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Infectious diseases > FINAL EXAM! > Flashcards

FINAL EXAM! Flashcards

1
Q

How do you differentiate between infectious agents?

A

Question #1: Is it living?
Yes= prokaryotes and eukaryotes.
No= Viruses + Prions

Question #2: For non-living, does it contain genetic material?
Yes= Viruses
No= Prions

Question #3: For living, does it contain nucleus and membrane bound organelles?
Yes= Eukaryotes (Protozoa, Fungi, Helminths)
No= Prokaryotes (Bacteria)

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2
Q

Viruses structural identity?

A
  • Protein coat
  • Double or single strand DNA or RNA
  • May have envelope
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3
Q

Prions Structural Identity?

A
  • Mis-folded proteins
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4
Q

Bacteria Structural Identity?

A
  • Cell wall made of peptidoglycan *
  • Cell Membrane
  • Circular double strand DNA
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5
Q

Protozoa Structural Identity?

A
  • Unicellular *
  • Cell Membrane
  • Double strand DNA in Nucleus
  • Organelles
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6
Q

Fungi Structural Identity?

A
  • Uni or Multi-Cellular
  • Cell wall containing Chitin*
  • Cell membrane
  • Double stranded DNA
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7
Q

Helminths Structural Identity?

A
  • Multicellular parasite
  • Cell membrane
  • Organ system *
  • DNA in nucleus
  • Organelles
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8
Q

What is the Gram reaction?

A
  1. Gm+: Have a thick peptidoglycan layer which will stain purple during the primary stain of the gram stain test due to the enhanced moisture retention, stain is then locked in by alcohol.
  2. Gm-: Have a thin peptidoglycan layer followed by a protective outer membrane made up of lipopolysaccharides (LPS) and porins, Stains pink from counter stain after LPS layer is dissolved using alcohol.
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9
Q

Nucleoid?

A
  • Central region with double stranded DNA chromosomes

- Not membrane bound (not a nucleus)

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10
Q

Plasmids?

A
  • Small circular double strand DNA
  • Can carry antibiotic resistance genes and other virulence factors*
  • extrachromosomal (Can be passed to another bacterium)
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11
Q

Ribosomes?

A
  • Translate mRNA to assemble proteins

- Structurally different than eukaryotic ribosomes*, can target w/out harming our own

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12
Q

Cytoplasm?

A
  • gel-like substance that contains dissolved nutrients + proteins
  • fills space within the cell
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13
Q

Cytoskeleton?

A
  • proteins that organize cytoplasm

- provides structure & support

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14
Q

Inclusions?

A
  • Granules that store polymerized neutrients (Ex. Glycogen, starch, sulfur, nitrate)
  • or materials used by the cell (Ex. Gas to change buoyancy, iron for navigation)
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15
Q

Plasma Membrane?

A
  • cell membrane, made of fluid phospholipid bilayer embedded with proteins.
  • controls what enters and exits the cell
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16
Q

Cell Wall?

A
  • Lies outside the plasma membrane
  • maintains cell morphology
  • protects cell from lysis due to osmotic changes
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17
Q

Morphology of GM+ bacteria?

A
  • Thick peptidoglycan layer ( Sugar chains cross-linked with peptides)
  • peptidoglycan is a target for antibodies within the immune system.
  • Teichoic acid (Acts as rebar in cement), stabilizes the cell wall and increases adhesion including pathogenicity.
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18
Q

Morphology of Gm- Bacteria?

A
  • Thin layer of peptidoglycan
  • outer membrane of lipopolysaccharides (LPS) and porins, makes bacteria harder to kill w/ drugs/chemicals
  • LPS= stabilizes outer membrane. Is an endotoxin which stimulates immune resonance (Fever or septic shock). Also increases adhesion (Pathogenicity, ex. To own cells) and can change to evade immune system.
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19
Q

What are the cell walls like of acid-fast bacteria?

A
  • thick outer peptidoglycan

- outer waxy layer of my colic acid (Inhibits gram stain)

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20
Q

Slime layers and capsules?

A
  • only some bacteria have
  • layer of sugars/proteins external or cell wall
  • capsule = tight, organized, slime layer = loose, unorganized.
  • helps form biofilm by increasing bacterial adhesion to surfaces and tissues.
  • protects bacteria from immune system
  • protects against dehydration, antibiotics and disinfectants
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21
Q

Fimbriae?

A
  • only some bacteria have

- numerous short, bristle-like proteins that cover some bacteria, increases bacterial adhesion (Ex. Biofilm)

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22
Q

Pilus/pili?

A
  • only some bacteria have

- like fimbrae but fewer in number and longer, increase to adhesion to tissues

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23
Q

Flagellum/Flagella?

A
  • only some bacteria have
  • propeller made of flagellin protein
  • allow bacteria to remove in response to stimuli
  • counterclockwise = run forwards
  • clockwise = tumble to change direction
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24
Q

Spors?

