Exam 2 Prep Flashcards

1
Q

Describe the relationship between “contamination”, “infection”, “disease”, ‘pathogenicity”, and “virulence”

A

“Contamination” is simply the presence of microbes in/on the body. Some microbes are capable of causing disease/harm and are known as pathogens. This ability to cause disease is known as “pathogenicity”.

When these pathogens successfully invade/enter the host body, this is known as “infection”. Once inside, if the pathogen alters or interferes with the normal body functions, “disease” results.

Pathogenicity does not guarantee a resulting disease or injection. “Virulence” is the degree of pathogenicity/relative ability of a pathogen to infect a host and cause disease.

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2
Q

Signs vs. symptoms? Name some examples.

A

Signs: objective manifestations of disease that are observable or measurable by others.

  • Fever (temperature)
  • Vomiting
  • Swelling/rash
  • WBC count
  • Tachycardia/bradycardia (increased/decreased heart rate)

Symptoms: subjective characteristics felt only by the person with the disease

  • Pain
  • Nausea
  • Headache
  • Itching
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3
Q

Why can signs and symptoms be helpful?

A

A group of signs and symptoms (known as a “syndrome”) can characterize a disease or abnormal condition and be useful in diagnosis.

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4
Q

Do infections and disease always present signs and symptoms?

A

No. Infections/disease can show no symptoms but still have signs. “Asymptomatic/subclinical” cases show no symptoms (i.e. headache/pain) but have signs (i.e. patient with leukocytosis has a sign, increased WBC count, but feels completely normal).

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5
Q

Define: etiology and epidemiology

A

Etiology - study of the cause of disease

Epidemiology - study of the occurrence, distribution, and spread of disease

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6
Q

What are some types of relationships between microbes and hosts?

What relationship do humans have with most of their microbiota?

A

Mutualism - both members benefit
Commensalism - one member benefits while the other is not affected
Parasitism - one member benefits at the expense/harm of the other

Humans/microbiota are mostly mutualistic in nature.

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7
Q

Describe the “human microbiome/normal flora”.

A

It is the collection of all normal microbes that live in and on a human and are important to our health and functioning.

“Resident” microbiota remain part of a human for most of their life and typically live on the skin, in mucous membranes, and GI or respiratory tracts. They normally do not cause disease (dysbiosis can influence disease)

“Transient” microbiota are only found on the body for short periods of time (hours, days, months) and found in the same area of resident microbes.

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8
Q

Describe “microbial antagonism”

A

Normal flora reduce the ability of arriving pathogens to grow in the body. This is due to their normal activities such as:

  • consuming nutrients
  • taking up space
  • releasing toxic waste
  • providing vitamins to promote health
  • stimulation of body’s immune system
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9
Q

Name some discoveries from the “Human Microbiome Project”

A
  • Microbes were found in locations previously thought to be sterile
  • 100 million viruses per gram of human feces
  • Healthy people normally harbor low numbers of potential pathogens
  • Intestinal biota influences overall health
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10
Q

Some human flora locations?

A

Main locations:

  • Skin
  • Mucous membranes
  • Upper respiratory tract
  • GI tract
  • Mouth
  • Genitals
  • Eye lids/membrane

Possible flora or their DNA locations:

  • Lungs (lower resp. tract)
  • Bladder and urine
  • Breasts and milk
  • Amniotic fluid and fetus

Possible DNA (of flora) locations:

  • Brain
  • Bloodstream
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11
Q

Unique facts about normal resident biota locations?

don’t need to memorize, this list not all-inclusive

A

Upper resp. tract: nose is cooler than the rest of resp. system

Upper GI tract: teeth and cheeks

Lower GI tract: mostly strict anaerobes found here

Reproductive systems: microbiota changes as acidity changes during menstrual cycle. Flow of urine prevents colonization of bladder/urethra.

Eyes: Tears wash away most microbiota

Skin: Mostly live on outer dead layers of skin.

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12
Q

When do we acquire normal microbiota?

A

During the birthing process. The birthing method also affects the ratio of microbiota a baby acquires.

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13
Q

Where can babies get their microbiome? (sources)

A

Utero, birth, milk, ,caregivers, environment

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14
Q

Factors that increase susceptibility to infection?

