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Lecture Exam 2 Flashcards

1
Q

Operon

A

Set of genes transcribed as a single mRNA, under the control of one promoter. Transcription/translation simultaneous.

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2
Q

Promoter

A

rRNA polymerase binding site, to do transcription. Produces mRNA.

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3
Q

Genes that code for proteins

A

Structural genes

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4
Q

Genes that regulate structural genes

A

Regulatory genes, make regulatory proteins

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5
Q

Genes that are always expressed (~75%)

A

Constitutive genes

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6
Q

Genes that are turned on/off as a cell’s needs change

A

Facultative genes. Inducible/repressible operons.

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7
Q

Inducible operons

A

Off by default. Activated by inducers. Lactose operon

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8
Q

Lactose operon

A

In absence of lactose operon is OFF. Repressor protein binds to operator, blocking RNA polymerase. In presence of lactose operon gets turned ON, RNA polymerase can work. Genes get turned back off when lactose levels go down

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9
Q

Repressible operon

A

ON by default. Must be turned off by co-repressors. Tryptophan operon.

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10
Q

Tryptophan operon

A

When tryp levels are low operon is ON, RNA polymerase is transcribing DNA. As long as levels are low operon will stay on. When tryp levels are high operon is turned off by allosteric activation.

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11
Q

Transfer of DNA between cells of the same generation

A

Horizontal gene transfer

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12
Q

3 Mechanisms of horizontal gene transfer

A
  1. Transformation
  2. Transduction
  3. Conjucation
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13
Q

Bacterial cell takes up naked DNA from environment

A

Transformation

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14
Q

Viral mistake, virus brings in new DNA

A

Transduction

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15
Q

DNA sharing via pilus, plasma DNA is shared

A

Conjugation

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16
Q

Property of cells that can naturally be transformed

A

Competency.

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17
Q

Manipulation of cells so they can be transformed

A

Artificial competency

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18
Q

Gene transfer via bacteriophage

A

Transduction

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19
Q

Generalized transduction

A

Lytic phage! Mistake made during the packaging of a random DNA fragment from the host bacterial chromosome into the bacteriophage.

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20
Q

Specialized transduction

A

Lysogenic phage! Mistake in the excision of a prophage from a host chromosome results in some bacterial DNA becoming attached to viral DNA.

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21
Q

Conjugation

A

Requires contact via sex pilus. F+ pilus holds to F-, each cell gets a copy of the other, allowing for exponential sharing of this plasmid. These plasmids often contain abs resistance genes.

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22
Q

Mutation

A

Change in the nucleotide (DNA) sequence of a gene. Can be repaired, sometimes.

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23
Q

Causes of mutation

A
  1. Spontaneous: unrepaired mistakes by replication enzymes. Cells 1 in 250, Viruses 1 in 250,000 bases replicated. Viruses mutate more rapidly.
  2. Induced: external forces increase the mutation rate, up to 1000x greater. Chemical or physical agents.
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24
Q

Mutagen

A

UV light = physical mutagen. Causes thymine dimers.

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25
Q

UV mutation repair (2)

A

Excision repair

Light repair - photo reactivation.

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26
Q

HA in influenza

A

Attachment to host cell. Primary target of vaccines.

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27
Q

Antigenic drift

A

Spontaneous mutations during RNA copying lead to minor changes in HAs. Increase in # of cases every 2 years.

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28
Q

Antigenic shift

A

Mistake during assembly with new combo of two segments. Very rare. ~10 years. 2009 H1N1 = pig, bird, human strains

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29
Q

Biotechnology

A

Use of biological system to make a product, does not require genetically engineered organisms.

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30
Q

Genetic engineering

A

Requires the use of biotechnology. Intentional modification of genomes for practical purposes. Change the genotype deliberately to change the phenotype. First example = insulin

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31
Q

DNA made from combining DNA from one or more sources into novel DNA molecules.

A

Recombinant DNA

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32
Q

Applications of biotechnology

A
  • Drugs/hormones
  • Vaccines
  • Genetic sequencing
  • Infection diagnosis
  • Industrial microbiology
  • Genomics
  • Microbiomes
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33
Q

Innate immunity

A

Not dependent on antigens. Immediate response upon exposure. No memory. First/second line of defense.

