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Mycology > Ch 12 > Flashcards

Ch 12 Flashcards

1
Q

Secondary metabolism

A
  • produce chemicals that inhibit growth of other microorganisms
  • slow down growth
  • mostly cannot be used to treat microorganisms
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2
Q

Antimicrobial Chemotherapy

ANTIBIOTICS

A

**goal: administer a drug to an infected person that destroys the infective agent without harming the host cells
-used to control infection
»Designed to act on bacteria

-any substance produced by the natural metabolic processes of some microorganisms that can inhibit or destroy other microbes-antagonism-
-antibiotics come mainly from aerobic spore forming bacteria and fungi (Streptomyces(2/3), Bacillus, etc)
> used to Control infection
-perfect drug dose doesn’t exist
-balancing drug char against one another compromise can be achieves

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3
Q

Semisynthetic

Symthetic

A
  • Chemically modified in lab after being isolated from a natural source
  • increase movement and spectrum

-antimicrobial compound synthesized in laboratory through chemical reactions

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4
Q

Common Drug strategies:

  • Prophylaxis
  • combines therapy
  • drug synergy
A 
(Prophylaxis)
-drugs are administered to Prevent and infection
-chemotherapeutic
(combines therapy)
-2+ drugs at once
-treats TB, HIV, gonorrhea
-prevents survival, treats mixed infections
(drug synergy)
-enhanced efficiency
-smaller amounts of drugs can be used
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5
Q

The spectrum of Antimicrobic Drug

  • Broad
    ex) Tetracyclin
  • intermediate
    ex) Ampicillin
  • Narrow(1&2)
    ex) Bactarin(1), Polymixin(2)
A

(Broad)
-greatest rage of activity
target cell components common to most pathogens-ribosomes-
>g+, g-, rickettsias, chlamydias, mycoplasms
(Intermediate)
>g+, g-, chlamydias(some), mycoplasmas(some)
(Narrow)
-effective on a small range of microbes
target a specific cell component that is found only in a cetain microbe
>group1
g+ only
> group2
g- only

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6
Q

Characteristics of ideal antimicrobic drugs

A
  • selectively toxic to the microbe, but nontoxic to host cells
  • Microbicidal
  • Potent long enough to act & is not broken down or excreted prematurely
  • isn’t subject to development of antimicrobial resistance
  • complements host defense activities
  • remains active
  • readily delivered to site of infection
  • reasonably priced
  • doesn’t disrupt host’s health by causing allergies or predisposing the host cell to other infections
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7
Q

selective toxicity**

A

> drugs should kill or inhibit microbial cells without simultaneously samaging host tissues

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8
Q

Mechanisms of Drug action(5)

A

-inhibit cell wall
-inhibit cell membrane
-inhibit DNA/RNA
-inhibit Protein Synthesis
>50S >30S >30S&50S
-inhibit Metabolism pathway

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9
Q

Inhibit cell wall

Drugs:
Beta-Lactom
-Penecilin
-Cephalosporin

Non-Betalactoms

  • Varcomycin
  • Bacitracin
  • Isoniazid(INH)
A

note: peptidoglycan protects against rupture
- bind and block peptidases cross-link glycan molec–interrupt completion of cell wall

:block synthesis and repair

Beta lactoms

Varcomycin(non-beta lactom, narrow spectrum)

Bacitracin(non-betalactom, narrow spectrum)
-block elongation of peptidoglycan

Isoniazid(INH)
-intf with synthesis of mycolid acid

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10
Q

Inhibit cell membrane

Drugs:
-Polymyxins(narrow spectrum with fatty acid component)
>B & E
-topical agents of ointments

A

-leakage of proteins and nitrogen bases from phospholipids

cause loss of selective permeability
-Target folic acid

:Dies from disruption in metabolism or lysis

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11
Q

Inhibit DNA/RNA

*analogs

Drugs:
Fluoroquinolones
-related to quinine
-bind to DNA gyrase and other enzymes

A

Inhibit replication and transcription

  • inhibit helicase
  • inhibit gyrase
  • inhibit RNA polymerase

(Analogs)
-insert viran n.acid like a normal base

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12
Q

Inhibit Protein Synthesis
-50S -30S -30S&50S

Drugs:
Aminoglycoside
Tetracycline
Chloramphenicol
Macrolides
A

> Bacteria
-50S -30S -30S&50S

> 50S
-prevents formation of peptide bonds
-inhibits translocation of subunit during transation
30S
-mireading of mRNA> lead to abnormal proteins
-block attatchment of tRNA on A-acceptor site
30S&50S
-blocks inhibition of protein synthesis

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13
Q

Inhibit Metabolism pathway

A

(commpetitive inhibition)-mimick normal substrate of an enxyme
-distract enzyme from substrate
:metabolism slows/stops bc enzyme is no longer able to produce needed product

:blocks pathway and inhibit metabolism

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14
Q

Antifungal drugs(5)

  • Polyenes
  • Marcolide polyenes
  • Griseofulvin(active in Dermatophytes)
  • Azoles
  • Flucytosine
A 
note:Fungi are eukaryotic
(Polyenes)
-attatck membranes b/c
Fungal membranes contain ergosterol
>Marcolide polyenes
-structure mimics the lipids in cell membranes

(Azoles)

  • broad spectrum antifungal
  • inhibit ergosterol and cell membrane synthesis
  • *choice treatment for menginitis

(Flucytosine)
-structural analog of cytosine that inhibits DNA and protein synthesis

