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RUSVM Principles of Infectious Disease Orange Semester 2016 > PID Exam 1 > Flashcards

PID Exam 1 Flashcards

1
Q

Define Symbiont

A

Organisms that live with another organism

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2
Q

Define Obligate Symbiont and Facultative Symbiont

A

Obligate Symbiont: Need host to survive

Facultative Symbiont: Can live with or without a host

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3
Q

Define Pathogenicity

A

Ability of an organism to cause disease

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4
Q

Define Facultative Pathogenic

A

Can cause disease depending on the circumstances

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5
Q

Define Endogenic Infection

A

Infection resulting from organism that was already present in the body.

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6
Q

Define Exogenic Infection

A

Infection from organisms that comes from outside the body (eg from another person)

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7
Q

Define Obligate Pathogenic

A

Always causes disease

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8
Q

Define Balanced Pathogenicity

A

Damage with recovery (the majority of infections)

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9
Q

Define Unbalanced Pathogenicity

A

High damage/death

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10
Q

Define Infection

A

Invasion and multiplication of microorganisms eventually with disease (symptoms)

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11
Q

Define Disease

A

Disorder of structure and function

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12
Q

Define Subclinical

A

Eg a decrease in production, but no other symptoms. Feeling under the weather, but no symptoms.

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13
Q

Define Opportunistic Pathogen

A

The pathogen needs a specific precondition (eg a viral infection, allergy, a younger animal with less immune system)

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14
Q

Define Septicaemiae/Bacteraemia

A

Bacteria in blood stream (Blood infection)

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15
Q

Define Hyperacute, Acute, Subacute, Chronic.

A

Hyperacute: very severe, death - very fast onset
Acute: fast onset
Subacute: between acute and chronic
Chronic: long/ongoing - gradual or waves (bacteria could be hiding somewhere)

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16
Q

Describe the “threshold” for our bodies and microorganisms.

A

We can handle microorganisms to a certain extent before there is disease. However, if we become immunocompromised then there may be a problem.

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17
Q

Describe the differences between bacteria and eukaryotes when it comes to: Size, Membrane bound organelles, Ribosomes, Nucleic acid, Nuclear membrane, Replication

A

Size: Bacteria = <5um, Eukaryotes = >10um
Membrane bound organelles: Not present in bacteria, present in eukaryotes (mitochondria, chloroplasts)
Ribosomes: Bacteria: 70 Eukaryotes: 80S
Nucleic Acid: Bacteria = Single molecule (circular), Eukaryotes: Chromosomes
Nuclear Membrane: Absent in bacteria, Present in eukaryotes
Replication: Bacteria replicate by binary fission, Eukaryotes replicate via mitosis.

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18
Q

Describe the shapes of cocci, bacilli, coccobaccilli and fusiform bacteria.

A

Cocci: round
Bacilli: rod
Coccobaccilli: between cocci & bacilli (think tic tac)
Fusiform: spindle shaped

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19
Q

Describe the morphology of Gram Negative vs. Gram Positive bacteria

A

Gram Negative - thin peptidoglycan layer, outer membrane with lipid A (O antigen)
Gram Positive - thick peptidoglycan layer

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20
Q

Describe how to write bacterial names.

A

Genus: Capital and italic
Species: italic
Subspecies: italic
Serovar or other: Captial, not italic

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21
Q

What are the 4 things that prokaryotic and eukaryotic cells have in common

A
  1. Cell Membrane 2. Cytoplasm 3. DNA 4. Ribosomes (but different types)
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22
Q

What are the 3 groups of molecules that cytoplasm contains?

A
  1. Macromolecules (proteins (enzymes), mRNA, RNA)
  2. Small molecules (energy sources, precursors of macromolecules, metabolites or vitamins)
  3. Various inorganic ions (required for enzymatic activity (cofactors))
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23
Q

What does the cytoplasm do?

A

Helps facilitate chemical reactions and helps to dissolve solutes (carbs and proteins), contains nucleoids and ribosomes.

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24
Q

What is a Nucleoid? What does a nucleoid contain?

A

It is a “nucleus-like” structure that contains: DNA (~60%), proteins, RNA

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25
Q

Describe Bacterial Chromosomal DNA

A

It is a large circular macromolecule (some bacteria have more than one). It contains the complete set of DNA for the bacteria (the whole bacterial genome)

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26
Q

Describe how DNA is compacted by proteins in the nucleoid.

A
  1. DNA loop formation caused by Nucleoid-Associated Proteins (NAPs) bound to DNA
  2. DNA supercoiling is mediated by enzymes: DNA gyrase and topolsomerase I (similar to coiling of rubber band)
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27
Q

What proteins are located in the nucleoid?

