Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Microbiology > Control of Microbial Populations (Bacterial and Fungal) > Flashcards

Control of Microbial Populations (Bacterial and Fungal) Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards
1
Q

Biocides

A
  • physical or chemical agents used to control microbes

- disinfectant, antiseptic or temperature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Disinfection

A
  • destruction of VEGETATIVE pathogens on inanimate surfaces
  • spores and other relatively resistant organisms (i.e. mycobacteria, viruses and fungi) may remain viable
  • too harsh to be used on tissues
  • may use physical or chemical methods
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Antisepsis

A
  • destruction of vegetative pathogens on living tissues
  • almost always be chemical methods
  • sporicidal action not implied
  • commonly used as components in soaps, hand gels
  • effectiveness determined by:
    a) microorganisms present
    b) the level of toxicity of the chemical to the tissues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Degerming

A
  • removal of microbes from a limited area (i.e. skin around injection site)
  • mostly mechanical removal by alcohol-soaked swab
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Sterilisation

A
  • absolute term - either something is sterile or it isn’t
  • destruction and removal of all forms of microbial life (including endospores)
  • prions may not be removed
  • i.e steam under pressure, sterilising gas (ethylene oxide)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Sanitisation

A
  • treatment intended to lower microbial counts to safe public health levels
  • usually eating/drinking utensils
  • i.e. high-temp washing, dipping into chemical disinfectant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

-Static

A
  • inhibition of further growth

- bacteria enters stationary phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

-Cidal

A
  • decreases cell numbers (killing effect)

- bacteria enters death phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Moist heat

A
  • physical sterilizing agent
  • steam at 121 degrees celsius and greater than atmospheric pressure (i.e. 2 atm)
  • sterilizes in 15 minutes
  • not for heat-sensitive objects (solutions, plastics)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Ethylene Oxide Gas

A
  • chemical sterilizing agent (used in gaseous form, it’s considered a physical agent)
  • objects placed in chemiclave and gas pumped in
  • alkylating agent; alkylation of terminal hydroxyl, carboxyl, amino, and sulfhydryl groups. This process blocks the reactive groups required for many essential metabolic processes (i.e. alkylates guanine and funtional groups of proteins -> prevents DNA replication)
  • used to sterilize heat-sensitive objects like sutures, bandages, and grafts
  • flammable, explosive and carcinogenic to lab animals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Generations

A
  • lab has altered the chemical composition of a naturally-occuring antibiotic
  • by altering the side chains, can change the properties of the antibiotic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Benzyl penicillin

A
  • natural penicillin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Ampicillin

A
  • aminopenicillin

- can be taken orally

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Methicillin

A
  • penicillinase-resistant penicillins

- overcome degrading enzymes that some bacteria possess to break down natural penicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Piperacillin

A
  • extended spectrum penicillin

- active against some gram - bacteria in addition to gram + bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Beta-lactams

A
  • Penicillins, Cephalosporins
  • cell wall synthesis inhibitor
  • binds penicillin-binding proteins (PBPs) - serine proteases (transpeptidases) that perform cross-linking of the peptidoglycan layer
  • binding inhibits assembly of peptidoglycan layer -> activates AUTOLYSIS (degrades cell wall -> cell death)
  • ineffective against mycobacteria (b/c cell wall is impenetrable) and mycoplasmas (b/c they lack a cell wall)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Isoniazid/ Ethionamide/ Ethambutol/ Cycloserine

A
  • cell wall synthesis inhibitors
  • treat mycobacterial infections

Cycloserine:
- inhibits D-alanine-D-alanine synthetase and alanine racemase (both enzymes catalyze cell wall synthesis)

18
Q

Bacitracin

A
  • cell wall synthesis inhibitors
  • topical treatment
  • treats gram + bacteria (Staphylococcus, Streptococcus)
  • gram - bacteria are resistant
  • interferes with dephosphorylation and recycling of lipid carrier responsible for moving peptidoglycan precursors through cytoplasmic membrane to cell wall
19
Q

Aminoglycosides

A
  • streptomycin, gentamicin
  • bind irreversibly to the 30S ribosomal subunit
  • induces codon misreading (changes the shape of the 30S portion and causes the code on the mRNA to be misread incorrectly)
  • not taken up by mammalian tissues
  • treats gram - bacterial infections
  • not effective against anaerobes (b/c oxidative phosphorylation is absent in anaerobes)
20
Q

Tetracyclines

A
  • binds reversibly to the 30S ribosomal subunit

- blocks binding of amioacylated tRNA to A site (on the mRNA-ribosome complex)

21
Q

Macrolides

A
  • erythromycin
  • binds 50S ribosomal subunit
  • inhibits transpeptidation and translocation
22
Q

Lincosamides

A
  • clindamycin
  • binds 50S ribosomal subunit
  • targets binding at A and P sites
23
Q

Streptogramins

A
  • chloramphenicol
  • binds 50S ribosomal subunit
  • inhibit peptide bond formation
24
Q

Quinolones

A
  • ciprofloxacin, levofloxacin (broad spectrum)
  • nucleic acid synthesis inhibitors
  • binds to both the alpha-subunit of DNA gyrase and topoisomerase IV -> inhibits DNA synthesis
25
Q

