Micro Exam 3 Flashcards

1
Q

Mutant

A
  • a strain of any cell or virus
  • carries a change in nucleotide sequence
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2
Q

Genotype

A
  • nucleotide sequence of the genome
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3
Q

phenotype

A
  • observable properties of the mutant
  • may be altered relative to parent
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4
Q

Wild Type Strain

A
  • Isolated from nature
  • the usual or native form of a gene
  • ORIGINAL FORM
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5
Q

4 Ways Genes can become Mutated

A
  1. Radiation
  2. Oxygen Radicals
  3. Chemicals
  4. Errors in base pairiing
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6
Q

Point Mutation

A

affecting only one nucleotide in a gene sequence.

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7
Q

Missense Mutation

A
  • Point Mutation
  • tyrosine to asparagine
  • diseases-Epidermolysis bullosa, sickle-cell disease
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8
Q

nonsense mutation

A
  • formation of stop codon
  • point mutation
  • premature stop codon
  • result is always bad
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9
Q

Silent Mutation

A
  • Point Mutation
  • Does not affect phenotype (first & second do)
  • almost always in the third base of the codon
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10
Q

Transition

A
  • purine pairs purine
  • prymidine pairs prymidine
  • type of substitution in a point mutation
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11
Q

Transversion

A
  • wrong purine/prymidine match up
  • point mutation
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12
Q

Frameshift mutation

A
  • codons are read in 3
  • chance sequence of polypeptide.
  • insertions or deletions (+1, or -1)
  • scrambles the entire polypeptide sequence after mutation point
  • result in complete loss of gene function
  • lethal
  • not reversible, like point mutations
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13
Q

Mutation Rate for Bacteria

A
  • 10-6 or 10-7 per kilobase pair
  • during single round of replication
  • 1 gene = 1000 base pairs
  • broth culture = 108 cells/mL
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14
Q

Selection

A
  • mutant cell are able to outgrow and replace parent.
  • allow isolation of a single mutant from a very large population
  • easy to detect under right environmental conditions
  • SELECTED BECAUSE IT IS A SURVIVOR IN A MILLION
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15
Q

Screening

A
  • examining large numbers of colonies and looking for the “different” ones.
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16
Q

Example of an Antibiotic resistant gene

A
  • selectable mutation
  • can grow in the presence of antibiotic concentrations that inhibit or kill the parent
  • thus is selected
  • SURVIVOR
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17
Q

auxotroph

A
  • mutant with a nutritional requirement for growth
  • may be derived from wild type, or mutant derivative of wild type
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18
Q

Screening for Nutritional Wild Type

A
  • Replica-plating
  • detect for nutritional mutants.
  • Has a master plate, stamped with growth
  • trasnfer imprint to fresh media, incubate
  • see what does not grow= auxotroph, lacked an amino acid
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19
Q

Mutagen

A
  • Chemical, physical and biological agents that increase mutation rate
  • induce mutations
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20
Q

Histones

A

protect DNA

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21
Q

Ames Test & Back Mutation

A
  • Test if compound is mutagen/carcinogen
  • If it goes from his- to his +
  • Only mutagens that revert back to their wild type can grow
  • Look for the presence rather than absense
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22
Q

Plasmid

A
  • An extrachromosomal genetic element that is NOT essential for growth and has NO extracellular form
  • Contorls Copy #
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23
Q

Chromosome

A
  • genetic element carrying genes essential to cellular function
  • Prokaryotes single circular
  • Eukarotes many linear DNA
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24
Q

Episome

A
  • a genetic element INSIDE bacteria
  • can replicate independently of the host and also in association with a chromosome with which it becomes integrated.
  • Does not control copy #
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25
Q

Copy Number

A
  • avg # of copies of a plasmid inside a host cell.
  • The higher the copy number, the more efficient the plasmid is at replicating itself.
  • (1-100s)
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26
Q

Pilus

A
  • present on fertile cells,
  • Hfr & F+
  • DNA transfer during conjugation
  • not motile, adhere to surfaces
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27
Q

how most plasmids enter cells

A
  • via conjugation through a pilus
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28
Q

where the genetic information encoding the pilus operon is located

A
  • tra region contains
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29
Q

what controls copy number (vegetative replication) of plasmids

A
  • Have their own origin of vegetative replication
  • Controlled by plasmid
  • Semi Conservative
  • Rolling Circle to maintain copy #
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30
Q

Function of OriT

A
  • Origin of TRANSFER during conjugation
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31
Q

