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Pre-Midterm Micro > Antimicrobials > Flashcards

Antimicrobials Flashcards

1
Q

Static antimicrobials

A

slow or inhibit growth
Slower onset of axn
Require a functional immune system– not used in imcp’d
or life threatening situations

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2
Q

Cidal

A

kills the microbes
Does not require a functional immune system– used in imcp’d and life-threatening situation.
Fast onset of axn

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3
Q

Situations to use broad-spectrums

A

1- Wide differential
2- waiting for identification would be dangerous
3- Tx of resistant pathogens to narrow spectrum compounds
4- polymicrobial infections

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4
Q

Natural sources for antibiotics

A

Actinomycetes
Filamentous fungi
Soil bacteria

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5
Q

Sulfonamides

A

Inhibitors of metabolism/Blocks NA synthesis
Synthetic antimicrobials
Block folic acid synthesis- they’re structural analogs of PABA (component of folic acid)

Used against bacteria bc humans don’t synthesize their own folic acid.

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6
Q

TMP-SMX synergy

A

TMP (trimethoprim) blocks dihydrofolate reductase- inhibits nucleic acid synthesis

SMX (sulfamethoxazole) block dihydropteroate synthetase

Together they are v effective at inhibiting folic acid synthesis in bacteria.

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7
Q

Cyclines

A

ex: Doxycycline
inhibit protein synthesis
Bind aminoacyl site of 30S– inhibits aminoacyl tRNA from binding

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8
Q

Aminoglycosides

A

ex: Streptomycin

Interferes with formation of 30S initiation complex

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9
Q

Macrolides

A

ex: Erythromycin

binds 23S component of 50S rRNA and blocks the exit of the peptide chain.

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10
Q

B-lactams

A

Inhibit PDG/cell wall synthesis
Includes: Penicillins, cephalosporins, monobactams, and carbapenems

All are only active on growing cells
No cross-linking of PDG– weakened cell wall– increased pressure with no support– lysis.

Does not work on mycoplasma bc they don’t have cell wall, or fungi, bc they don’t have PDG.

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11
Q

Mechanism of B-lactams

A

Antibiotic binds to PBPs involved in cross-linking the cells wall.
Blocks transpeptidation
Activates bacterial autolytic enzymes/removes autolysis inhibitor–> bacterial cell lyses

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12
Q

Quinolones and Fluoroquinolones

A

Inhibit nucleic acid synthesis
They are nalidixic acid analogs.

Ex: Ciprofloxacin (fluoroquinolone)

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13
Q

VRE

A

vancomycin resistant enterococci

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14
Q

KPC

A

Klebsiella pneumoniae carbapenemases

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15
Q

ESBL

A

Extended spectrum B-lactamases
Confer resistance to all B-lactam antibiotics (except cephamycins and carbapenems), and frequently many others like ahminoglycosides and fluoroquinolones

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16
Q

Why are enterococci resistant to SMX-TMP?

A

bc they lack folic acid synthesis pathway.

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17
Q

Amino glycosides are ineffective against what?

A

Anaerobes, bc they lack oxidative phosphorylation.

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18
Q

Glycopeptides are ineffective against what?

A

G-, bc they are too large to penetrate outer membrane

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19
Q

Nitroimidazoles are ineffective against what?

A

Aerobes, bc they lack flavodoxin which is required to activate nitroimidazoles.

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20
Q

Mechanisms of resistance

A

Altered uptake
Altered target
Drug inactivation

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21
Q

Altered uptake

A

prevents antibiotic intracellular accumulation to therapeutic level.

Often involves efflux pumps norm encoded by transposons, or membrane location transport proteins

Seen in G+ and G-

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22
Q

Altered target

A

mecA gene- encodes for PBP2a (modified transpeptidase) lowers binding affinity for B-lactam antibiotics. Transpeptidation still occurs.

Seen in S. aureus and S. pneumoniae spp.

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23
Q

Antibiotic inactivation

A

Hydrolytic enzymes cleave the antibiotic, making them inactive.
common in B-lactamase bacteria.
Solution: antibiotic with B-lactamase inhibitor (Clavulanic acid)

24
Q

Main ESBL producers

A

Enterobacteriacae:
E. coli (CTX-M enzymes)
Klebsiella spp.

25
Q

B-lactam antibiotics that ESBL aren’t resistant to

A

Cephamycins (cefoxitin and cefotetant)

Carbapenems

26
Q

Risks for ESBL exposure

A 
long-term antibiotics
prolonged ICU stay
Nursing homes
Severe illness
Residence in institution with high use of 3rd-gen cephalosporins
Instrumentation or catheterization
27
Q

Why is AST performed?

A

To give reliable estimate of activity of 2+ antimicrobial agents against a pathogen

Predict likely outcome of therapy

Survey development of resistance among a normally susceptible population of organisms

Predict therapeutic potential

28
Q

Why use antibiograms?

A

To guide treatment in advance of individual susceptibility results

Helps institutions determine and track their susceptibility trends

29
Q

Mechanisms of resistance for a plasmid or transposom

A

1- Transformation (DNA binding proteins)
2- Conjugation (plasmid)
3- Transduction (bacteriophage)

30
Q

What happens to newly acquired DNA?

A

1- destruction by bacterial endonucleases
2- Circularization and maintenance as a plasmid
3- Recombination and integration

31
Q

Types of recombination

A

1- Homologous (general)

2- Non-homologous (site-specific): “cut and paste” mechanism. Transposition

32
Q

Homologous recombination

A

between similar/identical DNA

For integration of DNA acquire by: conjugation, transduction or transformation

33
Q

Transformation

A

Uptake of free-floating DNA.
Facilitated by DNA binding proteins on the bacterial cell membrane.
Requires Ca2+

34
Q

Conjugation

A

Only in G- bacteria
Reliant of sex pilus encoded by F factor (tra) plasmid.
Pilus brings F+ and F- cells into contact, F+ gives F- some DNA and then they’re both F+

MDR bacteria are normally plasmid encoded

35
Q

Transduction

A

Bacteriophage injects DNA into host bacterial cell.