A
  • Bacterial spore protects DNA against harsh environmental conditions.
  • Allows bacteria to exist for years in dormant form.
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25
Q

What is Koch’s First Postulates and its limitations?

A
  1. Suspected pathogen must be found in every case of disease but not in healthy individuals

Limitations:
- Many pathogens are opportunistic
- can also be found in healthy individuals
Ex. S. aureus

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26
Q

What is Koch’s second postulates and its limitation?

A
  1. Suspected pathogen can be isolated and grown in pure culture

Limitations: Not all pathogens can be grown in pure cultures (Ex. Obligate intracellular bacteria viruses and dental plaque biofilm

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27
Q

What is Koch’s 3rd postulate and its limitation?

A
  1. Healthy subject infected with suspected pathogen must develop same symptoms and signs and disease

Limitations:

  • resident microbiota and subjects own immune system may result in different types and severity of signs and symptoms
  • not all pathogens van be grown in animal host
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28
Q

What is Koch’s 4th postulate and its limitation?

A
  1. Identical pathogen must be re-isolated from host

Limitation:

  • Pathogen my mutate, becomes more or less virulent
  • can be difficult to re-isolate
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29
Q

Pathogenicity?

A

Ability of microbial to cause disease

Whether it does or doesn’t cause disease

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30
Q

Virulence?

A

Degree of harm abused

How powerful it is ex. mild cough vs organ failure

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31
Q

What is pathogenesis? What are the 5 stages?

A

Ability to cause infection.
1. Contact and enter host
Pathogen present (air, food, water, environment, fomite, animals, human carrier) and enter through portal of entry (skin, mucus membranes (eyes, respiratory tract, Gi tract) and parenteral (breaks in the skin))
2. Adhere to host tissue
Bacterial structures and proteins allow adherence to tissues where bacteria can build biofilms
3. Invade tissue and obtain nutrients
Pathogens can stay on surface, enter or pass between cells. Virulence factors help spread through cells/tissues which often causes damage.
4. Replicate and multiply (Causes infection)
Infectious can be localized or systemic
5. To repeat cycle, pathogen must also be transmitted to new host
Pathogen leaves host via portal exit, (rubbing eyes, pus draining, sneezing/coughing, saliva, mucus, vomit, feces, urine, semen, blood, etc.)

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32
Q

Youre doing great

A
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33
Q

What are some Bacterial virulence factors?

A
  1. Structures (Flagella, fimbriae, LPS/otter membrane, capsule, plasmids)
  2. Proteins (adhesions, secretory systems)
  3. Enzymes (Hemolysin, proteases)
  4. Endotoxin (LPS)
  5. Exotoxins (damages issues, cannot be killed by cooking, cannot be reversed or removed)
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34
Q

What is a bacterial life cycle in good and poor conditions?

A

Good: Vegetative cell is growing (happily growing), larger vegetative cell, asexual reproduction cell division by binary fission, two daughter cells and then the cycle begins.

Poor: Vegetative cell is growing (happily growing), growth slows due to poor conditions, cell either dies or some bacteria can sporulate, dormant spore will germinate when in good conditions and will return back to a Vegetative cell that is growing.

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35
Q

What does bacterial growth depend on?

A

Appropriate/Sufficient levels of oxygen, nutrients, water, temperature, and pH.

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36
Q

Obligate aerobes?

A

Need oxygen to grow

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37
Q

Facultative anaerobes

A

Can grow with and without oxygen but prefer oxygen

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38
Q

Aerotolerant

A

Can grow in either, no preference.

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39
Q

Microaerophiles?

A

Grow in environments with very little oxygen

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40
Q

Obligate anaerobes

A

NO OXYGENNN

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41
Q

What is it called when bacteria grows in goooood conditions?

A

Exponentially.

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42
Q

What are bacteria growing in good conditions more sensitive to?

A

Disinfectants and antibiotics that target synthesis of cell wall, protein, and DNA

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43
Q

What happens to bacteria when conditions are poor?

A

Growth slows
Bacteria becomes LESS sensitive and MORE resistant to antibiotics
Endospores may form
If few cells can persist = chronic infection

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44
Q

Bacterial reproduction?

A

Asexual reproduction resulting in 2 genetically identical daughter cells. Also known as binary fission.

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45
Q

What are the 5 steps of binary fission?

A
  1. DNA replicates
  2. Cell elongates
  3. Septum forms
  4. Cell partitions
  5. Daughter cells separate
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46
Q

When does sporulation occur? What are spores?

A

In poor conditions.

  • metabolically inactive or dormant
  • highly resistant to starvation, heat, drying, freezing, radiation and chemicals
  • can last for years
  • can germinate within minutes when conditions are good
  • Spores are not reproductive, does not increase population.
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47
Q

What are the 5 steps of sporulation?

A
  1. DNA replicates
  2. DNA, ribosomes and enzymes are packaged into spore core
  3. Spore core is surrounded by layers resistant to heat and chemicals, forms endospores inside cell
  4. Endospores released = free spore
  5. Remaining cell dies
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48
Q

What is BACTERIAL genetic variation? What are the 3 kinds of it?

A

Bacteria that reproduce sexually and therefore does not result in genetic variation.

  1. Mutation
  2. Transposition
  3. Horizontal gene transfer
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49
Q

Mutation?

A
  • can be helpful or unhelpful to human body
  • can be induced by radiation or chemicals
  • can be spontaneous
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50
Q

Transposition?

A

Transponsons are able to jump to and from chromosomal DNA and plasmid DNA which results in the transfer of genes = information = abilities

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51
Q

Horizontal gene transfer?

A

The transfer of genes between bacterial cells of the same or different species
- occurs w/out cell division (Not reproduction)
A. Transformation: (Like eating a dead bird and growing wings)
- bacteria absorbed pieces of DNA from environment
- DNA environment can be from dying/dead catering or organisms
B.Transduction
- viruses can transfer DNA from one bacterium to another
C. Conjugation (Bacterial sex)
- some bacteria can produce pilus and transfer plasmids
- plasmids have gens for antibiotic resisntace or toxins
- can be transferred to bacteria of different species.

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52
Q

What are microbial communities?

A

Biofilms - a place where bacteria exists since they are nit free-floating

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53
Q

What are Biofilms?

A

A complex communities with many different species of microbes embedded in a protective matrix attached to some surface.

Fun fact, their is lots of communication, can look like cooperating or fighting.

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54
Q

What is the structure if Biofilms?

A

70% is made up of living and dead organisms, 30% extra cellular matrix.

Matrix:

  • consists of polysaccharides and proteins from saliva, GCF, and bacteria of biofilm.
  • acts as a food reservoir and glue (adherence)
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55
Q

Why do Bacteria live in Biofilms? (5 reasons)

A

Protects bacteria from..

  1. Dehydration
    - sugars in extracellular matrix draw in water
  2. For shortages
    - some bacteria may secret waste products that can be used by other bacteria as nutrients
  3. Immune system
    - extra cellular matrix blocks diffusion/entry of antibiotics and WBC
  4. Antimicrobials
    - extracellular matrix blocks diffusion of antimicrobial molecules
    - some antibiotic resistant bacteria can secrete enzymes that protect neighbouring bacteria.
    - bacteria in biofilm take turns being active and quiescent
  5. Transient competitors
    - resident bacteria bind/block receptors for adhesion, use up nutrients and release toxins (Fighting)
    - bacteria biofilms produce quorum-sensing molecules (allows cells to communicate, cooperate and share food along with to destroy dugs using specific proteins)
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56
Q

What is the relationship between plague biofilm and dental disease?

A
  • Stability of oral microbiome (symbiosis) is necessary for health, however a disturbance of oral microbiom (dysbiosis) leads to disease.
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57
Q

What does occurs to get to periodontitis disease?

A

Healthy: appropriate immune response (inflammation) + symbiotic biofilm.

Gingivitis: dysbiotic biofilm (decrease in diversity, increase in Gm- bacteria) appropriate i immune response however continuous inflammation.

Periodontitis: Pathogenic biofilm (mostly Gm- bacteria), excessive immune response, inflammation feeds pathogen in self-perpetuating pathogenic cycle.

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58
Q

What are the 3 different types of anti bacterial drugs?

A
  1. Antibiotics: produced by moles or other bacteria
  2. Semi-synthetic antimicrobials: modified naturally occurring antibiotic
  3. Synthetic antimicrobials: chemical found to have antimicrobial properties
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59
Q

What is the difference between bacterICIDAL and bacterIOSTATIC drugs?

A

bactericidal:

  • kill bacteria
  • target the cell wall, nuclei acids and the membrane
  • can be dangerous to patient since death of GM- cells release lots pf LPS (endotoxin (Located within the cell wall) = large immune response)

bacteriostatic:

  • prevents growth of bacteria
  • targets protein synthesis, metabolic pathways (Ex. Folic acid synthesis)
  • requires a healthy immune system to finish the job.
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60
Q

What causes a drug to be bateristatic or bactericidal?

A
  • Dose (amount and quantity)
  • Type of organism
  • Length of regime
  • Route of administration
  • Pathogen load (how much bacteria is in your body)
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61
Q

What factors affect the choice of antibacterial drugs being prescribed? (5 factors)

A
  1. Spectrum of activity:
    - broad spectrum: drugs work against many Gm+ and Gm-
    - narrow spectrum: drugs work against certain groups only.
  2. Drug safety:
    - selective toxicity (targets microbe, minimally damages host cells)
    - few side effects
    - does not include allergies
  3. Administration route:
    - oral drugs are easier to administer but need to resist digestive by acid and enzymes in stomach.
    - can also be given by parenteral route (Injection of infusion)
    - vein = intravenously
    - muscle = intramuscularly
    - skin = subcutaneously
  4. Drug stability and elimination:
    - half-life = time requires for half drug to be broken down by liver and eliminated by kidneys
  5. Drug interactions and contraindications:
    - most drugs have some interactions and contraindications
62
Q

What are the pros of using narrow or broad spectrum?

A

Narrow:

  • minimize effects of good bacterias
  • reduce chance of developing resistance

Broad:

  • if organism is unknown
  • not enough time to find out
  • before surgery to prevent infection
  • could be infected by multiple organisms
63
Q

What is the mechanism of action of common antibacterial?

A
  • to ensure selective toxicity, antibacterial drugs target bacterial structures not present in eukaryotic cells (Cell wall + ribosomes)
  • growing cells to make new or more cell wall(s), this requires transpepridase enzyme to complete the last step. Transpeptidase forms the peptide cross link that binds the sugar chains into chain link structure
64
Q

How does Beta-lactam antimicrobials prevent bacteria from building more/new cell walls?

A
  • chemical structure of drugs include beta-lactam ring, thing ring binds and blocks the transpeptidase enzyme which prohibits the cell wall from being build resulting in burst of bacterium.
65
Q

How does bacteria become antibiotic resistant when containing plasmids carrying the info to make beta-lactamase?

A
  • (Beta-lactamase is an enzyme that digests beta-lactam rings)
  • bacteria that make beta-lactamase are resistant to beta-lactum drugs
  • therefor combination drugs my work better.
66
Q

What are the characteristics of viruses?

A
  • Acellular
  • 10-100x smaller than bacteria
  • obligate intracellular parasites (Need host to make nucleus) due to not being able to make their own nuclei acids and proteins and to replicate using hosts organelles
  • infect every type of organism
67
Q

What is the viral structure like?

A
  • all viruses have a capsid band genetic material

- some contain envelopes and spikes

68
Q

What is a viral capsid?

A
  • protective shell or coat made by repeating protein subunits.
  • packages and protects the genome and may contain adhesion proteins.
69
Q

What is a viral envelope?

A
  • made up of envelope proteins that help virus invade cell.
  • once within cell, insert viral proteins into host cell membrane allowing it to steal part of membrane and leave via budding.
70
Q

What are viral spikes?

A
  • glycoprotein structures sticking out of capsid or envelope.
  • binds to specific factors on host, therefor derringers species and tissues that virus infects (Tropism)
  • helps virus attach and enter host cell
  • contributes to pathogenicity and virulence
  • can be recognized by specific immune systems cells abd antibiotics, however can change and escape immune system, which increases it virulence
71
Q

What are viral Genomes?

A
  • either DNA or RNA

deliver its DNA or RNA genome into the host cell so that the genome can be expressed (transcribed and translated) by the host cell.

72
Q

Double stranded DNA viral genome 1. replication of genome, 2. polymerase used to replicate and 3. proofreading capability of polymerase?

A
  1. DNA -> DNA
  2. host DNA pol
  3. Detects errors and Corey’s mismatch
73
Q

Singe strand DNA viral genome 1. replication of genome, 2. polymerase used to replicate and 3. proofreading capability of polymerase?

A
  1. DNA -> DNA
  2. Host DNA pol
  3. detects errors and corrects mismatch
74
Q

Double strand RNA viral genome 1. replication of genome, 2. polymerase used to replicate and 3. proofreading capability of polymerase?

A
  1. RNA -> RNA
  2. Viral RNA pol
  3. None = mutation
75
Q

Single strand RNA viral genome 1. replication of genome, 2. polymerase used to replicate and 3. proofreading capability of polymerase?

A
  1. RNA -> DNA -> RNA
  2. Viral reverse transcriptase -> host RNA pol
  3. Non = mutation
76
Q

What are the two ways viruses change over time?

A
  1. Mutations
    - DNA polymerase proof reading fails
    - no RNA polymerase proof reading
    - can’t cause minor changes to genome (viral proteins that immune system can’t recognize resulting in antigenic drift)
  2. Reassortment
    - 2 viral strains can coinfect the same cell, genome mixing during replication assembly, new viral strain created. Can lead to major antigenic shift, pandemics
77
Q

What are the two types of viral replication?

A
  1. Bacteriophage replication (in bacteria)
    - Lyric and Lysogenic replication
  2. Animal virus replication
78
Q

Lyric replication?