Use physical/chemical/mechanical barriers. Inflammation, fever. No specific target.

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34
Q

Acquired immunity

A

Dependent on antigens. Lag between exposure/response. Immunologic memory. Third line of defense

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35
Q

Normal microbiota

A

Beneficial bacteria/microorganisms found in/on the body. Promote overall health by providing vitamins to host, help stimulate immune system. Microbial antagonism. Produce conditions that do not promote growth of harmful bacteria.

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36
Q

Mechanical barriers for immunity

A

Peristalsis, urination, blinking, coughing, sneezing, vomiting

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37
Q

Physical barriers for immunity

A

Skin, mucus

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38
Q

Chemical barriers for immunity

A

pH, lysozyme (enzyme that breaks down peptidoglycan), lactoferrin, antimicrobial peptides, complement

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39
Q

Lysozyme

A

Enzyme that breaks down peptidoglycan, v effective agains G-pos bacteria. In tears, saliva, milk, mucus

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40
Q

Lactoferrin

A

Binds to iron, making it unavailable to microbes. Binds to LPS, leads to lysis.

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41
Q

Antimicrobial peptides

A

Small proteins, many are cations, attracted to negative charge of cells. Bind to cells and disrupt cell function.

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42
Q

Cathelicidins, Defensins

A

Macrophages, neutrophils

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43
Q

Dermicidins

A

Sweat glands

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44
Q

Complement

A

Set of >30 serum proteins.

  • Membrane attack complex: complement proteins form a ring in the membrane of a target cell, leading to lysis. Only for pathogens with a membrane.
  • Opsonization: increases likelihood of phagocytosis. Cell “tagged” for recognition.
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45
Q

Cellular barriers

A

Neutrophils

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46
Q

Neutrophil Extracellular Trap (NETs)

A

Type of programmed cell death. Neutrophil dies, spills out its DNA to trap cells, pathogens no longer can cause infection. Major component of pus

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47
Q

Phagocyte pathogen recognition

A
  • PAMPS (Pathogen-associated molecular patterns)
  • TLRs (toll-like receptors)
  • PRRs (pattern recognition receptors)
  • Flagellin, LPS, peptidoglycan, lipoteichoic acid
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48
Q

Inflammation

A

Nonspecific response to tissue damage. Dilation, increased permeability of blood vessels, triggered by mast cells, which release histamine. Red, swelling, heat, pain

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49
Q

Fever

A

Elevated body temp, increased overall metabolic rate

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50
Q

Antigens

A

Generate antibodies. Large, complex molecules

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51
Q

Exogenous antigen

A

Product/part of microbe in body

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52
Q

Endogenous antigen

A

Antigen from intracellular pathogen presented on surface of host cell. What our cells do when infected with a virus, telling others “come kill me!”

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53
Q

Epitope

A

The portion of an antigen structure that interacts with antibodies. Very specific. One molecule can have multiple epitopes.

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54
Q

Antibodies

A

Protein with 4 polypeptide chains, 2 heavy, 2 light. Human body can produce 10^23. Our cells interact with the constant region, variable region binds with epitopes.

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55
Q

Functions of antibodies

A
  1. Neutralization - before infection
  2. Opsonization
  3. Agglutination - clump together several cells to make phagocytosis more efficient
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56
Q

Helper T cells

A

activate other components of immunity

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57
Q

Cytotoxic T cells

A

Kill infected host cells

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58
Q

B cells

A

Strongest immune response is with B and T cells.

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59
Q

Plasma B cells

A

Produce large amounts of antibodies, only for a few days

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60
Q

Memory B cells

A

Point of vaccination! Can live as long as you do, immunologic memory.

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61
Q

Passive immunity

A

Receiving antibodies, no memory

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62
Q

Natural passive immunity

A

Immunoglobulins from placenta

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63
Q

Artificial passive immunity

A

Tetanus shot if infected with tetanus. Antivenin.