A
  • Weakened host defenses/immunocompromised
  • Old age/extreme youth
  • Surgery/organ transplants
  • Underlying disease
  • Chemotherapy
  • Physical and mental stress
  • Pregnancy
  • Other infections
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15
Q

Describe opportunistic pathogens

A

Normal microbiota that cause disease under certain conditions:

  • When normal microbiota are introduced to unusual site in body
  • Under immune suppression
  • Normal microbiota are decreased or changed in population

Polymicrobial infections - contributions from more than one microbe

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16
Q

What is virulence of a microbe determined by?

A

It’s ability to:

  • Establish itself in a host
  • Cause damage
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17
Q

Describe virulence factors

A

Characteristics or structures that contribute to the ability of a pathogen to establish itself in a host and cause disease

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18
Q

Name some examples of virulence factors

A
  • Adhesion factors (structures or molecules)
  • Biofilms
  • Extracellular enzymes
  • Toxins
  • Antiphagocytic factors
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19
Q

Describe the 5 steps in the Microbial Disease Process

A
  1. ) Find portal of entry
    - Respiratory tract, skin/wounds, etc.
  2. ) Attach firmly and negotiate the microbiome
    - Adhesion factors
  3. ) Survive host defenses
    - Avoid phagocytosis, death, hide from immune system
  4. ) Cause damage
    - Damage due to toxins, enzymes, induce extreme response, epigenetic changes
  5. ) Exit host
    - Usually through portal of entry, fluids, feces
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20
Q

Name some portals of entry

A

Skin:

  • Thick salty layers of dry, dead cells
  • Cuts/wounds/hair follicles/sweat glands

Mucous membrane:

  • Thin, moist, warm, living cell layers
  • Respiratory tract, conjunctiva, GI tract

Parenteral route:
- Normal tracts are circumvented (i.e. nails, thorns, needles, bites)

Placenta:
- Less than 2% of pregnancies

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21
Q

Exogenous vs. Endogenous microbes

A

Exogenous: originates from source outside the body (i.e. environment, person, animal)

Endogenous: already exists inside or on the body

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22
Q

What is an inoculating dose?

A

The minimum number of microbes needed to cause an infection to proceed. The smaller the number, the higher virulence.

(“ID50: 20” means 20 cells would result in infection in 50% of healthy adults)

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23
Q

Characteristics of adhesion?

A
  • Glycoproteins/lipoproteins (called ligands) can bind to complementary receptors (usually glycoproteins) on host cells. These ligands can be found on fimbriae, glycocalyces in bacteria or envelopes/capsids in viruses (AKA spikes).
  • Structures such as fimbriae, capsules, hooks(eukaryotes) can also adhere.
  • Adhesion is necessary to cause disease because the body has mechanisms to flush microbes such as tears.
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24
Q

What are phagocytes?

A

Cells that engulf and destroy pathogens with enzymes and chemicals.

  • An example is WBCs (AKA macrophages)
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25
Q

How do pathogens survive host defenses?

A
  • Virulence factors (help avoid phagocytes/macrophages)
  • Ability to kill phagocytes
  • Extracellular layer (capsule) makes it difficult to engulf
  • Adaption to survive within phagocyte after being engulfed
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26
Q

What are some antiphagocytic factors?

A

Capsule - not recognized as foreign and is slippery making it difficult to engulf

Chemicals - prevent fusion of lysosome with phagocytic vesicles, allowing bacteria to survive inside phagocytes.

Leukocidins - chemicals capable of killing WBCs/macrophages

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27
Q

What ways can pathogens cause damage?

A
  • Enzymes and toxins
  • Inducing excessive/inappropriate host defense response
  • Epigenetic changes
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28
Q

Examples of damage causing enzymes?

A

Hyaluronidase - breaks down hyaluronic acid, the “glue” that holds animal cells together

Collagenase - breaks down collagen, the body’s chief structural protein

Coagulase - causes blood to clot, provides pathogens a “hiding place” within clots

Kinases - digest blood clots, releasing “hidden” or trapped pathogens to cause damage

Keratinase/Mucinase - digest keratin/mucus lining of GI tract, respectively

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29
Q

How to toxins cause damage?