A

Proteins involved in DNA compaction & Transcription factors that regulate expression of the bacterial genome

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28
Q

What types of RNA are located in the nucleoid?

A

mRNA (messenger RNA - encodes for proteins), ncRNA (non-coding RNA - involved in DNA organization and expression of bacterial genome)

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29
Q

What is a plasmid? Are plasmids essential?

A

A plasmid is a circular molecule of DNA that replicated separately from the chromosome. It is NOT part of the nucleoid.
Plasmid genes are NOT essential under normal conditions (they are not part of the genome and not all bacteria have them).

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30
Q

Each plasmid has a defined copy number. What is a copy number? Is this copy number low or high for small plasmids? Large plasmids?

A

A copy number is the average number of plasmid copies per cell.
Small plasmids = high copy number
Large plasmids = low copy number

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31
Q

What is the importance of plasmids?

A 
Plasmids often contain genes associated with causing disease (virulence factors) or to survive in presence of antibiotics and other toxic compounds (resistance genes).
Some plasmids (conjugative plasmids) can transfer cell-to-cell by a process called conjugation
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32
Q

What does the bacterial envelope contain? What is it associated with?

A

Cytoplasmic membrane, cell wall (peptidoglycan layer), periplasmic space, outer membrane (gram-negative bacteria), capsule (some bacteria)
Envelope associated with: pili, fimbriae, flagella, secretion systems

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33
Q

What are the functions of the bacterial envelope? What about envelope-associated components?

A

Protects cell from environment/host, packages internal components, provides structural rigidity, produces energy, facilitates uptake of nutrients and efflux (removal) of toxic substances
Some envelope associated components can also (some bacteria): enable adhesion to surfaces or motility, provide resistance to some antibiotics or detergents, enable bacterial mating (conjugation)

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34
Q

In the gram staining technique - what colour does gram positive bacteria stain? gram negative?

A

Gram positive stains purple

Gram negative stains pink

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35
Q

What is present in the outer membrane of gram negative bacteria?

A

Lipopolysaccharides (LPS) aka endotoxins

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36
Q

What is the cytoplasmic membrane composed of? Where is it located?

A

Composed of phospholipid bilayer and proteins (transport proteins, energy generation and electron transport chain components required for the synthesis of ATP by the ATP synthase protein, proteins that function as anchors or help in the assembly of external structuring)
It is the inner most membrane - next to cytoplasm

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37
Q

What are the functions of the cytoplasmic membrane?

A

Functions as a selective permeability barrier (lipid soluble molecules can diffuse across membrane, transport proteins mediate the passage of hydrophilic substances into/out of the cell), plays key role in energy generation (protein motive force) and bacterial respiration (electron transport chain), serves as anchor for external structures

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38
Q

What is the cell wall? What does it do? What is in composed of?

A

Cell wall is a mesh-like essential structure that protects cell from osmotic lysis and provides mechanical protection. Consists of polymers of disaccharides that are cross linked with short chains of amino acids (peptides) by transpeptidase enzymes called Penicillin Binding Proteins (PBPs)

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39
Q

What type of bacteria is the outer membrane present in? What is its job?

A

Present in gram negative bacteria.
Prevents passive diffusion of hydrophobic/large compounds, provides resistance to toxic compounds that are hydrophobic/large (this includes several antibiotics), provides tolerance to detergents and bile salts

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40
Q

Describe the structure of the outer membrane.

A

Asymmetrical lipid bilayer - outer leaflet is mainly composed of lipopolysaccharide (LPS) (prevents diffusion of hydrophobic compounds), porin proteins, transport proteins.

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41
Q

Why does Lipopolysaccharide prevent hydrophobic substances from entering the cell?

A

Because it has a charge

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42
Q

What is the importance of the capsule of a bacteria?

A

Helps bacteria evade immune system - can prevent engulfment by white blood cells (phagocytes), aids in attachment to some surfaces, increased tolerance to antimicrobial agents

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43
Q

Describe the structure/appearance of the capsule.

A

Polysaccharide layer outside of the cell wall (in gram positive) or outer membrane (gram negative).

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44
Q

If a bacterial colony has a mucoid appearance what do the bacteria likely contain?

A

A capsule.

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45
Q

List the 4 main types of surface components and briefly describe them.

A
  1. Flagella - motility, long filamentous proteins structures
  2. Pili/Fimbriae - adhere to surfaces or bacterial interaction (biofilm), shorter/stiffer than flagella
  3. Sex pilus - bacterial conjugation (transfer of plasmids)
  4. Secretion systems - release of proteins into environment/host, secreted proteins are typically related to virulence or bacterial communication
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46
Q

List and describe the 4 types of flagellar arrangements.