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64
Q

Natural active immunity

A

Have the disease, then you make the antibodies

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65
Q

Artificial active immunity

A

Vaccines

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66
Q

Vaccination

A

Intentional introduction of antigens to elicit an immune response. Development of memory cells.

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67
Q

Variolation

A

First form of vaccination. Scab infection -> mild case

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68
Q

4 types of vaccines

A
  1. Attenuated
  2. Inactivated
  3. Toxoid
  4. Subunit
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69
Q

Attenuated vaccine

A

Viable, but weakened pathogen. Can’t cause disease but can cause infection. Strong immune response, but must be refrigerated, remote possibility of disease causation.

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70
Q

Inactivated vaccine

A

Organism is dead. More stable and safer than attenuated, but immune response not as strong, requires boosters.

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71
Q

Toxoid vaccine

A

Produce antibodies to toxins. No exposure to pathogen, only to toxin, but does require boosters.

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72
Q

Subunit/conjugate vaccine

A

Purified antigens that elicit an immune response. Never exposed to pathogen, only its antigens (HPV), so can be given to people with weakened immune systems. Very expensive, immune response is less strong, can require multiple doses

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73
Q

When enough members of a population are immunized to protect those who lack immunity

A

Herd immunity

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74
Q

Immune disorders

A
  1. Hypersensitivities: allergies
  2. Autoimmune diseases: lupus, MS, rheumatoid arth
  3. Immunodeficiencies: AIDS, SCID
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75
Q

Disease

A

Altered or impaired body function

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76
Q

Infection

A

When an organism evades the body’s external defenses, multiplies, becomes established in the body

77
Q

Signs

A

Objective manifestations that can be observed by others

78
Q

Syptoms

A

Subjective characteristics of disease felt by the pt

79
Q

Infectious disease

A

Illness due to a microbial pathogen

80
Q

Communicable disease

A

Infectious disease that is transmitted from person to person

81
Q

Contagious disease

A

Highly communicable disease

82
Q

Non-communicable disease

A

Infectious disease that is not typically transmitted person to person. (diabetes, heart disease)

83
Q

Zoonotic disease

A

Infectious disease acquired from an animal.

84
Q

Pathogen

A

Organism that causes infectious disease

85
Q

Primary (true) pathogen

A

Organism that causes disease in an otherwise healthy individual

86
Q

Opportunistic pathogen

A

Organism that causes disease in an immunocompromised host. Often resident microbiota

87
Q

Iatrogenic disease

A

Infection duet o a medical procedure/action fo a health care provider

88
Q

Nosocomial

A

Infection acquired in a hospital setting

89
Q

HAI

A

Healthcare associated infection

90
Q

Periods of disease

A
  1. Incubation (exposed, no signs/symptoms)
  2. Prodromal (effects slightly noticeable)
  3. Illness period
  4. Decline period
  5. Convalescence period

*Contagious times are pathogen specific!

91
Q

Koch’s postulates

A

Robert Koch 1850s. (Germ theory of disease)

  1. Organism must be found in all sick individuals and not in healthy indivs
  2. Microbe must be isolated and grown
  3. Microbe should cause disease when inoculate into healthy indivs
  4. Microbe must be re-isolated from newly diseased host, re-identified
92
Q

Pathogenicity

A

Ability of an organism to cause disease

93
Q

Virulence

A

Degree to which an organism can cause disease

94
Q

Infectious Dose (ID50)

A

of organisms necessary to cause disease

95
Q

Stages of pathogenesis

A
  1. Exposure (portal of entry)
  2. Attachment to host
  3. Invasion of host/Evasion of host defenses
  4. Infection of host
  5. Transmission (portal of exit)
96
Q

Virulence factors of pathogens

A

Adhesion via fimbriae (gonorrhea, shigella, E coli), pili, suckers, hooks (giardiasis, taeniasis), barbs, spikes (influenza)

97
Q

Virulence factors of invasion

A

Mucinase, collagenase, keratinase, staphylokinase

98
Q

Mucinase

A

Exoenzyme that digests mucus. Invasion.