Function of OriV

A
  • origin of vegetative replication
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32
Q

Function of tra Genes

A
  • genes that encode transfer functions
  • involved in mating pair formation
  • synthesis of sex pilus.
  • different plasmids may have slightl different tra regions.
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33
Q

how a plasmid becomes an episome

A
  • integrate into the host chromosome.
  • this is when genes can be transferred along with the plasmid
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34
Q

Rolling Circle Mechanism

A
  • unidirectional nucleic acid replication
  • rapidly synthesize multiple copies of circular molecules
  • (DNA , RNA, such as plasmids)
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35
Q

Transposable Elements x2

A
  1. Conservative
  2. Replicative
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36
Q

Conservative Transposable

A

Transposon is excised from one location and reinsterted at a second location. Copy number remains at one.

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37
Q

Replicative Transposon

A
  • a new copy is produced and insterted at the second location.
  • One copy remains at the original site, a second copy at the new site.
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38
Q

list features that are shared by insertion sequences and transposons and at least one
difference between the two, other than size

A
  • Both carry genes encoding transposase
  • both have short inverted terminal repeats at ends
  • IS are smaller, only code for proteins in transposition activity. Coding sequence is flanked by inverted repeats
  • transposons also carry accessory genes such as antibiotic resistance genes
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39
Q

Transposase

A
  • catalyzes the insertion of DNA segments into other DNA molecules
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40
Q

Homologous

A
  • common genetic ancestry; orthologs and paralogs.
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41
Q

RecA (chp.10 #30)

A
  • enzyme responsible for homologous recombination
  • binds strongly and in long clusters to ssDNA to form a nucleoprotein filament. The protein has more than one DNA binding site, and thus can hold a single strand and double strand together.
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42
Q

Homologous Recombination Sequence x5

A
  1. Endonuclease Nicks DNA
  2. Binding of SSB protein
  3. Strand invasion
  4. Development of cross strand exchange
  5. holiday junction a.k.a wifeswap
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43
Q
A

holliday junction

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44
Q

formation of Hfr Strain

A
  • integration of F-plasmid into chromosome occur where IS elements are located
  • HFR first to me transferred
  • lac last
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45
Q

why Hfr cells have such a high frequency of recombination???

A

If there are regions of homology, plasmids can recombine (integrate) into chromosomes

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46
Q

Presence of F Plasmid alters cell in 3 ways

A
  1. synthesize F-pilus
  2. mobilization of DNA
  3. alteration of surface receptors, cell can no longer act as recipient
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47
Q

R Plasmid

A
  • resistance plasmid
  • ability to resist the antimicrobial activity of some drugs.
  • REsist mercury, sulfonamide, strep, etc.
  • TRA genes,
  • pass it along
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48
Q

F-

A
  • Recipient
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49
Q

Role of Plasmids

A
  • impact metabolic functions on host cell
  • basis for genomic rearrangements via homologous recombination
  • horizontal gene transfer
  • examples phenotype class: antibiotic resistance, pigment production, tumor production in plants
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50
Q

3 Ways DNA can be exchanged

A
  1. Plasmids
  2. Transformation
  3. Transduction
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51
Q

Live Smooth Cells, Griffith Strep

A
  • Immune cannot kill encapsulated bacteria
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52
Q

Heat Killed Smooth Cells

A

alive

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53
Q

R Cells, Rough

A
  • no capsule, not pathogenic
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54
Q

Rough Cells + Heat Killed Capsule

A
  • heat killed S Cells TRANSFORMED the live R cells into live S cells!
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55
Q

why the donor cell in transformation likely is dead

A
  • competency- bind 1000 times more than noncompetent
  • because fragments are smaller, get degraded during the uptake process
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56
Q

list the size in bp of a typical gene and the size in bp of the DNA that typically is
taken up in transformation

A
  • Takes about 10 genes
  • 1 gene = 1000 bp
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57
Q

Ways that cells are not competent

A
  • low concentration
  • no peptide growth
  • Electroporation facilitates competency, by exposure to high voltage electrical pulses- makes cell wall permeable.
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58
Q

heteroduplex

A
  • double helix composed of single strands from 2 different DNA molecules
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59
Q

genotype of the daughter cells that form following heteroduplex
formation

A
  • 2 different genotypes
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60
Q

virulent vs. bactriophages

A
  • virulent do not integrate into host cell
  • Temperate ntegrate into the host DNA, causing LYSOGENY, a permanently infected state.
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61
Q

lytic

A
  • one of the two cycles of viral reproduction
  • destruction of the infected cell and membrane
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62
Q

transducing particle

A
  • A defective phage carrying part of the host genome in place of part of the phage genome.
  • When a bacterial cell is infected with a phage, lytic cycle may occur
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63
Q

why a transducing particle is a defective virus

A
  • during lytic infection, enzymes package host DNA accidentally.
  • These cannot lead to a viral infection b/c they contain no viral DNA.
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64
Q

lysogeny

A
  • a host bacterium that has incorporated a phage into its own genetic material;
  • evolutionary significance
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65
Q

Phage Conversion

examples??