A
  1. Attachment
    - binds to host cell sugars or proteins
  2. Penetration
    - capsid stays outside
    - injects nucleic acid
  3. Replication
    - makes cell produce viral genes and proteins
    - host cell DNA degraded
  4. Assembly
  5. Release (cell bursts)
    - by cell lysis
    - naked phases released
79
Q

Lysogenic release

A
  1. Attachment
    - binds to host cell sugars or proteins
  2. Penetration
    - capsid stays outside
    - injects nucleic acid
    - INTEGRATION= prophage (new info, new function)
    - cell division
    - host cell stressed
    - phage exits DNA to find new host
  3. Replication
    - makes cell produce viral genes and proteins
    - host cell DNA degraded
  4. Assembly
  5. Release (cell bursts)
    - by cell lysis
    - naked phases released
80
Q

What happens if a phage (bacterial virus) picks up bacterial DNA instead of Viral DNA during the assembly step of bacteriophage replication?

A

The phage could now carry genes for toxins to other bacteria (Transduction)

81
Q

What is the replication of most animal viruses?

A
  1. Attachment
    - via protein-protein interactions

2a) Penetration
- by fusion (enveloped only)
- or endocytosis

2b) uncoating
- breakdown of capsid to release genome

  1. Replication
  2. Assembly
  3. Release
    - budding or lysis
82
Q

What is the replication of SOME animal viruses?

A
  1. Attachment
    - via protein-protein interactions

2a) Penetration
- by fusion (enveloped only)
- or endocytosis

2b) uncoating
- breakdown of capsid to release genome
- integration (Viral RNA converted to DNA)
- cell division
- daughter cell carry vital DNA
- When host cell is stressed, virus can return to lytic cycle

  1. Replication
  2. Assembly
  3. Release
    - budding or lysis
83
Q

What are the two types of Viral infection?

A
  1. Productive infection
    - host cells replicate and release lots of virions, causes ACUTE INFECTION = immune system clears virus, infection done.
    Ex. Cold and flu viruses.
  2. Persistent infection
    - virus genome stays in host nucleus which can lead to CHRONIC INFECTION = continued release of virus. Without treatment virus count increases.
    - can lead to LATENT INFECTION = dormant periods alternating with flare ups.
    - this can lead to CANCER = if virus disrupts cell division control or proofreading genes
84
Q

What are 4 ways viruses can damage tissue and cause disease.

A
  1. Prophage interacting will host DNA can disrupt function and can even lead to cancer
  2. Replication within the cell degrades hots’ DNA, therefore disrupting cell function.
  3. Virus infected cells can create an immune response that not only kills the infected cells but also neighbouring healthy cells.
  4. During release, budding and lysis both kill the host cell.
85
Q

COVID-19:

A

-ethologies agent: SARS-CoV2

86
Q

What is the first line of defence (innate) of the immune system?

A

(Inhibits and prevents infection)

  1. Physical Barriers:
    - skin = tough, dry, neutrino poor
    - mucous membranes = traps microbes, ciliated cells sweep away
  2. Chemical barriers:
    - Acid (Sweat and stomach acid) = inhibits bacterial growth + kills
    - Lysozyme (in mucus, tears, saliva) = dissolved peptidoglycan in bacterial cell wall (GM+)
    - Definsin peptides (Made by neutrophils) = poke holes in bacterial membrane
    - mucus (Contains decoy molecules) = can block viruses
  3. Resident microbiota - live on tissue but cause no harm, can produce vitamins, take up space, resources, and can release chemicals that prevent growth.
87
Q

What is the innate second line i of defence?

A

(Deals with infection in early stages)

  1. Inflammation
  2. Fever
  3. Antimicrobial proteins
  4. Innate white blood cells
88
Q

What are the 5 signs of inflammation?

A
  1. Heat
  2. Redness
  3. Swelling
  4. Pain
  5. Loss of function
89
Q

How does inflammation occurs and what are the 2 types of inflammation?

A
  • Basophils, mast and damaged cells release histamine.
  1. Local vasodilation:
    - redness + heat
    - white blood cells, clotting factors, immune proteins, and nutrients are brought to the tissues faster due to the dilation
  2. Capillary Permeability:
    - swelling (pushes cells apart), pain, loss of function
    - allows WBC and materials to enter tissues
    - Edema dilutes toxins
    - Edema enhances lymphatic capillary uptake of microbes and dead cells
90
Q

How do fevers occur? What are the benefits?

A
  1. Neutrophils + macrophages release inerleukin-1, hypothalamus, increased temperature set point
  2. Metabolic activity = faster repair, increased interferon activity, causes liver and spleen to hoard Fe + Zn = less available for microbial reproduction
91
Q

What are the two types of Antimicrobial proteins?

A
  1. Interferons
    - secreted by virus infected cells
    - stimulate neighbouring cells to produce antiviral proteins
    - activate macrophages and NK cells
  2. Complement proteins
    - many different plasma proteins made by liver, circulate in inactive form. When one compliment protein is activated, all then become activated in a wave.
92
Q

What are the 3 ways compliment proteins become activated?