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15
Q

Antiparasitic chemotherapy

  • Antimalarial
  • Chemotherapy for protozoan infections
  • Antihilminthic
A

(Antimalarial)
-Quinine >Mefloquine–semisynthetic analog

(Antihelminthic)
-broad spectrum drugs

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16
Q

Antiviral Chemotherapeutic Agents

  • Drugs for treating influenza
  • Antiherpes drugs
  • Drugs for treatinv HIV and AIDS
A

(Drugs for treating influenza)

  • broader spectrum
  • inhibit neuaminidase
  • used prophycatically and must be giern early in infection

(Antiherpes drugs)

  • mimic the structure of neucleotides
  • compete for sites of replicating DNA

(Treating HIV and AIDS)

  • inhibit or block Reverse Transcriptase
  • use either NRTIa(directly top DNA) or NNRTIs(stop RT)
  • protease inhibitors block enzyme» result in faulty viruses
17
Q

Actions of Antiviral drugs
I. Inibition of virus entry or release
II. Inhibition of nucleic acid synthesis
III. Inhibition of HIV Insertion, Assembly, Release

A

I. Inibition of virus entry or release

II. Inhibition of nucleic acid synthesis

III. Inhibition of HIV Insertion, Assembly, Release

modes of action

  • barring virus penetration into host cell
  • blocking virus transcription and translation
  • preventing virus maturation
18
Q

Category of Anti-HIV drugs

  • Nucleoside revese transcriptase inhibitors
  • Nonnucleoside reverse transcriptase inhibitors
  • protease inhibitors
  • enrey of fusion blockers
  • integrase inhibitors
A

(Nucleoside revese transcriptase inhibitors)
-chemical analogsare inserted into HIV DNA and terminate its synthesis; competitive inhibition
eg)
retrovir
(Nonnucleoside reverse transcriptase inhibitors)
-drugs interact with reverse transcriptase and block its active site; noncompetitive inhibition
-bind directly to HIV RT enzyme
eg)
nevirapine
(protease inhibitors)
-HIV protease that completes viral assembly its blocked, leading to incomplete and dysfunctional viruses
-results in defective, immature, noninfective
eg)
amprenavir
(enrey of fusion blockers)
-maraviroc covers an entry receptor n the human cell (CCR5) nd keeps the virus from binding; enfuviritide stops the viral envelope from using with the cell emmbrane
eg)
maraviroc
(integrase inhibitors)
-interacts with HIV ntegrase;tops the action of the viral DNA
eg)
Raltegravir

19
Q

inferons (IFN)

A
  • glycoprotein produces primarily by fibroblasts and leukocytes in response to immune stimuli
  • antiviral, nticancer properties

therupeutic benefits:

  1. reducing time of healing
  2. preventing symptoms of cold and papiloma viruses
  3. slowing the progress of cancers
  4. treating rar e leukemias cancer
20
Q

Acquisition of Drug Resistance

  • how
  • due ot natural selection
A

(Drug Resistance)
-an adaptive response in which microorganisms begin to tolerate and amount of drug that would be normally inhibitory

(how)
-originates from resistance (R) factors being transferred though conjugation transformation, transduction

  1. spontaneous mutations in critical chromosomes
  2. acquire new genes via transfer from other species
21
Q

Mechanism of Drug Resistance(5)

A
  1. Inducement of alt enzymes can inactivate the drug(when 2.new genes acq)
  2. Permeability of into bacterium is decreased
  3. engages special drug transport pumps»remove drug
  4. Binding sites for drug decreased
  5. Affected metabolic pathway is shut down // alt pathway is used (when 1.mutation)
22
Q

Drug Inactivation Mechanism

  1. Drug inactivation
  2. Dec permeability
  3. Activation of drug pumps
  4. Change in drug binding site
  5. Use of alt metabolic pathway

ex)betalactomases hydrolyze beta-lactan of drugs

A
  1. Drug inactivation
    - producing enzymes
  2. Dec permeability
    - cell membrane
    - plasmid encoded proteins pump drug out of cell
  3. Activation of drug pumps
    - multi-drug resistant pumps use active transport to kick out drug
  4. Change in drug binding site
    - decreasing their synthesis of ergosterol(Fungi)
    - alteration of all proteins(Bacteria)
    - point mutations in ribosomal proteins asirse(Bacteria)
  5. Use of alt metabolic pathway
    - microbe develops alt metabolic pathay
23
Q

Allergy

A

(Allergy)
-occurs because the drug acts as an antigen

(antigen)-
foreign material capable of stimulating immune system

(super infection)-
microbed begin to overgrow and cause disease
ex) Candida albicans
Clostridium difficile

24
Q

Selecting Antimicrobial drug(3)

A
  1. Nature of microbe infection (ID organism)
    - examination of body fluids
  2. Test suseptibility of microbe
    - demonstating vitro activity of several drugs
    - expose pure culture to diff drugs
    - Kirby-Bauer Disc technique-agar diffusion
25
Q

Therapeutic index

A
  • high delective toxicity for infectious agent
  • low human toxicity

-higher therapeutic index, the lower potential for toxic drug reactions:)

26
Q

Therapeutic index

MIC

@ mic is therapeutic does

A
  • high delective toxicity for infectious agent
  • low human toxicity

-higher therapeutic index desired(the lower potential for toxic drug reactions:) )

ex) Amphoceritin B
- low therapeutic index . :needs to be controlled

27
Q

MIC

-describes the smallest concentration of a particular drug needed to kill/inhibit a microbe

A 
Type 1: "-cide"
-inhibit protein synthesis
ex) sulfa drugs
        -lead to kidney damage
Type 2: "-static"
-if does is increased, it can become "-cide"
28
Q

Biofilms

A

-form biofilms

|&raquo_space;difficult to control because buildup of cells makes it difficult for the antibiotic to reach a majority of the cells

Mycology (2 decks)

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