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Biology 2051 > Exam 5 > Flashcards

Exam 5 Flashcards

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1
Q

any situation in which a microbe is established and growing in a host; begins at mucous membranes found throughout the body

A

infection

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2
Q

pathogens adhere to mucosal surfaces through interactions between

A

pathogen and host macromolecules

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3
Q

4 adherence factors

A

capsule/slime layer, adherence proteins, lipoteichoic acid, fimbriae pili

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4
Q

Steps in pathogenesis

A
  1. Exposure to Pathogen
  2. Adherence
  3. Invasion
  4. Colonization & Growth
  5. Toxicity OR Invasiveness
  6. Tissue Damage/Disease
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5
Q

Describe invasion… what is needed?

A

pathogen penetrates the epithelium; needs nutrients and right growth conditions

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6
Q

substantial microbial growth in host tissue; dependent on location in the body

A

microbial colonization

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7
Q

microbial growth at the site of invasion

A

localized infection

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8
Q

spread of microbe throughout body via blood or lymphatic systems; more difficult to treat/ more likely to be deadly

A

systemic infection

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9
Q

microbe that cause disease; colonization early in life could be fatal

A

pathogen

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10
Q

microbe that causes disease when host defense is absent or compromised; some are resident flora (Staphylococcus or Candida)

A

opportunistic pathogen

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11
Q

damage or injury to the host that impairs host function; preceded by infection

A

disease

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12
Q

ability of a pathogen to cause disease

A

virulence

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13
Q

the number of pathogen required to kill 50% of the population

A

Lethal Dose 50

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14
Q

anything made by the pathogen to help it cause disease

A

virulent factors

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15
Q

help pathogen attach to host cell (ex. fimbrial protein subunit of E. coli)

A

adherence factors

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16
Q

help pathogen to invade host tissue (ex. Clostridium hyaluronidase breaks own hyaluronic acid that holds cells together)

A

invasive factors

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17
Q

help pathogen grow within host tissue (ex. Vibrio cholera secretes a protein (TcpF) that allows colonization of the small intestine)

A

Colonization Factors

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18
Q

help pathogen avoid phagocytosis (ex. Encapsulated Bacillus anthracis, Treponema pallidum binds host fibronectin for disguise)

A

Cell Surface Structures

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19
Q

soluble chemical excreted by viable pathogen

A

exotoxins

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20
Q

causes lysis of host cell (ex. Staphylococcal alpha-toxin)

A

cytolytic toxins

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21
Q

composed of two proteins covalently bound: B subunit binds to host cell and transfers the A subunit into the host cell to cause damage (ex. Diphtheria toxin produced by Corynebacterium diphtheriae)

A

A-B toxins

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22
Q

exotoxins that affect the small intestine, causing changes in intestinal permeability that lead to diarrhea (ex. Cholera toxin produced by Vibrio cholera)

A

enterotoxins

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23
Q

How is the cholera boxing produced by Vibrio cholera

A
  1. Normal ion movement, Na+ from lumen to blood, no net Cl- movement
  2. Colonization and toxin production
  3. Activation of epithelial adenyl cyclase by cholera toxin
  4. Na+ movement blocked, no net CL- movement to lumen
  5. Massive water movement to the lumen
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24
Q

stimulate large numbers of immune response cells causing extensive inflammatory reactions (ex. Staphylococcus aureus TSST-1 causes TSS)

A

superantigen toxin

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25
Q

toxic bacterial structural component released upon bacterial cell death; lipopolysaccharides derived from the outer membrane of gram-Neg bacteria

A

endotoxin

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26
Q

how do you detect endotoxins?

A

LAL assay

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27
Q

loss of virulence that can be attained by genetically engineered vaccines or naturally under non optimal growth conditions

A

attenuation

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28
Q

the ability of an organism to resist infection (ex. Bone marrow stem cells produce leukocytes)

A

Immunity

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29
Q

leukocytes

A

phagocytes & lymphocytes

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30
Q

4 types of phagocytes

A

dendritic cell
macrophage
neutrophil
mast cell

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31
Q

2 types of lymphocytes

A

t cell

plasma cells

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32
Q

where do all leukocytes come from

A

bone marrow stem cell

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33
Q

what body fluid systems transport immune cells throughout the body

A

circulatory and lymphatic systems

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34
Q

what is the first line of internal defense against pathogens

A

innate (non-specific) immunity

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35
Q

contact virus, bacterium, tumor cells; release perforin and granzymes to kill

A

Natural Killer Lymphocytes

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36
Q

if there is MHC 1 recognition, then the NK cell is deactivated

A

recognition of cells by Natural Killer cells

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37
Q

What happens when the Natural Killer cells recognizes cancer & viral infected cells

A

stress protein receptor recognizes stress protein on cell, then NK cell kills the cell

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38
Q

Neutrophils & Monocytes (macrophages and dendritic cells) that destroy the pathogen by phagocytosis

A

Phagocytes

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39
Q

pore forming protein

A

perforin

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40
Q

exogenous serine proteases

A

granzymes

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41
Q

steps in phagocytosis

A
  1. Phagocyte pattern-recognition molecules recognize pathogen-associated molecular pattern on pathogen
  2. phagocytosis
  3. Lysosome fuses with phagosome and secretes enzymes into the phagosome to digest the pathogen
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42
Q

What do phagocytes have on their cell surface to recognize pathogens?

A

phagocyte pattern-recognition molecules

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43
Q

What part of a pathogen is recognized by a phagocyte?

A

pathogen-associated molecular pattern

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44
Q

4 ways the pathogen can protect itself from phagocytosis

A
  1. Pigments to neutralize singlet oxygen (Staph aureus, carotenoids)
  2. Molecules scavenge toxic oxygen (Mycobacterium tuberculosis, cell wall glycolipids)
  3. Leukocidins kill phagocyte (Streptococcus pyogenes)
  4. Capsule prevents the adherence of phagocyte to the bacterial cell (Streptococcus pneumoniae)
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45
Q

localized nonspecific response to noxious stimuli (toxins, pathogens)

A

inflammation

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46
Q

arrive at site first in response to chemokine released from damaged host cells; release proteases, phospholipase, and collagenases to destroy bacteria; secrete chemokines such as Macrophage Inflammatory Proteins to signal macrophages to come help

A

neutrophils

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47
Q

secrete inflammatory cytokines (increase vascular permeability, swelling, reddening, heat); phagocytosis ensues if pathogen is present

A

macrophages

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48
Q

release histamines and cause vasodilation (increase in vascular capillary diameter)

A

mast cells

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49
Q

a systemic inflammatory response; life threatening

A

septic shock

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50
Q

main cause of septic shock

A

rupture of the large intestine causing leakage of gram negative enteric bacteria into sterile areas

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51
Q

adaptive (specific) immunity is defined by 3 properties

A

specificity, memory, and tolerance

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52
Q

immune cells recognize and react with antigens via direct molecular interaction

A

specificity property in adaptive immunity

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53
Q

memory T cells and B cells allow for faster and stronger secondary response

A

memory property in adaptive immunity

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54
Q

immune cells are not able to react with self antigen

A

tolerance property in adaptive immunity

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55
Q

Steps in adaptive immunity

A
  1. initial steps similar to innate immunity
  2. leukocyte displays digested pathogen peptide (antigen) on its cell surface thereby becoming an antigen-reseting cell
  3. t–cell recognizes the antigen on the antigen-presenting cell
  4. pathogen is destoyed
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56
Q

type of leukocytes and t cells in cell-mediated immunity

A

Leukocytes: Macrophages and Dendritic cells

Type of T-Cells: T-cytotoxic and T-helper 1 cells

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57
Q

type of leukocytes and t cells in antibody-mediated (humoral) immunity

A

Leukocytes: B cells

Type of T-Cells: T-helper 2 cells

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58
Q

positive selection in T cell tolerance

A

retains T-cells that recognize self MHC proteins

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59
Q

negative selection in T cell tolerance

A

retains T-cells that do not bind tightly to MHC/self-antigen complex

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60
Q

when T-cell receptor binds to antigen/MHC complex, T-cell:

  1. becomes activated
  2. divides to make more T-cells….
A

Effector Cells and Memory Cells

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61
Q

short lived and carry out function of T-cell

A

effector cell

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62
Q

remain inactive until they encounter the same antigen in the future; long-lived

A

memory cell

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63
Q

2 types of T-cell function in cell-mediated immunity

A
  1. t-cytotoxic cells destroy antigen-presenting cell (MHC 1 antigen presentation)
  2. t-helper 1 cells increase phagocytosis and cause inflammation (MHC 2 antigen presentation)
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64
Q

steps in antibody-mediated immunity

A
  1. Initial antigen exposure and primary response that leads to the production of antibodies and memory cells
  2. Secondary antigen exposure
  3. Subsequent antigen exposure
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65
Q

Steps of initial antigen exposure and primary response

A
  1. B cell uses antibody to recognize and bind antigen
  2. Antigen-antibody complex is internalized
  3. Antigen is processed and loaded onto MH II protein
  4. MHC-antigen complex is presented on the B cell surface
  5. Th2 Cell recognizes MHC-antigen complex stimulating cytokine production by Th2 Cell
  6. Cytokines stimulate nearby antigen-specific B cells to make antigen-specific antibodies (mostly IgM)
66
Q

make antibodies in the primary response, short-lived

A

plasma cells

67
Q

used upon future exposure to antigen, long-lived

A

memory cells

68
Q

faster than primary response, doesn’t require T-cells, memory cells transform into plasma cells and begin producing IgG

A

secondary response induced by reexposure to antigen

69
Q

over time, antibody titer _____

A

decreases

70
Q

subsequent antien exposure will lead to another

A

secondary immune response

71
Q

proteins activated by innate and adaptive immunities

A

complement proteins

72
Q

classical complement activation

A

uses antigen-antibody complex

  1. Antibody binds antigen and complement protein
  2. sequential binding of other complement proteins
  3. bacterial cell membrane damage and lysis
73
Q

alternative pathway of complement activation

A

host serum proteins bind to bacterial cell surface; C3 binding initiates binding of other complement proteins

74
Q

binding of antibodies or C3 enhances phagocytosis because phagocytes have antibody receptors that recognize constant domain and C3 receptors

A

opsonization

75
Q

inappropriate immune response resulting in host damage (four types)

A

hypersensitivities

76
Q

pathogen proteins that cause widespread stimulation of immune cells resulting in a massive inflammatory response damaging the host

A

superantigen

77
Q

antibody mediated; allergy; occurs within minutes of secondary antigen (allergen) exposure; reactions are mild to life-threatening

A

type I, immediate hypersensitivity

78
Q

primary response of type I, immediate hypersensitivity

A

allergens stimulate Th2 cells to secrete cytokines causing B cells to release IgE which bind to mast cell receptors

79
Q

secondary response of type I, immediate hypersensitivity

A

if allergen binds to nearby IgE antibodies to cross-link them, then degranulation occurs

80
Q

treatment of Type I, immediate hypersensitivity depends on severity

A

removal of allergen, antihistamines, steroids to reduce inflammation, adrenaline, desensitization

81
Q

activate abnormally large amounts of T cells; excess cytokine production causing systemic inflammatory reactions

A

superantigen

82
Q

Examples of Staph aureus as a superantigen

A

Food poisoning and TSS

83
Q

individual receives antibodies but did not make the antibodies

A

passive immunity

84
Q

natural passive immunity example

A

fetus gets IgG from mother in utero; newborns get IgA from breast milk

85
Q

artificial passive immunity example

A

injection of antiserum or antitoxin

86
Q

individual is exposed to antigen and memory cells are produced

A

active immunity

87
Q

natural active immunity example

A

infection

88
Q

artificial active immunity example

A

immunization

89
Q

found that milkmaids exposed to cowpox were immune to smallpox, so he started vaccinating people with cowpox

A

Edward Jenner

90
Q

resistance of a population to infection due to immunity of a high proportion of the individuals in that population

A

herd immunity

91
Q

What percentage of herd needs to be vaccinated to have herd immunity to measles

A

90%

92
Q

7 types of vaccines

A
  1. Toxoid
  2. Surface Protein
  3. Killed Bacteria Cel
  4. Inactivated Virus
  5. Live Cells/Activated Virus
  6. Purified Polysaccharide (Conjugated)
  7. Recombinant Antigen
  8. DNA Vaccine
93
Q

chemical modified exotoxin retains antigenicity but no toxicity (ex. Tetanus, Diphtheria, Anthrax)

A

Toxoid vaccine

94
Q

Formaldehyde create proteins from the bacteria (ex. Pertussis)