Rifampin

A
  • nucleic acid synthesis inhibitors

- binds to the beta-subunit of DNA dependant RNA polymerase complex -> inhibits transcription of mRNA

26
Q

Glycopeptides

A
  • vancomycin
  • cell wall synthesis inhibitor
  • interacts with the D-alanine-D-alanine termini of the pentapeptide side chains -> interferes sterically with the formation of the bridges between the peptidoglycan chain -> disrupts cell wall peptidoglycan synthesis in growing gram-positive bacteria.
  • ineffective against gram - bacteria (the molecule is large and cannot penetrate into the cell)
27
Q

Nitroimidazoles

A
  • metronidazole
  • Interact with DNA
  • Inhibit metabolism of glucose
  • Interfere with mitochondrial function
  • ineffective against aerobes (molecule requires activation by flavodoxin, which is absent in aerobes)
28
Q

Sulfamethoxazole/Trimethoprim combination treatment

A

Sulfamethoxazole (nucleic acid synthesis inhibitor)
- inhibits dihydropteroate synthetase (converts PABA -> dihydrofolic acid)

Trimethoprim (metabolism inhibitor)
- inhibits dihydrofolate reductase (converts Dihydrofolic acid -> tetrahydrofolic acid)

  • most bacteria synthesize their own folic acid, so this treatment works best against those bacteria
  • **exception: Enterococci use exogenous folic acid
29
Q

Antibiotic target modification (mechanism of resistance)

A
  • bacteria possess MecA gene - allows bacteria to produce alternative transpeptidase enzymes in the presence of antibiotics (i.e. beta-lactams like meticillin) so that the antibiotic cannot recognize the transpeptidase and the peptidoglycan layer can continue to grow in the presence of the antibiotic
30
Q

Inactivating enzymes (mechanism of resistance)

A

i. e. Beta-lactamases
- either constitutively produced, or produced in the presence of an antibiotic
- inactivate beta-lactam antibiotics

***can give the patient beta-lactamase inhibitors (i.e. clavulanic acid)

31
Q

Conjugation

A
  • only in gram - bacteria (only gram - bacteria have the F pilus)

prior to exchange:

donor: F+ cell (i.e. penicillin sensitive)
recipient: F- cell (i.e. penicillin resistant)

after exchange:
recipient: F+ cell (i.e. penicillin resistant)

  • single strand of plasmid transferred to recipient cell
  • once strand present in the recipient, complimentary strands formed in both cells
32
Q

High Frequency Recombination

A
  • happens in conjugation when there is a complete transfer of the F plasmid and it’s integration into the chromosome of the recipient cell
33
Q

Transformation

A
  • happens during the late lag phase
  • “free” DNA expelled into the environment and taken up by DNA binding protein on recipient cell

1st strand - degraded
2nd strand - recombination and incorportation into chromosome

34
Q

Transduction

A
  • DNA from bacteriophage incorporated into bacteria’s chromosome
  1. Virulent (lytic) bacteriophages - death of cell by lysis
  2. Temperate bacteriophages - switch between virulent and lytic phase
35
Q

Lysogeny

A
  • when bacteria are carrying a prophage
  1. The bacteria’s gene expression is repressed
  2. Phage gene expression and replication are triggered by certain conditions
36
Q

Transposition

A

Transposons (Tn)/ insertion sequences = jumping genes

chromosome -> plasmid
chromosome -> chromosome

  • transposons move around via non-homologous recombination, via the action of site-specific recombinases (Transposase)
  • simple transposon - no selectable genes
  • complex/ composite transposon - antibiotic resistance or other trait
  • plasmids may be numerous transposons together
37
Q

Polyenes

A
  • Amphotericin B
  • direct fungal membrane damage
  • lipid-loving compounds; bind to ergosterol in the membrane and form pores that result in leakage of internal cell contents out of cell
  • “cidal” to the fungi
  • doesn’t discriminate sterol attachment; also used as an antiparasitic (for Leishmania spp.) and -can be toxic to host cells as well
38
Q

Flucytosine

A
  • nucleic acid synthesis inhibitor/ antimetabolite
  • flucytosine (5-FC, 5-fluorocytosine) is an analog of cytosine
  • converted by fungal cytosine deaminase into 5-fluorouracil -> undergoes phosphorylation steps -> 5-fluorouridine triphosphate and 5-fluorodeoxyuridine monophosphate are incorporated into RNA/DNA synthesis process -> inhibition of synthesis
39
Q

Azoles

A
  • fluconazole
  • ergosterol biosynthesis inhibitor
  • inhibits 14alpha-demethylase (converts lanosterol -> ergosterol)
40
Q

Allylamines

A
  • terbinafine
  • ergosterol biosynthesis inhibitor
  • inhibits squalene expoxidase -> accumulation of squaline (which is incorporated into the cell membrane)
  • in addition, no lanosterol or ergosterol formed
  • total result is an increased membrane permeability
41
Q

Echinocandins

A
  • caspofungin
  • beta-glucan synthesis inhibitors
  • block (1,3)-beta-D-glucan synthetase

*active against Candida and Aspergillus, but not C. neoformas

42
Q

Nikkomycin Z

A
  • chitin synthesis inhibitors
  • competes with UDP-N-acetylglucosamine for chitin synthase
  • still under investigation for therapeutic potential

Microbiology (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions