosomal subunit (Willey, et al., 2011, pp.832-838).
Erythromycin inhibits peptide chain elongation while chloramphenicol inhibits peptidyl transferase reaction (Willey, et al., 2011, pp.832-838).
However, changes in 23S rRNA can decrease affinity of ribosome for erythromycin and chloramphenicol, thus these antibiotics cannot function anymore (Willey, et al., 2011, pp.832-838).

References: Willey, J.M., Sherwood, L.M., Woolverton, C.J. (2011) Prescott’s Microbiology. 8th edn. New York: McGraw-Hill.

20
Q

Describe how bacteria can use an alternate pathway to develop drug resistance.

A

Antibiotics work by influencing target molecules to inhibit certain pathways of important processes, for example protein synthesis inhibitors etc (Willey, et al., 2011, pp.832-838).
However, bacteria can gain resistance to antibiotics if they use an alternate pathway instead, or if they increase the target metabolite production to oppose the effects of the antibiotic (Willey, et al., 2011, pp.832-838).
For example, resistance to sulfanomides can be gained by using preformed folic acid from the environment or by increasing folic acid production to counteract sulfanomide inhibition (Willey, et al., 2011, pp.832-838).

References: Willey, J.M., Sherwood, L.M., Woolverton, C.J. (2011) Prescott’s Microbiology. 8th edn. New York: McGraw-Hill.

21
Q

Describe some ways to overcome drug resistance.

A

Use high drug concentration.
Use a mixture of drugs simultaneously (drug cocktail) so bacteria die without gaining resistance, as it will be difficult for it to gain resistance to multiple drugs at the same time.
Ensure patients are completing the full drug course to prevent full mutation to resistant phenotypes. Otherwise, surviving bacteria could gain resistance and thus the antibiotic may not work in the future.
Find new antimicrobial agents.
Strict control of therapeutic drugs.
Identify new targets for antibiotics.
Research more about the use of bacteriophages as antibiotics.

Microbiology (20 decks)

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