A

Surface Protein vaccine

95
Q

formaldehyde, heat (ex. Typhoid Fever)

A

Killed Bacteria Cell vaccine

96
Q

formaldehyde (ex. Rotavirus, IPV, flu)

A

Inactivated Virus vaccine

97
Q

attenuated strains; more effective for viral immunity (MMR, Var, BCG)

A

Live Cells/Active Virus vaccine

98
Q

antigenic polysaccharide from capsule is attached to a protein (ex. MCV4, PCV7, Hib)

A

Purified Polysaccharide (Conjugated) vaccine

99
Q

pathogen gene that codes for an antigen is put into a harmless microbial host (yeast) to make lots of th antigen (ex. HAV, HBV, HPV)

A

Recombinant Antigen vaccine

100
Q

bacterial plasmid containing a pathogen antigen (ex. HIV clinical trials)

A

DNA vaccine

101
Q

viral size

A

~20-44nm; smaller than their host cell

102
Q

viral structure

A

a nucleocapsid made of nucleic acid (viral genome) surrounded by a protective protein coat (capsid)

103
Q

made of capsomeres containing one or more proteins; arranged to give vision symmetry

A

capsid

104
Q

rod-shaped; protein subunits twist up; length of virus is determined by length of nucleic acid

A

helical symmetry

105
Q

roughly spherical; 20 equilateral triangles with 3 or more capsomeres in each

A

Icosahedral symmetry

106
Q

outer membrane (lipid bilayer) around capsid derived from the host cell

A

enveloped viral structure

107
Q

multiple parts of the viral structure assembled separately

A

complex viral structure

108
Q

What are the two forms of a virus? In which form does the virus do harm?

A
  • extracellular and intracellular

- the virus does harm in the intracellular

109
Q

how are viruses classified?

A

their genomes and how they make DNA

110
Q

Steps in viral replication of a virulent phage

A

Attachement, Penetration, Synthesis of nuclei acid and protein, Assembly and packaging, Release (lysis)

111
Q

bacteriophage that leaves by budding

A

M13

112
Q

bacteriophage act injects a phage and kills it

A

T4

113
Q

Packaging of DNA into T4 phage head

A

Packaging motor attaches to proceed. dsDNA moves into the head by a proton motive force. Scaffold proteins discarded. Other assembly steps. Packaging motor discarded.

114
Q

Temperate virus infects the cell and has two options

A

Lytic Cycle or Lysogeny

115
Q

viral genome integrates into host chromosome

A

lysogeny

116
Q

the virus when its genome exists as part of host genome

A

prophage

117
Q

host cell that harbors prophage

A

lysogen

118
Q

transfer of a specific region of bacterial chromosome to another bacterium via a virus; requires a lysogen to be moved incorrectly (rare)

A

specialized transduction

119
Q

represses genes involved in lysis; required in low concentrations to maintain lysogeny

A

CI (lambda repressor)

120
Q

represses genes involved in lysogeny; needed in greater amount than CI to force lambda into lytic cycle

A

Cro

121
Q

when lysogeny occurs, this can survive in a dormant host cell while virulent phages need active host cellular biosynthetic machinery

A

prophage

122
Q

When does Lysis occur?

A

if cell has DNA damage.
in nutrient-rich environments when many proteases are present in the host cell.
CI is destroyed by host protease -> Cro Protein accumulates -> lytic cycle begins

123
Q

How does a dsDNA virus make new dsDNA genomes and mRNA

A

The DNA of the viral genome enters the cell’s nucleus. New viral DNA is synthesized in the nucleus. Transcription produces mRNAs that are translated on cytoplasmic ribosomes into capsid and spike proteins. Capsid proteins enter the nucleus and combine with viral genomes to form new nucleocapsids. The viruses bud through eh nuclear membrane but do no acquire their final envelope and spikes until reaching a Golgi Complex.

124
Q

What is the structure of a typical retrovirus

A

RNA and enzymes surrounded by a core protein, surrounded by a core shell protein, surrounded by a lipid membrane bilayer with surface envelope proteins and transmembrane envelope proteins

125
Q

What is the genome of a retrovirus?