36
Q

Transposition

A

Mobile genetic elements Tn or IS are transferred between bacteria– helps confer resistance.

37
Q

Fluoropyrimidine analogs

A

Target nucleic acid synthesis in fungi.

Flucytosin= artificial pyrimidine.
Causes intracellular deamination by fingal cytosine deaminase to 5-fluorouracil– inhibits NA synthesis

Works against: Candid, cryptococcus fungi

anti-protozoal against” Leishmania, and acanthamoebae

38
Q

Polyenes

A

Target ergosterol synthesis
Lipophilic
Ex: amphotericin B
Binds ergosterol in fungal cell membrane– disrupts osmotic integrity–> ion leakage and membrane destabilization –> lyses the cell.

Fungicidal against most yeasts and filamentous fungi

Anti-protozoal against amoebas

39
Q

Azoles

A

Target ergosterol synthesis by inhibiting 14a-demethylase (converts lanosterol to ergosterol)

Most widely used antifungal

Imidazole’s (2Ns): Ketoconazole
Triazoles (3Ns): Fluconazole, Voriconazole
have reduced toxicity and higher efficacy to imidazoles
Can be fungicidal or fungistatic

40
Q

Terbinafine

A

an Allylamine anti fungal often in topical creams

Inhibits squalene epoxidase–> squalene can’t be converted to lanosterol–> can’t form ergosterol

41
Q

Echinocandins

A

Inhibit chitin synthesis

ex: Caspofungin

Block (1,3)-B-D-glucan synthetase involved in chitin formation

42
Q

Resistance to azoles

A

due to:
Efflux mediated by multi drug transporters
Mutations that decrease affinity to the fungi
Upregulation of demthylase
Alteration in the ergosterol biosynthetic pathway

43
Q

Neuraminidase inhibitors

A

Target viral release (influenza virus)
Ex: Osteltamivir
Blocks neuraminidase –> virus forms aggregates at cell surface and their release is blocked

44
Q

IFNs as anti-virals

A

Both Type I and type II IFNs stimulate uninfected cells to produce antiviral proteins.

Produced in response to:

  • live virus
  • inactivated virus
  • viral nucleic acids

IFN-a2b used for chronic Hep C
IFN-a used against Hep B
IFN-a-n3 used against genital and perianal HPV warts.

45
Q

Adamantanes

A

Antivirals that inhibit uncoating
Ex: Amantadine
Blocks M2 ion channel– viral RNAs then remain bound to M1 and can’t enter the nucleus. Viral replication is halted.

46
Q

Integrase strand transfer inhibitors (INSTIs)

A

Antiretrovirals, target viral synthesis
Ex: Raltegravir, Elvitegravir
Inhibits viral DNA from combining to integrase which blocks it from bonding with the host DNA.

47
Q

NRTIs and NtRTIs

A

anti-virals. Reverse transcriptase inhibitors

Both lack 3-hydroxyl group (have N3 instead). Incorporation into DNA results in chain termination. Aka inhibits DNA synthesis.

48
Q

Acyclovir

A

NRTI (nucleoside analog reverse transcriptase inhibitor)

Requires intracellular phosphorylation to a triphosphate form.

Selective toxicity against viral thymidine kinase. Causes chain termination

Activity against: HSV-1 and HSV-2

49
Q

Viral load

A

measures treatment efficacy

Most frequently used to monitor antiretroviral therapy

50
Q

Nitazoxanide

A

Thiazolide. Interferes with pyruvate ferredoxin oxidoreductase.

Activity against:
Helminths
  - nematodes
  - cestodes
  - trematodes
Protozoa (guardia, cryptosporidium)
  - interferes w anaerobic metabolism
51
Q

Nitroimidazoles

A

Anti-protozoal and anti-bacterial for anaerobes.

Ex: Metronidazole
Causes DNA damage and strand breakage– loss of helical structure, impaired ability to act as template.

52
Q

Pentamidine

A

Interferes w NA and protein synthesis

Anti-fungal (P. jirovecii)
Antiprotozoa (giardiasis, cryptospoirodsis)
Toxic with lots of side effects

53
Q

Antimalarials

A

Quinines: interferes with parasite’s hematin detoxification. Targets blood schizontocides
- chloroquine, mefloquine, quinine

Protein synth inhibitors: Inhibits 70S ribosomes and apicoplast. Targets blood and liver stages.
- Doxycycline

Sesquiterpenes: Artemisinin. Release free-radicals into parasite vacuoles and damage membranes. Inhibits metab processes (glycolysis)

54
Q

Ivermectin

A

Anti-helminthic
Interferes with glutamate gated Cl- channel–> disrupts neural and neuromuscular transmission.

Acts against: nematodes, cestodes and trematodes.
For: onchocerciasis and lymphatic filariasis

55
Q

Benzimidazoles

A

Anti-helminthic.
Binds Beta-tubulin, and inhibits polymerization, glucose transport and fumarate reductase

Exs: Albendazole, Mebendazole

Activity against intestinal nematodes and cestode spp.

56
Q

Praziquantel

A

Anti-helminthic
Interferes with calcium transport (tegument). Causes worm paralysis –> detachment, breakdown and expulsion.

Activity against: trematodes and cestodes.
Tx for: schistosomiasis, liver flukes and cysticercosis.

Pre-Midterm Micro (8 decks)

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