A
  • The conversion of non toxin producing strains of Corynebacterium to toxin producing strains following lysogeny
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66
Q

plasmid vector

A
  • proceeds independently of direct chromosomal controal.
  • natural vectors b/c they carry othere genes that confer imporatant properties on their hosts.
  • small size- easy to isolate, multiply copy number , & presence of selectable markers (antibiotic resistant genes)
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67
Q

polylinker

A
  • a segment of artificial DNA with cut site for many restriction enzymes
  • multiple cloning site
  • inserted into lacZ gene
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68
Q

transformant

A
  • cells that have taken up DNA (foreign, artificial or modified) and express genes on the introduced DNA.
69
Q

restriction site and enzyme

A
  • enzymes can chemically modify DNA
  • recognize base sequences and cut the DNA
  • used in invitro, gave birth to genetic engineering
70
Q

sticky ends (image)

A
  • Type II Restriction Enzymes
  • make staggering cuts, leaving short, single stranded overhangs
  • used in molecular cloning.
71
Q

role of ligase in cloning????

A
  • complementary sticky ends are generated
72
Q

a recombinant plasmid may be introduced into a
bacterial cell

A
  • transformation
  • conjucation
  • electroporation
  • calcium enchilling
  • transduction
73
Q

how tranformants may be selected using an ampicillin

A
  • selection or plasmid
  • cloning
  • cell takes up DNA
  • amp must for resistiance on plasmid
74
Q

Xgal

A
  • Cells transformed with vectors containing recombinant DNA will produce white colonies;
  • non-recombinant plasmids (i.e. only the vector) grow into blue colonies.
75
Q

Chp 9

Virus vs Plasmid

A
  • Both are not considered to be a form of life
  • Viruses have an extracellular form, enables them to exist outside host. Transmits from one cell to another.
  • Plasmids are NAKED DNA NO CAPSID
    • do NOt encode genes for transfer to a new host
    • Viruses DO
76
Q

Virus vs Living Cell

A
  • Viruses are not living cells
  • have no metabolism
  • Both Compartmentalize
  • Both evolve
  • Virus- reproduces by invading a host cell
  • Smaller than a Cell, (400nm), Bacteria is (1000nm)
  • Virus does not have a cell wall
77
Q

2 Components of the Simplest Virus ???

A
  • DNA
  • or RNA????
78
Q

Capsid

A
  • Protein shell
  • surrounds the nucleic acid of virion
79
Q

Capsomeres

A
  • subunit of the capsid,
  • outer covering protects the genetic material of a virus.
  • self-assemble, form the capsid.
  • Clog Shoes
80
Q

Nucleocapsid

A
  • complete complex of n.acid & protein packaged in virion
81
Q

Envelope

A
  • Some viruses are Naked,
  • others possess lipid containing layers around nucleocapsid.
82
Q

Spikes

A
  • attach virus to the to-be-infected cell
  • project from enveloped viruses
  • glycoproteins
83
Q

Viral Receptor

A
  • found on the surface
  • not on the host cell, but host physiology
  • an adsorption target
  • place that a virus attaches to begin its infection
84
Q

Viral Matrix

A
  • link the viral envelope w/core.
  • play a crucial role in virus assembly
  • interact w/ the RNP complex & viral membrane.
85
Q

2 Major Shapes of Animal Viruses & Symmetry for each

A
  • Icosahedral- Spherical
  • Helical- ROD
86
Q

Icosahedron

A
  • 20 triangular faces
  • 12 vertices
  • spherical
  • more efficient because it uses the smalles number of capsomeres to build the shell
87
Q

DDDP

A
  • DNA, Dependent, DNA Polymerase
    *
88
Q

RDRP

A
  • RNA Dependent RNA Polymerase
  • RNA replicase
  • required by positive, negative, and double stranded
89
Q

DDRP

A
  • DNA Dependent RNA Polymerase
90
Q

RDDP

A
  • RNA Dependent DNA Polymerase
91
Q

Naked Virus

A
  • Has no envelope
  • Capsomeres form the outer layer
92
Q

How a virus obtains is envelope

A
  • derived from the membranes of the host cell
  • makes initial contact with host
  • critical for the attachment of the virion
93
Q

How most animal viruses enter cells

A
  • entire viroin enters animal cell
  • Replicate in animal cell’s NUCLEUS
94
Q

How attachment process determines host specificity for animal viruses ?