99
Q

Collagenase

A

Exoenzyme that breaks down connective tissue. Invasion

100
Q

Keratinase

A

Exoenzyme that breaks down keratin of skin. Invasion

101
Q

Staphylokinase

A

Exoenzyme that breaks down blood clots. Invasion

102
Q

Virulence factors of evasion

A

Leukocidins, capsules, coagulase/kinase, DNAse, listeriolysin O, phospholipase

103
Q

Capsules

A

Prevent adherence of phagocytes/opsonization. Evasion

104
Q

Coagulase/kinase

A

Exoenzymes that form blood clots around cells to hid from phagocytes. S. Aureus. Evasion.

105
Q

DNAse

A

Exoenzyme that dissolves NETs. Evasion

106
Q

Listeriolysin O, Phospholipase

A

Escape phagosome before digestion. Evasion

107
Q

Virulence factors of toxins

A

Molecules that harm tissues or trigger host immune responses.

108
Q

Endotoxin

A

LPS of a G-neg bacteria. Causes an intense and overwhelming immune response, leading to endotoxic shock.

109
Q

Exotoxins (4 types)

A

Secreted by G-neg, G-pos, fungi.

  1. Neurotoxins
  2. Cytotoxins
  3. Enterotoxins
  4. Mycotoxins
110
Q

Neurotoxins

A
  • Botulism toxin: excitatory signal blocked, flaccid paralysis.
  • Tetanus toxin: inhibitory signal blocked, spasmodic paralysis.
111
Q

Cytotoxins

A
  • Alpha toxin: phospholipase
  • Diptheria toxin: blocks protein synthesis, leading to cell death
  • Hemolysins: lysis of RBCs to release iron/other nutrients.
112
Q

Enterotoxins - infections

A
  • Cholera toxin: disrupts osmolarity, leads to severe diarrhea
  • Shiga toxin: kills epithelial cells of intestines, leading to dystenary
113
Q

Enterotoxins - intoxication

A

Staphylococcal enterotoxin: heat stable, common cause of food poisoning. Vomiting. S aureus.

114
Q

Mycotoxins

A
  • Aflatoxin: highly mutagenic and carcinogenic. Acute hepatic necrosis.
  • Ergot alkaloids: hallucinatory. Burning, itching skin. Claviceps purpurea.
115
Q

Antimicrobial resistance

A

Decreased susceptibility of an organism to a drug. Acquired through new mutations of chromosomal genes, or through acquisition of plasmids/other DNA that harbors resistance genes.

116
Q

Problem of resistance

A

CDC estimates in 2013 2 million illnesses, 2-3 deaths due to antimicrobial resistance.

117
Q

Mechanisms of antimicrobial resistance

A
  • Production of enzymes that destroy drugs
  • Alteration of drug target
  • After metabolic pathway: resistance to sulfa drugs
  • Pump antimicrobial drug out of the cell. Active transport.
  • Formation of biofilm that drugs cannot penetrate
118
Q

Multiple resistance

A

Pathogen carries multiple genes that confer resistance to multiple drugs. Super-bugs

119
Q

Cross resistance

A

Single mechanism that provides resistance to multiple drugs. Efflux pumps

120
Q

Efficacy

A

Effectiveness of an antimicrobial against its intended target organism.

  • Disk diffusion assay
  • MIC serial dilution (rapid, expensive, machine. Tells concentrations)
  • E tests
121
Q

Antibiogram

A

Table that outlines susceptibility of tested isolates. Used in clinical setting to aid in decision on what drugs to prescribe.

122
Q

Preventing resistance

A

Use antimicrobials only when necessary. Use drugs for entire time prescribed. Reduce use in agricultural settings. Combination therapy. Development of new vaccines/new antimicrobials.