A

Monotrichous - one tail
Lophotrichous - multiple tails, all on one end
Peritrichous - multiple tails, all around the bacterium
Amphitricous - two tails, one on either end

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47
Q

What are endospores?

A

Dormant bacteria that can survive in adverse environmental conditions (harsh environments) and for long periods of time.
When endospores enter a host they can revert to “active” state, multiply and cause disease

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48
Q

Which type of bacteria is more likely to be a spore-forming bacteria?

A

Gram positive

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49
Q

Define obligate aerobe, obligate anaerobe, facultative anaerobe, aerotolerant anaerobes. Which is most common in clinical practice?

A

Obligate aerobe - need oxygen to grow
Obligate anaerobe - only grow in anaerobic environment (no oxygen)
Facultative Anaerobe - typically better growth in oxygen environment (but grows in both )
Aerotolerant Anaerobes - grows better in anaerobic environment but can grow in oxygen.

Facultative Anaerobe is most common in clinical practice.

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50
Q

List the gram positive, aerobic cocci

A

Staphylococcus, Streptococcus, Enterococcus

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51
Q

List the gram positive, aerobic rods

A

Actinomycetes, Bacillus, Coryne bacterium/Nocardia, Listeria, Mycobacterium, Rodococcus

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52
Q

List the gram positive, anaerobic ros

A

Clostridium

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53
Q

List the gram negative, enterobacteriaceae (rod)

A

Escherichia coli/Shigella, Salmonella, Klebsiella/Enterobacter, Proteus, Yersinia

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54
Q

List the gram negative, non-fermentative rods

A

Bordetella, Pseudomonas/Burkholderia, Aeromonas/Vibrio, Pasteurella/Mannheimia, Haemophilus/Histophilus, Brucella, Francisella

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55
Q

List the gram negative, anaerobic rods

A

Clostridium (pilifome), Fuscobacterium

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56
Q

List the miscellaneous, curved/spiral bacteria

A

Campylobacter/Helicobacter, Brachyspira, Lawsonia, Leptospira, Treponema/Borrelia

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57
Q

List the miscellaneous, obligate intracellular bacteria

A

Anaplasma/Ehrlichia, Chlamydia/Chlamydophila, Coxiella, Rickettsia

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58
Q

List the miscellaneous, bacteria without a cell wall

A

Mycoplasma

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59
Q

Describe the phases of infection.

A

Susceptible: Not yet infected, just at risk
Latent Period: Infected, the agent is multiplying in the body, immune system is working
Infectious Period: Infected and Shedding
Noninfectious Period: Removed (dead) or recovered (immune, carrier, susceptible)

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60
Q

Describe the phases of disease.

A

Susceptible
Incubation Period: No symptoms. Lasts longer than infectious latent period.
Symptomatic Period
Non-infectious Period: removed (dead), recovered

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61
Q

Why is it important that the incubation period of disease lasts longer than the latent period of infection?

A

Because the animal can not be showing any symptoms when they become infectious.

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62
Q

Define mutualism, commensalism and parasitism.

A

Mutualism: Both are necessary and the relationship is beneficial to both.
Commensalism: Good for one, no problem for the other
Parasitism: One takes advantage of/harms the other.

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63
Q

Describe the process of disease.

A

Adhesion: bacteria adheres to something inside/outside of the body
Invasion: replicates
Toxin Release: can make you sick

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64
Q

Where is the H-antigen found? What is an antigen?

A

H-antigen is found in flagella of motile bacteria

An antigen is a toxin that induces immune system response in body

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65
Q

In what type of bacteria would you more commonly find a flagella?

A

Gram negative.

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66
Q

What is the structural protein of bacterial flagella called?

A

Flagelin

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67
Q

Where is F-antigen found?

A

Pili, Fimbria, Fibrillae

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68
Q

Define extracellular invasion. What can it lead to?

A

Do not invade cells, proliferate in extracellular environment.
Can lead to thromboses (blood clots), local use of nutrients and oxygen (that the host needs)

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69
Q

What is the immunological reaction to extracellular invasion?

A

Oxygen radicals/enzymes produced by the macrophages and neutrophils (to kill the bacteria)

70
Q

Define facultative intracellular invasion

A

Invades cells when it gives them selective advantage. Causes cell lysis in the host.

71
Q

Define obligate intracellular invasion

A

Needs host cells (can’t live outside hose cell). Causes cell lysis.

72
Q

What is a virulence factor?

