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Chapter 20 Flashcards

1
Q

A) What was the first documented example of a chemical used successfully as antimicrobial medication?

A

??

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2
Q

B) What was Prontosil found to be useful in treating?

A

red dye called Protonsil which killed steptococci in animals

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3
Q

C) How were sulfanilamide’s discovered?

A

when protonsils break down in blood into sulfanilamide which acted against the strep

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4
Q

D) What are chemotherapeutic agents? Are they the same thing as antimicrobial drugs?

A

chemicals used to treat disease. yes

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5
Q

E) How was penicillin discovered?

A

alexander flemming was studying the staph areus and saw that colonies growing near a mold seemed to be disolving.. He identified the mold as a Penicillium and so he called the substance produced by it as penicilin. he used it on mice, and it worked, but he couldn’t get to purify the compound.
later chain and florey were able to purify penicillin and used it to treat a police officer

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6
Q

F) What are antibiotics?

A

antimicrobial drugs produced by microorganisms

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7
Q

G) How can you alter penicillin to give it new properties? [Figure 20.1]

A

take penicillin G ( kills gram positive) alter it so it produces ampicilin (kills Gram negatives. It can also be changed to produce menthylcillin which is less suscepatble to enzymes produced by some bacteria which destroy penicillin

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8
Q

A) Where do most antibiotics come from?

A

they come form microorganisms found in the soil like strptomyces, penicillium, cephillosporium

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9
Q

B) What does selective toxicity mean?

A

causing greater harm to microbes than to humans

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10
Q

C) What does the therapeutic index tell us?

A

lowest dose toxic to the patient devided by the normal dose used in therapy. This is an expession of the toxicity of a drug. Thos with high theraputic index are less toxic.

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11
Q

D) What do bacteriostatic drugs do?

A

inhibit bacterial growth: ex. sulfa drugs. They inhibit/ stop growth, but the persons body must eliminate the infection.

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12
Q

E) What do bactericidal drugs do?

A

kill bacteria: these damage the cells so the bacteria cannot eliminate the reactive oxygen and results in extensive oxidative damage

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13
Q

F) What do broad-spectrum antibiotic affect? When are they used?

A

are used in treating acute life-threatening diseases that why do not have time to identify the specific type of bacteria. This can cause issues thought with normal microbiota

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14
Q

G) What do narrow-spectrum antimicrobials affect? When are they used?

A

affect a limited range of bacteria. this is used when the bacteria is identified and tested for antimicrobial suceptability

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15
Q

H) When are a combination of antimicrobials used and how?

A

when you use different antibicrobials to eliminate an infection. You have to be careful because bacteriostatic drugs interfere with drugs that kill only actively dividing cells. So some combos are antagonistic

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16
Q

I) What must an antimicrobial do to treat meningitis?

A

it must be able to cross from blood into the cerebral spinal fluid

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17
Q

J) How do you administer drugs that are unstable at low pH?

A

through Iv or injection. not oral or stomach acid will destroy it

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18
Q

K) What is the half-life of a antimicrobial drug and why is it important?

A

the time it takes in seum to react 50%. This determines the frequency of doses.

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19
Q

L) What are some adverse effects associated with antimicrobial drugs?

A

allergic reactions
Supress normal microbiota
Toxic Effects: some are toxic at high concentrations and can damage the body

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20
Q

M) What is intrinsic resistance? What is acquired resistance?

A

inrtinsic: innate resistance. when a bacteria has always had innate characteristics protecting them from antibiotics
Aquired: is when the cell mutates ect and it becomes resistant to an antibiotic

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21
Q

A) What are the targets of antibacterial drugs? [Figure 20.2]

A

q

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22
Q

B) What are the characteristics of β-lactam drugs? [Table 20.1 and Figure 20.4]

A

Inclued penicillins, an cephalosporins. These drugs are composed of a Beta lactam ring. they disrupt the formation of peptiloglycan. the inhibit enzymes (penicillin binding protien ,by penicilin binding to them.) that catalyze peptide bridges between glycan strands. This causes weakness in cell walls causing the cell to lyce

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23
Q

C) Why can antimicrobials that interfere with cell wall synthesis be advantageous? [Figure 20.3]

A

because they can inhibit growth of infection as well as they are not likely to damage eukaryotic cells

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24
Q

D) What are penicillin-binding proteins? How do they relate to β-lactam drugs?

A

they are the enzymes that make the peptide briged between glycan strands. they call them penicillin- binding because penicillin can bind to them inactivating them.