And what are its 3 main actions?

A

Activation:

  1. Binding to antibodies on surface of bacteria
  2. Spontaneous breakdown
  3. Binding to sugars on bacterial surface

Actions:

  1. Inflammation and attract WBC
  2. Label bacteria for phagocytosis
  3. Form membrane attack complex (MAC) =channel in membranes -> lysis (Makes hole in virus resulting in blowing up)
93
Q

what are the 6 types of innate white blood cells involved in innate immune response?

A
  1. Basophils
  2. Eosinophils
  3. Neutrophils
  4. Natural killer cells
  5. Monocytes
  6. Dendritic cells
94
Q

Basophils? Process?

A
  1. Basophils and mast cells secrete histamine which creates inflammation. (Make up 0.5% of WBC)
  2. Vasodilation = increased blood flow = redness + heat. = permeability (spaces between cells enlarge) allow materials to enter tissues = edema (WBC, nutrients and repair proteins can help)
95
Q

Eosinophils?

A
  1. Produce H2O2 and superoxide (harmful toxins) against parasites.
    - stimulate basophils
    - secrete enzyme to limit histamine action
96
Q

Neutrophils?

A

Kill bacteria 3 ways:

  1. Phagocytosis:
    - engulf bacteria into a membrane bag. Granules fuse and kill, lysosomes fuse and digest. (Will day after 1-2 times)
    - makes of 60% of WBC
  2. Oxidative burst:
    - try to engulf however some H2O2 escapes and can damage the body.
  3. Netosis:
    - neutrophil extracellular traps, neutrophils burst open releasing a sticky DNA that traps the bacteria.
97
Q

Natural killer cells? Process?

A
  1. Kills own infected cells (cancer)
    - lymphocyte
  2. Patrols for virus-infected cells, cancer cells or other cells lacking or missing MHC 1
    - release perforin (pokes holes in cell’s membrane) and granzymes (digests cell)
    - virus infected cell dies via apoptosis, debris removed by macrophages.
98
Q

Monocytes/Macrophages? Process?

A
  1. Eats microbes, dead neutrophils and damaged cells
  2. Detention:
    - can decider if bacteria has peptidoglycan, LPS or antibodies/compliments
    - works best wen pathogen is labeled with antibodies
    - works best if labeled with complement.
99
Q

Dendritic cells? Process?

A
  1. Link innate and adaptive immunities
  2. Phagocytosis (cellular process for ingesting and eliminating particles), mature DC present bacterial antigen, DC travels to lymph node to present antigen to T-helper cells (mature DC present viral antigens to Thelper and Tcytotoxic cells in lymph)
100
Q

Innate vs adaptive immunity?

A

Innate: which an organism is born with

adaptive: which an organism acquires following disease exposure

101
Q

Why is innate immunity nonspecific where as adaptive immunity is specific?

A

Innate: Responds to common, conserves pathogen markers (LPS, peptidoglycan)

Adaptive: 100 million different lymphocytes exist, each with receptor for 1 antigen.

102
Q

What is involved in innate immunity?

A
  • inflammation
  • fever
  • lysozyme, complement, interferon
  • basophils
  • neutrophils
  • macrophages, dendritic cells
  • eosinophils
  • NK cells
    … (ETC)
103
Q

What is involved in adaptive immunity?

A
  • T cells
  • B cells
  • antibodies
104
Q

What is the response time difference between innate and adaptive immunity, why?

A

Innate: immediate -> always present and ready, same each time.

Adaptive: needs to be activated (take 7-10 days when first time in contact with pathogen): pool of possibilities -> selection -> activation expansion -> effector cells + memory cells produced.
- effector cells eliminate pathogen then die, memory cells last for decades.

With each exposure, effectiveness of response improves:
- hyper mutation and selection creates B cells + antibodies with increased infinity for antigen. Labeling/recognition improves + memory cells are activated faster

105
Q

What is the difference of symptoms between innate and adaptive immunities?

A

Innate: no or few symptoms

Adaptive: symptoms occur when innate is unable to cope and adaptive immunity starts ramping up.

-recovery occurs when adaptive immunity enhances and innate immune both work to remove pathogen.

106
Q

What is clonal selection and where does it occur?

A

The process of establishing the idea that only those cells capable of recognizing an antigen will proliferate, while other cells are selected against. Clonal selection calls both B and T cells. (Leads to adaptive immunity)

Occurs in the bone marrow.

107
Q

What are the 4 stages of the clonal selection?

A
  1. Random generation: billions of lymphocytes, each wih different specificity. (Hopefully one will fit a pathogen. Could be against self-antigens)
  2. Maturation in thymus and brown marrow: involves testing against self-antigens. Self-reactive lymphocytes are killed.
    - they get killed because Tcells are binding to own antigens.
  3. Pool f 100 million different possibilities: only a few lymphocytes of each type are present.
  4. Selection: by binding of foreign antigen leads to activation and clonal expansion.
    - hypermutation in B cells results in even better antigen binding, leads to stronger response next time = adaptive immunity.
    - effector cells eliminate antigen then die, memory cells last for decades.
108
Q

Which step of the clonal selection would result in an autoimmune disease?