Chp 9 #16

A
  • Macromolecules for cell-to-cell contact
  • via the immune system
  • specific receptors
  • determines host
95
Q

Plus Sense RNA Viral Strategy

A
  • RNA Replicase
  • makes complementary strands
  • uses a template to make more plus strands
96
Q

Minus Sense RNA Viral Strategy

A
  • Must carry enzymes in viroins
  • plus strand synthesized by RDRP and used as mRNA
  • plus strand used as a template to make more negative strands
97
Q

Double Strand RNA viral Strategy

A
  • Viroin contains plus strand RNA
  • cannot be released as mRNA
  • Must contain RDRP, transcribes DSRNA
  • produce positive mRNA upon entry to host
98
Q

Retrovirus Viral Strategy

A
  • ssRNA in viroins
  • replicate through dsDNA
  • require REVERSE transcripticase
99
Q

Reverse Transcription

A

RNA to DNA

100
Q

Double Strand DNA viral Strategy

A
  • replicate through RNA intermediate
  • transcription of minus strand
  • only partially double stranded
101
Q

Explain Why some viruses must carry proteins inside the capsid and list the types of viruses and the types of proteins they carry?

Chp 9 #19

A
  1. Negative RNA
  2. Double Stranded RNA
  3. Retro Virus
102
Q

Why Naked Virus must kill host cell??????????

A
  • destroy host cell cyoplasmic membrane
  • can’t bud out
  • lytic, no way to get out
103
Q

syncytia

A
  • fusion of multiple nuclei
  • example : skeletal muscle
104
Q

2 types of Microscopes for Viruses ???

A
  1. Transmission Electron Microscope
  2. Electron Crio Microscopy
105
Q

list
 6
 
outcomes
 to 
cells 
following 
infection
 with
 an 
animal
 virus
 and 
give
 an

example
 of
 a 
virus 
that 
has 
each
 outcome


A
  1. Cell fusion
  2. Transformation into Tumor Cell
  3. Tumor Cell Division
  4. Death of cell and realease of virus
  5. Slow release of virus without cell death
  6. Virus present but not replicating
106
Q

symbiotic 
relationship
 between
 parasitic
 wasps
 and
 the
 virus 
that

infects
 them
 and
 why 
this 
changes
 our 
view
 of 
host‐virus 
relationships


A
  • Does not replicate to new viruses
  • affects the caterpillar’s immune system
  • Without the virus infection, phagocytic hemocytes (blood cells) will encapsulate and kill the wasp egg but the immune suppression caused by the virus allows for survival of the wasp egg
  • genes expressed from the polydnavirus alter host development and metabolism to be beneficial for the growth and survival
107
Q

parasitic wasp virus vs transducing virus vs lysogenetic virus ???

A
  • Transducing- DNA is transferred from one bacterium to another by a virus
  • Lysogeny- integration of the bacteriophage nucleic acid into the host bacterium’s genome.
108
Q
  • shape
 of
 bacteriophage 
T4 & animal 
viruses
  • role
 of 
the
 tail
 in 
infection

A
  • Animal Virus- has no defined shape, enveloped virus. Virions are 80 nm
  • Tail= attachment of viroin to the host and injection of nucleic acid
109
Q

proteins
 that 
regulate 
early, 
middle 
and 
late 
gene 
transcription
 in 
T4


A
  • Eary & Middle- mRNA is produced, codes for nucleases, DNA poly, new phage, proteins
  • Late- mRNA codes for structural proteins of phage virion and for T4 lysozymes. used to lyse the cell and release new phage particles.
  • SIGMA
110
Q

lysogeny

A
  • viral genome is replicated as a prophage along with genome of the host
111
Q

agar
 overlay
 method


A
  • dilution of a virus is mixed in melted agar with the sensitive host bacteria.
  • mixture is poured on surface of agar plate
  • host bacteria grow and form a lawn of confluent growth
  • Virion infected cells are lysed forming plaques in the lawn
  • Top
 agar
 is 
very
 soft to
 allow 
easy
 spread 
to 
adjacent 
cells

112
Q

Plaque

A
  • a zone of lysis or cell inhibition caused by virus infection on a lawn of cells
113
Q

Plaque Forming Unit

A
  • a measure of the number of particles capable of forming plaques per unit volume
  • viral particles that are defective or which fail to infect their target cell will not produce a plaque and thus will not be counted.
114
Q

How are animal viruses grown in the laboratory ?????

