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Pre-Midterm Micro > Antimicrobials > Flashcards

Antimicrobials Flashcards

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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

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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

Study These Flashcards
A

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

25
B-lactam antibiotics that ESBL aren't resistant to
Cephamycins (cefoxitin and cefotetant) | Carbapenems
26
Risks for ESBL exposure
``` long-term antibiotics prolonged ICU stay Nursing homes Severe illness Residence in institution with high use of 3rd-gen cephalosporins Instrumentation or catheterization ```
27
Why is AST performed?
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
Why use antibiograms?
To guide treatment in advance of individual susceptibility results Helps institutions determine and track their susceptibility trends
29
Mechanisms of resistance for a plasmid or transposom
1- Transformation (DNA binding proteins) 2- Conjugation (plasmid) 3- Transduction (bacteriophage)
30
What happens to newly acquired DNA?
1- destruction by bacterial endonucleases 2- Circularization and maintenance as a plasmid 3- Recombination and integration
31
Types of recombination
1- Homologous (general) | 2- Non-homologous (site-specific): "cut and paste" mechanism. Transposition
32
Homologous recombination
between similar/identical DNA | For integration of DNA acquire by: conjugation, transduction or transformation
33
Transformation
Uptake of free-floating DNA. Facilitated by DNA binding proteins on the bacterial cell membrane. Requires Ca2+
34
Conjugation
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
Transduction
Bacteriophage injects DNA into host bacterial cell.
36
Transposition
Mobile genetic elements Tn or IS are transferred between bacteria-- helps confer resistance.
37
Fluoropyrimidine analogs
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
Polyenes
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
Azoles
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
Terbinafine
an Allylamine anti fungal often in topical creams | Inhibits squalene epoxidase--> squalene can't be converted to lanosterol--> can't form ergosterol
41
Echinocandins
Inhibit chitin synthesis ex: Caspofungin Block (1,3)-B-D-glucan synthetase involved in chitin formation
42
Resistance to azoles
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
Neuraminidase inhibitors
Target viral release (influenza virus) Ex: Osteltamivir Blocks neuraminidase --> virus forms aggregates at cell surface and their release is blocked
44
IFNs as anti-virals
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
Adamantanes
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
Integrase strand transfer inhibitors (INSTIs)
Antiretrovirals, target viral synthesis Ex: Raltegravir, Elvitegravir Inhibits viral DNA from combining to integrase which blocks it from bonding with the host DNA.
47
NRTIs and NtRTIs
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
Acyclovir
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
Viral load
measures treatment efficacy Most frequently used to monitor antiretroviral therapy
50
Nitazoxanide
Thiazolide. Interferes with pyruvate ferredoxin oxidoreductase. ``` Activity against: Helminths - nematodes - cestodes - trematodes Protozoa (guardia, cryptosporidium) - interferes w anaerobic metabolism ```
51
Nitroimidazoles
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
Pentamidine
Interferes w NA and protein synthesis Anti-fungal (P. jirovecii) Antiprotozoa (giardiasis, cryptospoirodsis) Toxic with lots of side effects
53
Antimalarials
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
Ivermectin
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
Benzimidazoles
Anti-helminthic. Binds Beta-tubulin, and inhibits polymerization, glucose transport and fumarate reductase Exs: Albendazole, Mebendazole Activity against intestinal nematodes and cestode spp.
56
Praziquantel
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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