A

Molecules produced by pathogens (bacteria, viruses, fungi, protozoa) that contribute to the pathogenicity of that organism

73
Q

List some virulence factors that bacteria utilize.

A

Capsule
Proteins that circumvent innate immunity
Iron uptake (bacteria need iron for growth, host body hides it)
Production of extracellular enzymes (eg that kill off WBC)

74
Q

What type of antigens do capsules contain? What are capsules made of?

A

K-antigens; made of polysaccharides, protein

75
Q

How does a capsule act as a virulence factor?

A

Colonization, invasion, adhesion, protection against phagocytosis and complement (receptor - no relation so no initiation of host defence)

76
Q

What are the 2 ways that a bacterium can get an exotoxin into the cell?

A
  1. Bacterium exports toxin into the environment (not directly into the cell) - can be taken up by pores, can cleave part of surface molecules with enzymes, can bind to receptor.
  2. Injects toxin directly into the cell.
77
Q

What are exotoxins?

A

Bacterial metabolites, proteins with high molecular weight (are antigenic) (exceptions = heat stable enterotoxin (Sta, Stb) of ETEC)

78
Q

What are anatoxins?

A

Chemically treated toxins: Toxicity decreases, antigenicity increases (used for vaccinations!)

79
Q

List the 3 types of exotoxins.

A

Type I, Type II and Type III

80
Q

How does Type I exotoxin work? Give some examples.

A

Binds to a receptor. Disturbs cellular metabolism.

Sta of ETEC, Clostridium perfringens, Staphylococci, Streptococci

81
Q

How does Type II exotoxin work? Give some examples.

A 
Causes cell wall damage. 
Staphylococcuc aureus (alfatoxin (hemolysis)), Actinobacillus pleuropneumoniae
82
Q

How does Type III exotoxins work? Give some examples.

A

Intracellular toxins.
A component: Goes intracellular.
B component: Binds the membrane
Heat labile toxin (LT) of ETEC, Shiga Toxin of VTEC, EHEV, Botulinum toxin, tetanospasmin

83
Q

What do endotoxins cause as far as disease goes?

A

Fever, general sickness, tissue damage, cardiovascular shock, death

84
Q

Why can’t you vaccinate against endotoxins?

A

Because there is a limited immune reaction to them.

85
Q

What are the functions of LPS?

A

Protection against toxic products and complement (receptors), acts as an endotoxin

86
Q

Describe the structure of LPS

A

Long external polysaccharide chain (O antigen)
Lipid A chains (hydrophobic)
Core polysaccharides connecting the O antigen to Lipid A

87
Q

What is the purpose of the O-antigen?

A

Stimulates antibody production by host cells. Host immune ells include: mast cells, coagulation factors and macrophages –> immune response = fever, tissue damage

88
Q

What is the purpose of Lipid A portion of LPS?

A

Component of endotoxic activity. Composition excludes hydrophobic molecules making it resistant to many detergents. Allows the cells to multiply. When bacterial cell lyses, LPS become endotoxin.

89
Q

List the toxins that can be present in the cell wall of gram positive bacteria.

A 
Lipoteichoic acid (LTA)
Lipoarabinomannan (mycobacteria) (LAM)
Peptidoglycan
90
Q

How many types of protein secretion systems are there? Describe Type III.

A

There are 7 types.

Type 3 is a needle-like structure that is directly inserted into the host cell and through which the protein can pass.

91
Q

How are membrane vesicles formed? What do they contain?

A

They are formed from the outer membrane. It closes in on itself forming a spheric structure.
Contain enzymes, exotoxins, DNA, signal molecules.

92
Q

List the roles of membrane vesicles.

A

Pathogenesis, signaling (quorum sensing), excretion of toxic products, killing of competitors, immunomodulation, excretion of bacterial toxic products, transformation.

93
Q

Describe how biofilms are formed.

A

Formed when bacteria switch from planktonic (free) to sessile (attached, not active). The bacteria attach to a surface and colonize. Then they produce bacteria and excrete polymers.

94
Q

What are biofilms composed of?

A

Polysaccharides, proteins, nucleic acids (DNA)

95
Q

What is the role of biofilms?

A

Reduction of host immunity, local damage, reduced susceptibility to antibiotics

96
Q

List some mechanisms bacteria have evolved to obtain iron from host cells.

A

iron-chelating compounds remove iron from host proteins (transferrin, lactoferrin), lyse erythrocytes, use an alternative (eg manganese)

97
Q

Why is iron uptake considered a virulence factor?

A

Inadequate iron interferes with the bacterial ability to infect the host cell, therefore, iron uptake systems can be considered a virulence factor.

98
Q

List 2 virulence factors related to bacteria overcoming innate immunity.