A
  • Use tissue
  • ex, hela cells,

monolayer

115
Q

calculate
 the
 titer 
of 
a 
virus 
preparation
 given 
the 
dilution,
the 
amount
 plated 
and

the
 numbers
 of 
plaques 
counted


???

A
  • by counting the number of plaque forminug units
  • number of virus infectious units present in the virus sample
  • 50
 pfu/ml 

/

 10‐5 
=
 
5
 X
 10
6
 pfu/ml

116
Q

Viroid

A
  • small circular single-stranded RNA that causes certain plant diseases
  • resembles a short double-stranded molecule with closed ends.
  • can exist oustide host cell
  • lacks a capsid, does not use a receptor to enter host cell.
  • enters a PLANT cell through a wound, from insect or other mechanical damage.
  • move via plasmodesmata (thins strands of cytoplasm)
  • no protein encoding genes
  • dependent on host function for replication.
  • Result= multimeric RNA with many viroid units joined end to end.
117
Q

Prion

A
  • an infectious protein whose extracellular form contains no nucleic acid. misfolded

  • encodes native form of prion protein.
  • found in neurons of healthy animals (brain).
  • more b-sheet regions
  • Scrapie(sheep), Mad Cow Disease, Kuru (cannibals), Creutzfeldt-Jakob (in humans), Chronic Wasting Disease (deer, elk)
118
Q

why 
autoclaving 
is
 NOT
 adequate 
for 
sterilizing
 instruments 
contaminated

with
 prions


A
  • because they are already misfolded
  • must be incinerated
119
Q

sterilization

A
  • No viable microbes
  • not always attainable, ex: fresh foods
120
Q

pasteurization

A
  • Uses heat
  • first used for controlling wine
  • NOT sterilization does not kill microorganims
  • Reduces load of microbes
121
Q

disinfection

A
  • lowering the number of microbes to decrease number of pathogens
  • inhibit growth of microbes
  • ex: Bleach
122
Q

High Temp Sterilization: Dry Heat vs. Wet Heat

A
  • Macromolecules lose structure and function in heat
  • Dry heat is more heat resistant, takes longer.
  • Steam under pressure can achieve higher temperatures (autoclave)
  • Wet heat is more effective
  • faster reduction
  • better penetrating power
123
Q

Most difficult microbe to render via autoclave

A
  • Bacterial Endospores
  • Endospores are dryer requiring more heat.
  • Prions cannot be autoclaves
124
Q

Infectious Agent cannot be sterilized by autoclave and what must be done to sterilize equpiment contaminated

A
  • Prions
  • must be incinerated to ash
125
Q

Sterility using an autoclave

A
  • not the pressure, but high temperature achieved with steam. kills microorganisms
126
Q

Advantages/Disadvantages of Autoclave tape + Endospore Strips

A
  • tape- changes color after exposure to temperatures commonly used in sterilization processes, typically 121°C in a steam autoclave.
  • does not ensure, product is sterile, tape will change color upon exposure only.
  • cannot use disinfectants on endos
127
Q

2 Methods to Sterilize Plastic ware

A
  • Cationic Detergents
  • sterilants
  • disinfectants
  • sterilizers
128
Q

How microbes can be removed from air, but liquids that cannot be autoclaved

A
  • UV
  • Microwaves
  • gamma rays
  • X-rays
  • steam can remove microbes, liquids may boil over
129
Q

HEPA

A
  • High Efficiency Particulate Air Filters
  • Expensive
130
Q

Disinfectant considered “Gold Standard”

A

Phenol

131
Q

Advantages/Disadvantages of Phenol

A
  • Too toxic to use, except in small quantities
  • Protein denaturant
132
Q

Advantages/Disadvantages of Phenolics

A
  • Disrupts Membranes
  • Inhibits fatty acid synthesis
133
Q

Advantages/Disadvantages of Triclosan

A
  • antibacterial and antifungal agent.
  • polychloro phenoxy phenol
  • negative effects on environment & toothpaste
134
Q