A
  • Harm tissues or trigger host immune responses that cause damage
  • Toxemia refers to presence of toxins in bloodstream
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30
Q

How to extracellular enzymes cause damage?

A

Most dissolve/digest structural chemicals in the host

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31
Q

Types/categories of toxins?

A

Exotoxins - secreted by microbes to destroy host cells or interfere with metabolism

Endotoxins - the lipid A portion of membrane’s lipopolysaccharide (gram negative cell walls) that is released when these cells die/divide/are digested

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32
Q

How do endotoxins affect the host?

A

Dead gram-negative bacteria release lipid A which cause systemic damage - cause fever, inflammation, diarrhea, hemorrhaging, shock, blood coagulation

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33
Q

How to exotoxins affect the host?

A

Cytotoxins - kill host cells

Neurotoxins - interfere with nerve cell function

Enterotoxins - affect lining of GI tract

Nephrotoxins - damage kidneys

Hemotoxins - lyse RBCs

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34
Q

Some characteristics of exotoxins?

A
  • Toxic in small amounts
  • Specific to cell type
  • Composed of small proteins
  • Stimulates antitoxins
  • Usually no fever
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35
Q

Some characteristics of endotoxins?

A
  • Toxic in high doses
  • Systemic reaction (fever, inflammation)
  • Composed of lipid A
  • Doesn’t stimulate antitoxins
  • Gram-negative only sources
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36
Q

Classify infectious diseases/infections

A

Local infection - limited to small area of body

Systemic infection - throughout the body

Focal infection - begins as local infection and spreads through body

Primary infection - acute infection that causes initial illness

Secondary infection - opportunistic infection arises due to primary infection

Subclinical disease - no noticeable symptoms or signs

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37
Q

Types of infections in the blood

A

Leukocytosis - increase in WBC levels

Leukopenia - decrease in WBC levels (ex. HIV)

Septicemia - microorganisms are multiplying in blood and present in large numbers

Bacteremia/viremia - bacteria/viruses are present in blood but not multiplying

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38
Q

How do pathogens exit the body?

A

Often leave in the same way they entered or leave in materials the body releases:

  • Secretions: tears, saliva, respiratory droplets, earwax
  • Excretions: feces, urine
  • Blood: arthropod bites, needles, wounds
  • Milk, semen
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39
Q

What are the 5 stages of infection?

A
  1. ) Incubation period - time between infection and first signs/symptoms
  2. ) Prodromal period - short time of mild symptoms, pathogens are reproducing
  3. ) Illness - most severe stage of disease, pathogens are highest in number
  4. ) Decline - immune system responds, body returning to normal state
  5. ) Convalescence - patient recovers and tissues are repaired. Returns to normal
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40
Q

How is the incubation period influenced?

A

Host resistance, degree of virulence, distance between target organ and portal of entry

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41
Q

What is the acute phase of infection?

A

Can occur after prodromal period:

  • pathogen/agent multiplies at high levels
  • greatest virulence, becomes well established
  • fever occurs
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42
Q

What is a continuation phase in an infection?

A

Only some chronic infections:

- lingers for months or years

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43
Q

What are the reservoirs of infectious diseases?

A

Most pathogens can’t survive for long outside of host:

Animal reservoirs

Human carriers

Nonliving reservoirs

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44
Q

What are diseases that spread from animals to humans?

A

Zoonoses

Acquired through:

  • direct contact
  • consumption
  • arthropods
45
Q

Characteristics of human carriers

A

Humans with active disease are reservoirs for other humans

Can be asymptomatic - show no apparent symptoms

Carriers - incubate pathogen, some develop illness but others do not

46
Q

Transmission of pathogen/agents

A

Communicable - can be spread from one host to another

Contagious - very easily spread from one host to another

Noncommunicable - arises from outside of host, or can be opportunistic pathogen

47
Q

Communicable disease transmission

A

Contact transmission:

  • Direct: person to person
  • Indirect: spread through fomite (needle/toothbrush/tissue/toys/medical equipment, etc.)
  • Droplet: coughing/sneezing (occurring less than 1 meter)

Vehicle transmission:

  • Airborne: droplet or dust more than 1 meter via aerosol
  • Waterborne: fecal-oral usually
  • Foodborne
  • Bodily fluid

Vector transmission:

  • Biological vector: transmit/host for pathogen (ex. biting arthropods like mosquito)
  • Mechanical vector: transmit pathogens present on body like feet (ex. flies)
48
Q

Factors associated with healthcare-associated infections (AKA nosocomial infections)

A
  • Immunocompromised patients
  • Collection point/presence of many pathogens
  • Acquired from fomites, medical equipment, other patients, medical personnel, food/water
49
Q

Most common HAIs

A
  • Pneumonia
  • Surgical site infections
  • GI illness
  • UTIs
50
Q

How to control HAIs

A
  • Hand washing/disinfection techniques
  • Infection control officers implement proper procedures
  • Training for personnel
  • Universal standards and precautions
51
Q

Describe quorum sensing in biofilms

A
  • Microbes secrete quorum sensing molecules (AKA auto-inducers)
  • These molecules bind to receptors in other microbes.
  • As density increases, more molecules are secreted and available to bind.
  • Results in change in gene expression and/or damage
52
Q

Why is quorum sensing important to biofilms?

A

Quorum sensing allows individual bacteria within colonies to coordinate and carry out colony-wide functions such as: sporulation, bioluminescence, virulence, conjugation, competence and biofilm formation

53
Q

Incidence vs. Prevalence (in epidemiology)

A

Incidence - number of new cases in given area

Prevalence - total number of cases in area

54
Q

Occurrence of disease terms

A

Endemic: constantly present in area or population

Sporadic: occurs occasionally in area or population

Epidemic: higher than normal number of cases in area (one continent)

Pandemic: higher than normal number of cases on more than one continent

55
Q

What are some differences between the genetic material in eukaryotes vs. prokaryotes?

A

Prokaryotes:

  • DNA is typically circular
  • Usually one chromosome (haploid)
  • Plasmids - non-essential DNA pieces that can replicate independently (can produce secondary metabolites for survivability)
  • In nucleoid region with cytosol
  • Smaller (less bp in length)

Eukaryotes:

  • DNA is linear
  • Usually in pairs (diploid)
  • In the nucleus
  • Presence of histones
  • Longer (more bp in length)

Viruses:

  • DNA or RNA
  • Within capsid
56
Q

What is the difference between a gene and genome?

A

A “gene” is a specific sequence of nucleotides with codes for a product (such as a protein)

Genome refers to the sum of ALL genetic material in an organism

Genetics is the study of inheritance and inheritable traits in an organism’s genetic material

57
Q

What are the three categories of genes?

A
  • Structural genes: code for proteins (building blocks, enzymes)
  • Genes that code for ribosomal RNA (rRNA)
  • Regulatory genes: control gene expression (which proteins are made under which conditions)
58
Q

What is meant by “gene expression”?

A
  • Transcription and translation processes with the end result a polypeptide

(Also known as “central dogma of biology” and the “flow of information”)

59
Q

When you hear the word “genotype” what should you think of?

A

Instructions for proteins/enzymes; DNA; genetic code determines phenotype

60
Q

When you hear the word “phenotype” what should you think of?

A

Expresses the trait/characteristic; protein; RNA

61
Q

Structure of nucleic acids (NA)?

A

NA’s monomer: nucleotides
- Phosphate
- 5-carbon (pentose) sugar: deoxyribose in DNA, ribose in RNA
- Nitrogenous base
(Adenine paired with Thymine; Guanine paired with Cytosine….in RNA Thymine is replaced by Uracil)

62
Q

Which nitrogenous bases are purine? Which are pyrimidines?

A

Purines (two ring structure):

  • Adenine
  • Guanine

Pyrimidines (one ring structure):

  • Thymine
  • Cytosine
  • Uracil
63
Q

Describe the bonds between the nucleotides

A

Covalent bonds link the phosphate (5’) to the sugar (3’) of another nucleotide.

(This bond is also referred to as a glycosidic bond)

64
Q

Describe the backbone structure of nucleic acids

A

Polymerization - the alternating 5’ to 3’ covalent bonds create the linear structure of DNA.