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25
E) What is β-lactamase?
enzyme released by some bacteria that breaks down the Beta lactam ring
26
F) What are the different members of the penicillin family and what are their structure and characteristics?[Figure 20.6]
penicillin V: 0CH2 (acid ressistant) Methylcillin: OCH3(penicillinase- resistant) Dicloxacillin:Cl, N and CH3(acid and penicillinase resistant) Ampicillin: CH, NH2(broad spectrum and acid resistant) Amoxicillin: H0, CH, NH2( like ampicillum, but more active and requires less frequent doses) Tricaracillin:Ch.COONa( most active against gram neg rods) Pipercillin: CH, NH, C,O,( like ticaracillin, but broader spectrum)
27
G) What are the cephalosporins, what are the difference among the generations?
derived from the antibiotic produced by fungi Acremonuim cephalosporium, and closely related ab's produced by bacteria streptomyces. Resistant to Beta lactanases. Some are not as effective on gram positives because they have a low affinity for pbp's. 1-4th generations cephalexan& cephradine (1st) cefacloe and cefprozil (2nd) cefixime and ceftibuten(3rd) cefepime(4 later gens are better agianst gram neg, and more b-lactamase resistant.
28
H) What are carbapenems and monobactams?
beta lactum drugs 2 groups that are b-lactamase resistant Carbapenems: They are effective against wide range of gram neg, and pos. -impenem -meropenem -ertapenem -doripenem Monobactams: aztrenoman- work against enterobacteria. diff structure and can be given to those with penicillin allergies
29
I) How does vancomycin work and what are they used to treat?
block peptiglycogen synthesis by binding to NAM molecules preventing the formation of glycan chains. - can kill bacteria that are gram positive and are resistant to beta lactam drugs - kill clostridium difficle - gen last resort
30
J) How does bacitracin work and how is it used?
inhibits cell wall biosynthesis by preventing transfers of peptilogycan precursors across the cytoplasmic membrane. -used topically because of it's toxicity
31
K) Which antimicrobials inhibit prokaryotic protein synthesis, how and when are they used? [Figure 20.7 and Antibiotic Protein video] 8
- Aminoglycosides - Tetracyclines - Glycyclines - Macrolides - Chloramphenicol - Lincosamides - Oxolidines - Streptogramins
32
L) Which antimicrobials target enzymes used in nucleic acid synthesis, how do they work and when are they used? 3
Fluoroquinonlones: synthetic drgs that inhibit enzymes (topiosemereases) which maintain the supercoiling of dna. - bacterialcidal gram neg and pos - resistnace is due to alteration in dna gyrase target Rifamycins: block polymerase from initiating transcription. - Rifpamin (type). bacteriocidal to gram neg, pos, and mycobacterium. and is used in treating leporacy, tb, and prevent those exposed from getting Neisseria meningitis - redish pigment apears in tears and urine Metronidazole: interferes with DNA synthersis and function, but only in anaerobic microorg. because the metaboism of cell is what activates it. - treats vaginosis and Clostriduim difficile
33
M) Which antimicrobials interfere with metabolic pathways, how do they work and when are they used? [Figure 20.8]
Sulfonamids: reffered to as sulfa drugs. inhibit the growth of gram pos and neg. They are similair structure to PABA (substrate used in the pathway) the enzyme that usually binds to PABA is taken over by sulfa drugs. - Human cells lack enzymes in folate synthesis and are no harmed by the sulfa drugs. - resistance is aquired through a plasmid bound to enzyme making affinity for sulfa Trimethoprim: inhibits enzyme invovled in another metabolic step. - This has little affect in human counterparts. - resistence is like that of sulfonamids - combined with sulfonamids is used to treat UTI's
34
N) Which antimicrobials damage bacterial membranes, how do they work and when are they used?
Daptomycin: inserts itself into the cytoplasmic membrane in gram pos cells resistent to other drugs Polymyxin: damaged gram neg membranes, but it can also to eukaryotic cells and so is used only topically
35
O) Why are not many antimicrobials effective against Mycobacterium?
their waxy cell wall, and slow cell growth.
36
P) What are first line drugs? What are second line drugs?
used against tb (a mycobacterium) First line: combos of diff. antibiotics to reduce chance of bacteria becoming resistant. -Isonaizid inhibits mycolic acids, which are used in making cell wall. -Ethambutol also inhibits the cell wall components Second line: used for strain resistant to first line drugs, but usually are less effective, or have greater risk of toxicity.
37
A) What is the minimum inhibitor concentration? How is it determined? [Figure 20.1]
lowest concentration of a specific drug needed to prevent growth of a given strain invitro. This is determined by growing cultures with fixed amount of bacterium that have different concentrations of antibiotics. then incubated for 16 hrs. the one with the lowest concentration with no growth
38
B) What is the minimum bactericidal concentration? How is it determined?
lowest amount of antibacetial drug that kills 99.9% of cells of a specific strain. They take samples of MIC and then transfer them on a plate to see if they will grow. if no growth it was bacterialcidal
39
D) How can commercial modifications of antimicrobial susceptibility testing be advantageous?[Figure 20.11 and Figur20.12]
- results within 3 hours | - less labor intensive
40
A) How does antimicrobial drug resistance develop? [Figure 20.13]
resistant strains survive and multiply and the others will die off
41
B) What are the different mechanisms of acquired resistance? [Figure 20.14]