A

ssRNA

has a Gag, Pol, and Env regions

126
Q

makes structural proteins like protease

A

Gag

127
Q

makes reverse transcriptase and integrase (DNA endonuclease)

A

Pol

128
Q

makes envelope glycoproteins

A

Env

129
Q

Replication of a retrovirus

A
  1. Entry and uncoating of the retrovirus
  2. Reverse transcriptase (2 steps)
  3. Viral DNA enters nucleus and integrates into the host genome
  4. Transcription by host RNA polymerase forms viral mRNA and genome copies
  5. Translation of mRNA forms viral proteins; new nucleocapsids assembled and released by budding
130
Q

Where does the envelope come from that surrounds some viruses?

A

from host cytoplasmic membrane

131
Q

Destruction of host cells (ex. Pox viruses, Poliovirus)

A

Lytic

132
Q

enveloped viruses, new visions leave host by budding, cell does not die but remains infected and will produce visions indefinitely, influenza virus

A

Persistent

133
Q

virus is not actively replicating, formant; some integrate into host cell genome, but others don’t. Symptoms appear only when virus emerges from latency. (ex. Herpes simplex, Varicella-Zoster), herpesvirus, HIV

A

Latent

134
Q

Virus can transform from a norma cell to a cancer cell. Genetic changes that relate growth. (ex. Human Papillomavirus, Epstein-Barr, Cytomegalovirus)

A

Oncogenic

135
Q

genes who products are key components of signaling pathways that stimulate cell proliferation

A

oncogene normally found in cells

136
Q

normal gene that can be converted into an oncogene

A

Proto-oncogene (Oncogene normally found in cells)

137
Q

extra genes not needed for viral replication

A

oncogene found in oncogenic viruses

138
Q

misimpression of oncogene in the wrong cell type or prolonged expression can lead to

A

uncontrolled cell proliferation

139
Q

oncogene off ->

A

normal cell growth an division

140
Q

oncogene on ->

A

uncontrolled cell growth and division (tumor)

141
Q

protein particle, no nucleic acid; cause animal neurodegenerative diseases called transmissible spongiform encelphalpathies

A

prions

142
Q

Creutzfeldt-Jakob Disease

A

human disease caused by prions

143
Q

Bovine Spongiform Encephalopathy

A

mad cow disease, vCJD if transmitted to humans ….. caused by prions

144
Q

chronic wasting disease

A

disease in deer and elk caused by prions

145
Q

3 ways to get prion disease

A
  1. Infectious - ingestion of nervous tissue from infected animal
  2. Sporadic - having a mutation in the prnp DNA of a neuronal cell
  3. Inherited - mutation in germ line cells
146
Q

smallest known pathogens; circular, ssRNA; no protein; cause plant diseases

A

viroids

147
Q

Host defense from viruses in eukaryotes

A

immune system; RNA interface (RNAi)

148
Q

dsRNA nuclease

A

dicer

149
Q

short interfering RNA

A

siRNA

150
Q

RNA-induced silencing complex

A

RISC

151
Q

ssRNA nuclease

A

slicer

152
Q

the CRISPR antiviral defense system

A

DNA is transcribed into CRISPR RNA. Cutting of DNA by Cas proteins. Foreign sequence is recognized by CRISPR RNA. Can proteins cut and destroy foreign nucleic acid

153
Q

Host defense from viruses in prokaryotes

A

Restriction & Methylation

154
Q

using restriction endonuclease to cut viral dsDNA at specific sequences

A

Restriction defense in prokaryotes

155
Q

DNA methylates to methylate their own DNA to prevent cleavage by their own and viral restriction endonucleases

A

methylation defense in prokaryotes

156
Q

unaffected by restriction systems

A

ssDNA and RNA

157
Q

modify their DNA to avoid digestion by the host’s restrict endonuclease

A

dsDNA viruses

158
Q

disguising with sugar

A

glucosylation

159
Q

encode proteins to inhibit host restriction systems

A

viral genomes

160
Q

3 Anti-HIV drugs

A

Fusion inhibitors, Reverse transcriptase inhibitors, Protease inhibitors

161
Q

synthetic peptide that binds to an HIV membrane protein preventing the viral membrane from binding to the host cell membrane

A

fusion inhibitors

162
Q

bind HIV protease, preventing the protease fro processing viral polypeptides

A

protease inhibitors

Biology 2051 (7 decks)

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