When two DNA strands’ nitrogenous bases are linked together by hydrogen bonds, this forms an anti-parallel double helix (opposite orientation - 5’ matched with 3’ on both ends)

65
Q

Describe complementary base pairs (bp) in nucleic acids

A

Since DNA is usually double stranded, each nitrogenous base specifically match with another specific nitrogenous base:

  • Adenine forms double hydrogen bond with Thymine
  • Guanine forms triple hydrogen bond with Cytosine

(During transcription, Uracil takes the place of Thymine in the mRNA)

66
Q

What are plasmids and what are they made of?

A
  • Plasmids are non-essential circular pieces of DNA found mostly in prokaryotes. They can replication independently and usually code for a secondary metabolite that increases chances of survival.
  • They are also made up of nucleotide monomers, just like chromosomes, but are smaller and usually 1-20% the size of the normal chromosome.
67
Q

What the 4 types of plasmids?

A
  • Fertility (F) plasmids: instructions/codes for conjugation via pili
  • Resistance factors: resistant to antimicrobial agent(s)
  • Bacteriocin plasmids: codes for protein toxins that kill other bacteria without the plasmid
  • Virulence plasmids: codes for enzymes/toxins enabling pathogenicity
68
Q

What enables RNA viruses to have their RNA converted to DNA?

A

The enzyme, reverse transcriptase

69
Q

Where does DNA replication begin? Where does it stop?

A

It starts:
- At the ‘origin’ of replication

It ends:
- Where converging replication forks meet (‘termination’ of replication)

70
Q

What enzymes assist in DNA replication and what are their functions?

A

Helicase - unwinds the DNA/breaks about the hydrogen bonds between complementary bp

Primase - adds the RNA primer which provides the 3’ start point for DNA polymerase to begin

DNA polymerase - synthesizes DNA by adding free nucleotides to the 3’ end of the daughter DNA strand

Ligase - connects sugar-phosphate backbones of the Okazaki fragments

71
Q

Explain semi-conservative, bi-directional, and semi-discontinuous in DNA replication

A

Semi-conservative: each new DNA molecule will consist of an original template/parental strand as well as a daughter strand

Bi-directional: starts at origin and replicates in opposing directions. This creates 2 replication forks, as well as a leading strand and a lagging strand

Semi-discontinuous: the leading strand is created continuously towards the replication fork while the lagging strand is synthesized away from the replication fork in segments (Okazaki fragments)

72
Q

What are some types of RNA can be transcribed from DNA?

A

Messenger RNA - carries genetic information from chromosomes to ribosomes

Ribosomal RNA - combines with ribosomal proteins to form ribosomes

Transfer RNA - deliver amino acids to ribosomes based on mRNA’s codons

RNA primer - provided 3’ start point for DNA polymerase during replication

73
Q

Where does transcription begin? Where does it end?

A

It beings:

  • At a specific DNA sequence called a “promoter”.
  • RNA polymerase contains “sigma factors” which are required to recognize these promoters.
  • These promoters are usually located between 10-35 nucleotides away from where transcription actually begins

It ends:
- At a terminator sequence

74
Q

In what ways is RNA polymerase different than DNA polymerase?

A

RNA polymerase unwinds DNA by itself, it does not need helicase

RNA polymerase does not need a primer (it uses sigma factors to recognize promoter)

RNA polymerase adds Uracil instead of Thymine nucleotides

75
Q

How do sigma factors help regulate gene expression?

A

Different sigma factors recognize different promoter regions. In other words, sigma factors can help maintain which proteins are eventually synthesized at certain times.

This is important to ensure energy is not wasted unnecessarily

76
Q

What are some differences between prokaryotic and eukaryotic translation?

A

Prokaryotes:

  • Translation can occur because transcription ends (both happen in cytosol)
  • One mRNA often codes for several different proteins

Eukaryotes:

  • Translation begins after completion of transcription (mRNA must be sent to cytosol from nucleus first)
  • Typically codes for single protein
77
Q

Where does translation start? Where does it stop?

A

It starts:
- The Shine-Dalgarno sequence (ribosome binding site) used to align the ribosome’s “P-site” with start codon to begin

It ends:
- Release factors recognize stop codons resulting in the release the of polypeptide

78
Q

Why is regulating gene expression important?