Drug inactivating enzymes Alteration in target molecule decreased uptake of drug increased elimination of the drug
42
C) How do spontaneous mutations lead to antimicrobial resistance?
this is because it changes and can prevent binding to the drug
43
1) How does combination therapy get around this?
this is so the ones that form mutations and become resistent to the one drug is then killed off by the other. the likelyhood of it developing to both is slim
44
D) How does gene transfer lead to antimicrobial resistance? What does the R plasmid have to do with it?
R plasmid is shared via conjugation to another cell. this carries the codes for different resistance and therefore become resistant to multiple drugs instantaneously
45
E) What sort of resistance does enterococci exhibit?
they have low affinity for b-lactam drugs, Have R plasmids. Resistant to vancomyosin
46
F) What makes MRSA, VISA, and VRSA so dangerous?
have low affinity for b-lactam drugs
47
G) What sort of resistance does Streptococcus pneumoniae have?
there are changes in the penicillin binding protiens. this is due to aquisition of chromosomal dna
48
H) What are the problems with treating M. tuberculosis?
many patients do not keep up with the complex schedule of first line combination drugs. As a result they build resistance against first line drugs.
49
I) What sort of resistance does Enterobacteriaceae have?
outer membrane doesn't allow drugs in and then they developed ability to produce b-lactamase. some extended further to be resistant to cephalosporins and aztreonam. and some produce an enzyme which inactivate carbapenem
50
J) What can physicians and healthcare workers do to slow the spread of antimicrobial resistance?
increase efforts to discover source of infection so they can perscribe the right antibiotic, and so better at educating the pts.
51
K) How can patients slow the spread of antimicrobial resistance?
Follow instructions. complete it
52
L) How can public education slow the spread of antimicrobial resistance?
people need to know antibiotic are not effective against viruses.
53
B) What are targets for antiviral drugs? [Figure 20.15 and Antiviral Agents video]
viral entry into the cell: bind to HIV protien that binds to cells and blocks it interfere with viral uncoating: amatadine and rimantadine they interfere with the uncoating step and so it cannot replicate interfere with nucliec acid synthesis: -nucleoside annalogs: drug converted in the eukaryotic cell to become analogs. Then virally encoded enzymes are likely to incorperate them resulting in permature synthesis. Non-nuclioside polymerase inhibitors: inhibit the viral polymerases by binding to it Non-nucleoside reverse transcriptase inhibitors: bind to viral revers transcriptase -typically used with nucleoside analogs.
54
1) How do antivirals do their job?
you also have ones that target the enzymes required for viral assembly and release. protease inhibitors: inhibits protease which is important in providing protien components to make a virus Neuraminidase inhibitors: in influenzae. important for the release of viral particles.
55
C) What are the characteristics of antiviral drugs? [Table 20.2]
475
56
A) What type of drugs are used to treat fungal infections and how do they work? [Table 20.3 and Figure 20.16]
477
57
A) Why is there less research done on antiparasitic drugs?
because they occur in poorere countries where drugs cannot be afforded
58
B) What are the more important antiparasitic drugs and what are their characteristics? [Table 20.4]
479
59
Aminoglycosides-
irreversably attatches to 30S. This alters the shape preventing translation and misreading of mrna.enters cell via active transport ( so only respiratory cells. This can make them risky with possible side effects. often combined with b-lsctam drugs which will make cell walls penetrable by them in bacteria they normally could not. - one, trobamyosin can be administered through inhilation for pts. with cistic fibrosis - another neomyocin is too toxic and is used topically
60
-Tetracyclines
reversibly bind to 30S blocking trna from attaching and therefore prevents translation. brought into prokaryotes via active transport. gram neg and gram pos. Ressistance can be built to them by cell regulating/ limiting the amount they allow in the cell -doxycycline has longer half life
61
Glycyclines
related to tetracylines. wider spectrum of activity, and is used if tetra. is ressisted. -Tygecycline is the only approved one
62
Macrolides
reversably bind to 50S. and prevents the continuation of translation. works against grm pos. they also fight against walking pneumonia, but not enterobacteriae. - "drug of choice for pts. with allergies to penicillin. " - resistance occurs through changes in rna target, it produced enzymes which alter the drug, and alterations that result in decreased uptake. - ( -omyosins)
63
Chloramphenicol
binds to 50S. prevents ptptide bonds from being formed and blocks translation. This is active against a range of bacteria, but used as a last resort to avoid rare, but lethal side effect (aplastic anemia, which lead to no production wbc and rbc)
64
Lincosamides
50s. inhibits gram neg and pos. - used in treating intestinal perforation because it inhibits norm microbiota, Baceriodes fragilis - people who take it are more likely to develop C difficile which are resistant to it - clindmyosin
65
Oxalidinones
bind 50s. gram pos. | -used in treating those who have resistance to b-lact. drugs and vancomysin
66
Streptogramins
50S preventing distinct steps of translation. | -synercide composed of two (individually they are bacteriostatic) together they are bacteriocidal

Micro Biology (25 decks)

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