123
Q

Options for new antimicrobials

A
  • Alter existing drugs
  • Find drugs that inactivate the resistance mechanism
  • Research new targets in pathogens
  • Antimicrobial peptides
  • Use of bacteriophage
124
Q

Bacteriophage therapy

A
  • Specific to bacteria, will not infect humans
  • Multiple strains for a given bacterium already isolated
  • Mutate on their own, resistance circumvented
  • Oral application, eye treatment, wound dressings
125
Q

John Snow

A

1854 London cholera outbreak. Tracked incidence of disease vs water sources.

126
Q

Florence Nightingale

A
  1. Crimean war. Kept records on morbidity/mortality of soldiers.
127
Q

Epidemiology

A

Study of disease transmission

128
Q

Etiology

A

Study of causes of disease

129
Q

Morbidity

A

Presence of disease

130
Q

Mortality

A

Death due to disease

131
Q

Prevalence

A

Total # of cases of disease in a population in a given time period

132
Q

Incidence

A

Total # of new cases of disease in a population in a given time period

133
Q

Patterns of incident (4)

A
  1. Sporadic
  2. Endemic
  3. Epidemic
  4. Pandemic
134
Q

Sporadic disease

A

Very small #s, occurs occasionally and unexpectedly. Prevalence and incidence usually zero. Tetanus, plague, rabies

135
Q

Endemic disease

A

Constant low #s of disease. Prevalence/incidence never zero. Salmonella.

136
Q

Epidemic disease

A

Greater than expected #s in a geographical region. Increased incidence and prevalence. Influenza, salmonella.

137
Q

Pandemic disease

A

Widespread/worldwide epidemic. Yellow fever, cholera, TB

138
Q

Spread of epidemics (2)

A
  1. Common source: single, shared source. Foodborne. Shorter.

2. Propagated: spread person-person. Harder to stop. Longer duration.

139
Q

Reservoirs and carriers

A

Where pathogens are maintained in nature. Nonliving reservoirs = soil, water. Living reservoirs= humans (carriers), animals.

140
Q

Carriers

A

Humans who unknowingly shelter pathogens and spread them to others.

141
Q

Asymptomatic carrier

A

Person who is infected but has no symptoms

142
Q

Passive carrier

A

Person who is contaminated, but no infection. Often health care worker.

143
Q

Contact transmission (4)

A

Direct/horizontal contact: person to person
Vertical: birth canal
Droplet: respiratory liquids
Indirect: via inanimate object called fomite.

144
Q

Vehicle transmission

A

Pathogen enters body by consumption/intake of it in water, milk, food etc. Sometimes air.

145
Q

Biological vectors

A

Arthropod harbors pathogen within its body. Ticks, mosquitoes, please. Lyme, rickets, plague, malaria

146
Q

Mechanical vectors

A

Pathogen is found on surface of arthropod. Flies, cockroaches. Dysentery, salmonella, cholera.

147
Q

endogenous HAI

A

Infectious agent from microbiota of a pt

148
Q

exogenous HAI

A

Infection introduced in medical setting

149
Q

Emerging infectious disease

A

Diseases new to humans or increasing in prevalence and geographic range. Reemerging diseases reappear after a decline.

150
Q

Louis Pasteur

A
  1. Noted that heat treatment prevented microbial contamination in wine
151
Q

Joseph Lister

A
  1. Used carbolic acid (phenol) to treat dressings, antiseptics prior to surgery
152
Q

-static

A

Inhibition of growth of target organisms

153
Q

Disinfection

A

A process to destroy vegetative pathogens on inanimate objects. Reduces # of bacteria

154
Q

Sanitization

A

Disinfection to meet public health standards.

155
Q

Sterilization

A

A process that destroys all viable microbes, including endospores

156
Q

Antisepsis

A

Destroy vegetative pathogens on living tissue. Reduces # of bacteria

157
Q

Degerming

A

Mechanical removal of microbes from skin. (Hand washing)

158
Q

Physical methods of control (4)

A

Temperature
Radiation
Filtration
Desiccation

159
Q

Temperature (5)

A
  1. Incineration: dry heat. Long time, high heat
  2. Autoclave: wet heat. More efficient
  3. Pasteurization: kills vegetative pathogens, reduces spoilage organisms. Milder than autoclaving.
  4. Refrigeration: slows growth except in psychrophilic microbes
  5. Freezing: decreases microbial metabolism, limits amount of available water
160
Q

Radiation (2)

A

Nonionizing: UV light, does not kill endospores. Disinfection.

Ionizing: gamma rays and x rays, break covalent bonds in DNA. Good penetrating power, useful for packaged, heat sensitive items. Sterilization.