A

Gene expression regulation ensures that non-essential polypeptides are only created in response to a change in the environment because if these polypeptides are always being created but not needed at the time, this is a massive waste of a cell’s energy

79
Q

What do prokaryotes use to regulate gene expression?

A

Operons: Clusters/blocks of genes that code for proteins needed for a specific function. Operons consist of: a promoter, operator, and set of genes.

For example, all of the genes needed to use lactose as an energy source are coded next to each other in an operon. If lactose is not available, the operon is not needed because there is no lactose to be used as energy.

Basically, all of the genes in an operon will be needed at the same time, or none will be needed at all.

80
Q

What are the two types of operons?

A

Inducible operons:

  • Inactive and must be “turned on” by inducers
  • “On” when substrate is present (catabolism)

Repressible operons:

  • Typically always active and must be “turned off” by repressors
  • “Off” when product is synthesized (anabolism)
81
Q

What is the difference between catabolism and anabolism?

A
  • Catabolism is where complex and large molecules are broken down into small ones.
  • Anabolism is the metabolic process that transforms simple substances into complex molecules.
82
Q

What are 3 main mechanisms for genetic variability?

A
  1. Mutations
  2. Recombination
  3. Vertical and horizontal gene transfer
    (4. Transposons)
83
Q

Describe mutations

A
  • Permanent, inheritable change in the nucleotide base sequence of a genome.
  • Occurs because of errors in DNA replication or due to mutagens (physical like radiation or chemical agents)
  • Completely random - they don’t happen to help the organism
84
Q

What are some types of mutations?

A

Point mutations: one nucleotide base pair is changed/swapped out for a different base pair

  • Silent mutations
  • Missense mutations
  • Nonsense mutations

Frameshift mutations: insertion or deletion of a nucleotide base pair shifts and changes the rest of the entire amino acid sequence

  • Insertions
  • Deletions
85
Q

Briefly explain:

  • Silent mutations
  • Missense mutations
  • Nonsense mutations
A

Silent mutations
- The base pair change results in no change in amino acid selection (because some codons can specify for the same amino acid)

Missense mutations
- The change results in a different amino acid selection

Nonsense mutations
- The change results in a stop codon creation instead of amino acid

86
Q

What is genetic recombination?

A

Refers to the exchange of nucleotide sequences between two DNA molecules, usually between segments that are similar.

Typical example is homologous recombination/”crossing over” in meiosis.

87
Q

Vertical vs. horizontal gene transfer?

A

Vertical
- Passing of genes to the next generation

Horizontal

  • Acquisition of genes from other microbes of the same generation
  • Donor cell provides DNA to recipient cell
  • If recipient cell inserts donor DNA into chromosome, it becomes “recombinant”
88
Q

What are the 3 types of horizontal gene transfer?

A
  1. Transformation
  2. Transduction
  3. Conjugation
89
Q

Describe transformation

A
  • Process where recipient cells take up DNA from their environment. No contact required.
  • IMPORTANT: New DNA must have replication instructions or be incorporated into DNA/plasmid to affect recipient cell.

“Competency” is the ability to take up DNA:
Natural examples - Streptococcus, Staphylococcus, Pseudomonas
Artificial example - E. coli in a lab

90
Q

Describe Transduction

A
  • Transfer of DNA from one cell to another by a virus
  • Virus must be able to infect both donor and recipient cells

Steps:

  • During viral synthesis/assembly, host DNA is accidentally incorporated into new viruses.
  • These “transducing phages” are released and find new recipients.
  • They inject the DNA into these new hosts.
  • New DNA may be incorporated into their chromosome/plasmid by recombination
91
Q

Describe conjugation

A

DNA transferred by a pili and requires physical contact between donor and recipient

Donor requires Fertility plasmid (F+) and recipients must lack F plasmid (F-):
- The (F-) recipient becomes (F+) after conjugation

Note: HFR is much different than (F+)

92
Q

What is the difference between (F+) and HFR conjugation?