A

Maturation in thymus and bone marrow because (?)

109
Q

Immunizations take advantage of what step of the clonal selection?

A

Selection, activations + expansions because provides antigens in a reasonable load? There for antibodies and memory cells can already be created?

110
Q

What is the third line of defence for the immune system?

A

Enhance innate response (B-cells, Antibodies and Thelper cells) and deal with intracellular pathogens (Tcytotoxic)

111
Q

What are the 4 different specific types if immunity?

A
  1. Natural active - ex. exposure to virus
  2. Artificial active - ex. Immunization
  3. Natural passive - ex. Mothers antibodies
  4. Artificial passive - ex. Antibodies to snakes venom
112
Q

What do activated Thelper cells do?

A
  • effector CD4
  • activate B +Tcytotoxic cells in lymphoid tissue
  • return to site of infection and increase effectiveness of innate cells
  • produce memory Thelper cells
113
Q

What do activated Tcytocells do?

A
  • effector CD8
  • will return to site of infection and destroy infected or cancerous body cells
  • bind to MHC 1 + antigen on infected cell, release perforin (Poke holes) -> release granzymes (digestive enzymes) -> apoptosis.
    Will produce monetary Tcytotoxic cells
114
Q

What do activated B Cells do?

A
  • activated B cells = effector B cells = plasma cells)
  • produce memory B cells
  • produce highly specific antibodies
115
Q

What do antibodies do?

A

Return to site of infection where they will:

  1. Neutralize: block pathogens from entering + damaging cells
  2. Opsonize: label to help neutrophils, macrophages, dendritic cells and NK cells recognize pathogens
  3. Aggregate: clump pathogens for quick removal
  4. Activate complement: including inflammation, initiate cell lysis with MAC
116
Q

What is the purpose of MCH II?

A

present processed antigens, which are derived primarily from exogenous sources, to CD4(+) T-lymphocytes.

117
Q

T helper cells function and add-ons?

A
  • help activate B cells to secrete antibodies and macrophages to destroy ingested microbes, but they also help activate cytotoxic T cells to kill infected target cells by
  • TCR = binds specific antigen held in MHC protein
  • CD4 = protein binds MCH ll (protein) on dendritic cells, B cells abd macrophages.
118
Q

What are the 4 signals used by dendritic cells activate thelper cells?

A

1: MCH ll + antigen - Finds matching Thelper
2: costimulatory protein - activates Thelper, regulate the activation of T cells and the generation of effector T-cell responses.
3: cytokines - tell Thelper cells what’s to do (communicating chemical)
4: vita,mins - tells Thelper where to go

119
Q

What are the 5 types of vaccines?

A
  1. Live attenuated (weakened)
  2. Inactivated (killed)
  3. Subunit + recombinant
  4. toxoid
  5. mRNA
120
Q

Live attenuated vaccines?

Advantages and disadvantages?

A
  • attenuated = grown in lab for 30-80 generations till virus can no longer cause disease (weakened)
  • whole virus = more sited where immune cells can bind, more Ab and memory cells
  • live virus = can infect cells, stimulate Tcytotoxic response

adv: closest to natural infection, stimulate strong long lasting immunity.
Dis: cant be used by immunocompromised ppl
Dis: can become virulent if circulates to unimmunized ppl
Dis: requires refrigeration

121
Q

Inactivated vaccines?

Advantages and disadvantages?

A
  • killed, cannot infect cells or cause diseases
  • will stimulate Ab response, memory Thelper and memory B cells
  • relies on production of neutralizing Ab to prevent future infection

Adv: cannot cause diseases, can be used by immunocompromised ppl
Adv: doesn’t require refrigeration
Dis: doesn’t stimulate Tcytotoxic or Tc memory cells
Dis: doesn’t create long lasting immunity, requires booster shots

122
Q

Subunit and recombinant vaccines:

Adv, Dis?

A
  • purified parts of antigenic proteins instead of whole microbe
  • includes an adjuvant to activate dendritic cells, make costimulatory protein (signal 2)
  • small section of antigen = less Ab, memory Thelper and B cells
  • relied on production of neutralizing Ab to prevent future infection

Adv: cannot cause diseases, can be used by immunocompromised ppl
Dis: doesn’t stimulate Tcytotoxic or Tc memory cells
Dis: doesn’t create long lasting immunity, requires booster shots

123
Q

Toxoid vaccines?

A
  • inactivated bacteria toxins
  • stimulates Ab response for early neutralization against toxin but not bacteria.
  • Includes adjuvant
  • requires booster shot
124
Q

mRNA vaccines?