161
Q

Filtration

A

Physical barrier to trap microbes. Used for heat-sensitive materials and high volumes. Can be used to sterilize if pores are small enough

162
Q

Desiccation

A

Lowers water activity

163
Q

Disinfect…

A

…inanimate objects

164
Q

Antiseptics used on…

A

…animate objects

165
Q

Phenolics

A

Based on phenol. Hand soap, cleaners

166
Q

Alcohols

A

70% most effective. Antiseptic and disinfectant.

167
Q

Halogens

A

React w/non-target molecules, inactivated by sunlight. Iodine/betadine, chlorine/bleach, fluoride

168
Q

Heavy Metals

A

Metal ions bind of proteins and other molecules, disrupting function. Topical!

169
Q

Quats

A

Quaternary ammonium compounds. Antiseptics and disinfectants, easily inactivated by soaps

170
Q

Bisbiguanides

A

Surgical prep, hand washing. Chlorhexidine, alexidine, hibiclens

171
Q

Soaps/detergents

A

Disrupt binding of bacteria to surfaces. Degerming. Handwashing.

172
Q

Paul Ehrlich and Sahachiro Hata

A
  1. “Magic bullet” chemical to target microorganisms but not us
173
Q

Alexander Flemming

A
  1. Penicillin.
174
Q

Antibiotic

A

Naturally occurring antibacterial

175
Q

Spectrum of activity

A

Types of #s of organisms that a drug is active on

176
Q

Superinfection

A

Consequence of broad-spectrum drugs. Secondary infection of opportunistic pathogen due to disruption of normal microbiota. C. Dificile.

177
Q

Selective toxicity

A

Drug is more toxic to target organisms than humans (host) due to differences in cellular physiology and metabolism. The greater the cellular difference the better the selective toxicity. # antibacterials > #antifungals > # antivirals

178
Q

Therapeutic index

A

Ratio of the amount of drug that is toxic to humans to the amount that is toxic to target cell.

TI= Amt of drug toxic to human/amt toxic to target

Want large number over small number

179
Q

Drug toxicity

A

Property of drugs that causes damage to human cells and tissues. Usually to kidneys, liver, nerves.

180
Q

Mode of action (6)

A

How an antimicrobial works against a target organism.

  1. Cell wall synthesis
  2. Protein synthesis
  3. Cell membrane structure
  4. Metabolic pathways
  5. Nucleic acid synthesis
  6. Host attachment/entry/exit
181
Q

Cell wall - antibacterials (5)

A 
Beta-lactams: penicillin, ampicillin
Glycopeptides: Vancomycin
Antibacterial peptide: Bacitracin
Carbapenems: Imipenem
Echinocandins
182
Q

Protein synthesis - antibacterials (4)

A

Chloramphenicol
Aminoglycosides: streptomycin, neomycin
Tetracyclines: doxy
Macrolides: azithromycin, erythromycin

183
Q

Cytoplasmic membrane disruption - antibacterials (1)

A

Polymixin B, Polymixin E

184
Q

Inhibition of metabolic pathways - antibacterials (3)

A

Folic acid:

  • sulfonamides: sulfamethoxazole
  • trimethoprim

Mycolic acid:
- isoniazid

185
Q

Inhibition of nucleic acid synthesis

A

Fluoroquionolones: cipro, levofloxacin

186
Q

Antifungal mode of action

A

Disruption of cytoplasmic membranes.

  • Azoles: fluconazole target ergosterol synthesis
  • Polyenes: amphotericin B target ergosterol binding. Only used in severe cases.
187
Q

Block attachment/entry/exit - Antivirals

A

Tamiflu, zanamivir, oseltamavir

188
Q

Inhibition of nucleic acid synthesis - Antivirals

A

Acyclovir, ribavirin

189
Q

Anti retroviral therapy

A
  • Protease inhibitors: Ritonavir
  • Reverse transcriptase inhibitors: Etravirine, tenofovir
  • Integrase inhibitors - Raltegravir. Blocks insertion of viral DNA into chromosome

Microbiology (7 decks)

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