A

(F+) has conjugation instructions on an F plasmid:

  • One strand of (F+) plasmid transferred into recipient and complementary strand is created
  • Recipient becomes (F+) afterwards

HFR (high frequency of recombination) F plasmid is integrated into donor’s chromosome:

  • Piece of F plasmid (along with some of the chromosome) is transferred to and incorporated with recipient chromosome (recombination)
  • Recipient stays (F-)
93
Q

What are transposons?

A
  • Segments of DNA that move themselves from one location to another (“jumping genes”).
  • Can move within same DNA or to different DNA (plasmid, diploid, etc.)
  • Do not require homology

(Important because transposons can include genes for antibacterial resistance)

94
Q

What are two types of transposons?

A

Insertion sequences (IS):

  • Made of the gene (for the enzyme, “transposase”) between 2 inverted repeats (like palindromes)
  • Transposase cuts/copies “insertion sequence” and inserts/pastes at target site

Complex transposons:

  • Made of two insertion sequences with a gene in the middle
  • This gene in middle may be antibiotic resistant
95
Q

What is transposition?

A

Process where transposons replicate or move from place to place within, among, and between chromosomes and plasmids.

Plasmids can carry transposons to and from cells.

96
Q

What is the different between “biotechnology” and “recombinant DNA technology”?

A
  • Biotechnology is the use of microorganisms to make practical products
  • Recombinant DNA technology, AKA “genetic engineering”, is the intentional modification of the genomes of organisms
97
Q

What are restriction enzymes / restriction endonucleases?

A
  • Enzymes that cut DNA at specific nucleotide sequences and produce restriction fragments
  • Necessary for recombinant DNA technology to cut DNA at a desired location
  • They are capable of recognizing foreign DNA and breaking down the sugar-phosphate backbone
98
Q

What is the purpose of polymerase chain reaction (PCR)?

A

Process that produces a large number (billions in a few hours) of identical molecules of a specific segment of DNA.

It uses cycles of heat to break apart strands, enabling enzymes to synthesize complementary strands, at an exponential rate.

99
Q

What are some medical uses of PCR?

A

Replication of DNA can:

  • be used to detect viruses
  • monitor treatment effectiveness in patients
  • assist the process of recombinant DNA (plasmids may come from PCR)
100
Q

What is the purpose of gel electrophoresis?

A

Use electricity to separate DNA fragments based on their electrical charge, size, and shape.

Fragments are placed in wells/agarose and the fragments move towards the positive charge when current is applied. Larger fragments take slower.

Size is determined by comparing against known sizes.

101
Q

What are some medical uses of gel electrophoresis?

A
  • Can be used to detect specific DNA molecules

- The fragments can be used in plasmids or PCR

102
Q

What is DNA sequencing?

A

Determining the exact order of nucleotides in a segment of DNA.

Next-generation DNA sequencing allows us to sequence billions of bases in a few days.

103
Q

What are medical uses of DNA sequencing?

A
  • Enables scientists to study pathogens
  • Aids development of drugs/vaccines
  • Aids understanding of protein synthesis
  • Aids understanding of microbiome
104
Q

What is a vector (regarding recombinant DNA technology)?

A

Plasmid, virus, or transposon that carries DNA into cells.

It can alter the gene.

105
Q

What are medically relevant uses of recombinant DNA technology?

A

Producing:

  • Hormones
  • Enzymes
  • Vaccines

Gene therapy

Genetic screening

Medical Diagnosis

106
Q

What is gene therapy?

A
  • Using recombinant DNA technology to introduce DNA into a patient’s cells to treat or cure a disease.
  • Uses a specific virus to replace/correct a defective gene
107
Q

Briefly explain CRISPR

A

Uses bacterial Cas-enzymes (which are to protect the bacteria from viruses) to find a specific segment of DNA and then edit it (cut and/or replace) with extreme precision.

108
Q

What is phylogeny? What is a branch point?

A

Phylogeny - visual hypothesis of evolutionary history (avoids analogous traits)

Branch point - common ancestor between two groups

109
Q

Homologous vs. analogous traits

A

Homologous - derived from common ancestor and share similar structure. May or may not be adapted to perform different function (i.e. arm bones similar in humans, dogs, birds but function differently)

Analogous - same function but not sharing or derived from a common ancestor (i.e. bird’s wings vs. butterfly’s wings)