Advantages/Disadvantages of Halogens

A
  • inactivate proteins by iodination or oxidation
  • Iodine/Chlornie lose potency w/ time or proteinaceous materials
135
Q

+/- Of Alcohols

A
  • Denature Proteins
  • Not good against naked viruses or endospores
136
Q

+/- Cationic

A
  • Disrupts Membranes
  • Inactive against endospores/naked viruses b/c no membranes
  • ex:Lysol
137
Q

+/- Anionic Detergents

A
  • soaps contain esterified fatty acids, NaOH, KOH
  • No antimicrobial properties
  • hand washing for 20-30 seconds, reduce count by 99.9%
  • gentle
  • ex: ivory
138
Q

Bacteriostatic

A
  • inhibits growth while in contact
139
Q

Bacteriocidal

A
  • makes microbe non-viable
140
Q

Bacteriolytic

A
  • destroys microbe immediately
141
Q

Best way to remove microbes from hands

A

Washing with soap & water

142
Q

Antimicrobial Agents x 6

A
  1. penicillins
  2. cephalosporins
  3. tetracyclines
  4. sulfonamides
  5. aminoglycosides
  6. quinolones
143
Q

Penicillins

A
  • beta lactamase
  • Target Cell Walls
  • low host toxicity
  • broad spectrum
  • inhibit transpeptidation
144
Q

Cephalosporins

A
  • derived from fungus
  • beta lactamase
  • Target Cell Wall
  • low host toxicity
  • broad spectrum
145
Q

Tetracyclines

A
  • interfere with protein synthesis
146
Q

Sulfoamides

A
  • inhibitor to PABA
  • folic acid metabolism
147
Q

Aminoglycosides

A
  • amino sugars bonded by glycosidic linkage
  • against grame negative
  • nerve and neurological adverse effects
148
Q

Quinolones

A
  • inhibit DNA gyrase
  • little effect on Euks
  • $$$
  • inhibit Gram + & Gram -
149
Q

2 Classes of antimicrobial agents that contain Beta-Lactim Ring

A
  • penicillins
  • cephalosporins
150
Q

Beta-Lactamase

A
  • splits actam ring
  • inactivating antibioticy
  • CELL WALL synthesis
151
Q

Sulbactam

A
  • bind to b-lactamase
  • get penicillin
152
Q

Clavulanic Acid

A
  • bind to b-lactamase
  • get penicillin
153
Q

Synergism

A
  • combinations of antibiotics that works better together
154
Q

Antagonism

A
  • antibiotics that do the opposite
155
Q

Why are Trimethoprim & Sulfamethoxazole is a Synergistic

A
  • combo makes them work better together than alone
156
Q

Why Penicillin + Sulfonamides are antagonistic

A
  • sulfs- cell wall will not divid until it gets folic acid
  • no affec on dividing cells- penicillin
157
Q

Side Effects for Tetracyclines + Aminoglycoside

A
  • can’t use on children
  • sun sensitive
  • overgrowth of fungi
158
Q

Bacterial Resistance Mechanisms x5

A
  1. Reduced permeability
  2. inactivation of antibiotic
  3. alter target
  4. resistant to biochemical pathways
  5. efflux (pumping out of cell)
159
Q

Why antifungals & antiviral drugs are more toxic than antibacterial drugs

A
  • closer to our cells
  • anti-virals use our biochemistry
160
Q

Superbug

A
  • can’t treat them
  • developing faster with time
  • genetics-plasmids
161
Q

2 Common Mechanisms Bacteria acquire Resistance

A
  1. random mutation, gene transfer
  2. secrete enzymes that detroy
162
Q

MIC

A
  • minimal inhibitory concentration
  • 2 fold serial dilution
  • what serum level to achieve
163
Q

MBC

A
  • minimal bacteriocidal combination
164
Q

Kirby Bauer Agar Disk Diffusion Test

A
  • controls right pH
  • turbidity
  • swab lawn
165
Q

Susceptible

A
166
Q

Intermediate (susceptibility testing)

A
167
Q

Resistant (susceptibility testing)

A
168
Q

2 Reason Zone Size CANNOT be used to determine most effective antimicrobial agent

A
  1. because you don’t know MIC
  2. Diffuse Really fast
169
Q

Zone of Inhibition

A
  • The clear region around the paper disc saturated with an antimicrobial agent on the agar surface.