Adv, Dis?

A
  • laboratory made sequences are given to produce proteins and antigen

Adv: doesn’t contain infectious agent, cannot cause infection or diseas
Adv: doesn’t require adjuvant to stimulate DC or formaldehyde to kill infectious agent
Adv: mRNA is rapidly degraded, cannot combine with DNA or integrate with hosts DNA
Adv: can be rapidly produced and modified
Dis: some require extreme cold storage
Dis: new technology, no long term data

125
Q

Reservoir?

A

A place where pathogens reside for long periods of time, a place to reside

126
Q

Passive carrier?

A

Something that is contaminated with the pathogen and mechanically transmits it to another host, however it itself is not infected.

127
Q

Active carrier?

A

And infected individual who can transmit a pathogen to another host.

128
Q

Asymptomatic carrier

A

An individual who is infected and can pass it to another host however does not show any symptoms.

129
Q

Definitive host?

A

A preferred host for the organism for a parasite where it reaches maturity and may reproduce asexually.

130
Q

Intermediate host?

A

A host that a parasite will reside in for a few parts of its life cycle however will move to another host.

131
Q

Vertical contact transmission?

A

Pathogens transferred mother -> child

132
Q

Horizontal transmission

A

Pathogen gets transferred via sex = example

133
Q

Droplet transmission

A

Coughing and sneezing results in transmission of pathogen

134
Q

Via formite?

A

Inanimate objects harbour pathogens that you can pick up.

135
Q

Waterborne, airborne/areosols and foodborne

A
  1. Pathogens transmitted through water
  2. Pathogens that float in they air
  3. Contamination of food with harmful pathogens
136
Q

Mechanical vector

Biological vector

A
  1. An animal that transmitted a pathogen from one anti Al to the other w/out being infected
  2. Pathogen reproduces W/in a biological vector that transmitted the pathogen form one host to another
137
Q

Communicable vs noncommunicable

A
  1. Disease that spreads from person to person using direct or indirect mechanisms
  2. Infectious disease that isn’t spread from person to person
138
Q

Contagious?

A

Disease that can spread from one to person to another

139
Q

Morbidity vs mortality rate?

A
  1. # of infected people/population

2. # of dead people / population

140
Q

Sporadic disease?

A

Diseases seen sporadically and w/out geographic concentration.

141
Q

Endemic disease?

A

A disease that happens in a short amount of time w/ more cases than expected in a geographic region.

142
Q

Outbreak vs epidemic vs pandemic?

A
  1. The occurrence of disease cases is excess than expected
  2. A widespread occurrence of an infectious disease in a community @ a particular time
  3. A disease that is prevalent across a whole country or the world.
143
Q

Etiologic agent?

A

He cause of the/a disease

144
Q

Propagated spread?

A

The progression of an infectious diseases from person to person directly or indirectly through population of susceptible ppl as one infected person transmits to others via sex or coughing (EX.)

145
Q

Point source spread vs continuous point source spread vs intermittent common source spread?

A
  1. Transmission from the source occurs for a brief period that is less than the pathogens incubation period.
  2. A mode of disease transmission in which every infected originates from the same source the is produced for longer than incubation period.
  3. Mode of transmission where every infection originates from the same source that produced infectious for a period before stopping and starting again.
146
Q

Antibacterial agents : penicillin V + C, cephalosporin, ampicillin, amoxicillin and methicillin mechanisms of action?

A
  • B lactic ring blocks transpeptidase enzyme.
  • inhibits cell wall synthesis
  • bactericidal
147
Q

Antibacterial agent: erythromycin, clindamycin and tetracycline mechanisms of action?

A
  • bind bacterial ribosomes

- block protein synthesis

148
Q

Antibacterial agents, sulfonamides mechanisms of action?

A
  • interferes with folic acid synthesis

- needed for DNA replication and division.

149
Q

What ingredients are included in vaccines?

A
  1. Adjuvant - stimulate dendritic cells -> costimulatory protein -> activate Th
  2. Formaldehyde - used to kill viruses and inactivate bacterial toxins during purification
  3. Antibiotics - prevent the growth of bacteria when growing viruses
  4. Stabilizers - Help viruses withstand the freeze-drying process
  5. Preservative - prevent the growth of bacteria and fungus
150
Q

How are vaccines tested?

A
  • 10-15 years
    1. Exploratory stage = lab research
    2. Pre-clinical stage = test vaccine in-culture and on animals (immune response)
    3. Phase 1 vaccine trials = 20-80 healthy adults (immune response)
    4. Phase 2 vaccine trials = 100-1000 random ppl (safety, dose, schedule/mode of delivery)
    5. Phase 3 vaccine trials = 1000 - 30,000 random ppl (rare side effects, ability to prevent disease and infection)

Infectious diseases (3 decks)

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