A
  1. Inhibition of the complement mediated inflammation (membrane vesicles, expel of complement factors)
  2. Intracellular multiplication - bacteria hide in cells to prevent immune system from recognizing
99
Q

What are the aspects of the cellular mechanism of innate immunity?

A

Phagocytes (Macrophages, Neutrophils), Natural Killer Cells

100
Q

List 2 phagocytes.

A

Macrophages, Neutrophils.

101
Q

List some virulence factors that overcome phagocytes?

A

Extracellular bacteria (capsule, metabolites-exotoxins), biofilm, facultative intracellular

102
Q

Define definitive host, intermediate host, and incidental host.

A

Definitive host: harbours adult or sexual stage of parasite
Intermediate host: harbours larval or asexual stage of parasite
Incidental host: unusual host, unnecessary for the maintenance of parasite in nature

103
Q

Define ectoparasite and endoparasite.

A

Ectoparasite: lives on host, causes infestations.
Endoparasite: lives in host, causes infections.

104
Q

Define acquired immunity.

A

Conferred by a host’s specific immunity response developed as a results of a previous parasitic infections.

105
Q

Define premunition.

A

resistance to reinfection or superinfection conferred by a presence of parasites that are alive but are in check by host immunity (malaria, toxoplasmosis)

106
Q

List common routes of parasite entry.

A
  1. Ingestion
  2. Skin or mucosal penetration
  3. Transplacental (prenatal)
  4. Transmammary (milk)
  5. Arthropod bite (vector)
  6. Sexual contact.
107
Q

What are the 2 ways by which parasites can cause cell and tissue damage?

A
  1. Mechanical damage

2. Toxic Products

108
Q

What are the 3 ways by which parasites can cause mechanical tissue damage?

A
  1. Blockage of internal organs (Ascans, tapeworms, schistosomes, filorial worms).
  2. Pressure atrophy (echinococcus, Cysticerci)
  3. Migration through tissues (helminthic larvae)
109
Q

What are the 3 ways that parasites create toxic products?

A
  1. destructive enzymes (Anasakiasis, schistosome cercariae, hookworms).
  2. endotoxins (african trypanosomes, malaria)
  3. toxic secretions (tick paralysis)
110
Q

List some ways by which parasites create a loss of nutrients?

A

Competition with host for nutrients (Diphyllobothrium latum), interference with nutrient absorption (Giardia duodenalis, Strongylodus stercoralis), nutrient loss (hookworm), iron loss

111
Q

What is Ancylostoma coninum and list some important aspects of it.

A

Hookworm. Latches onto mucosa of small intestine. 3 pairs of marginal teeth. Sucks blood. Transmammary into puppies - puppies usually anemic (pale mm)

112
Q

What is Ctenocephalides felis and list some important aspects of it.

A

Cat flea. Flea allergy dermatitis.

113
Q

What are the 3 main classes of parasites that can cause disease in humans?

A

Helminths, Ectoparasites, Protozoa

114
Q

What are the 3 most important things to remember when trying to diagnose a parasite?

A

SIS:
Host Species
Site of Infection
Size of Parasite

115
Q

What are the phylums and classes of parasites that are of veterinary medical importance?

A

Phylum Nemathelminthes - Class Nematoda
Phylum Platyhelminthes - Class Cestoda and Class Trematoda
Phylum Arthropoda - Class Insecta and Class Arachnida
Subkingdom Protozoa - Phylum Mastigophora and Phylum Apicomplexa (5 orders)

116
Q

What is the common name for class nematoda, cestoda and trematoda?

A 
Nematodes = Roundworms
Cestodes = Tapeworms
Trematodes = Flukes
117
Q

List all important characteristics of nematodes.

A

Free-living or parasitic, elongate/cylindrical, alimentary canal present (mouth, anus), sexes usually separate (female bigger), life cycle direct or indirect

118
Q

List all important characteristics of cestodes

A

Flat body, no alimentary canal (have specialized integument - absorb everything), scolex (holdfast organ), strobila (body) with proglottides, each proglottid is hermaphroditic, , indirect lifecycle, types of characteristic larval stages

119
Q

List all important characteristics of trematodes.

A

-dorso-ventrally flattened, leaf-like in shape, oral and ventral suckers, indirect lifecycle, usually genitally independent

120
Q

List important characteristics of insects.

A

Adults have 3 pairs of legs, segmented body (head, thorax, abdomen), antenna.

121
Q

List common insect groups in veterinary medicine.

A

Flies (Diptera), Fleas (Siphonaptera), Lice (Phthiroptera), Hemptera (bed bugs)

122
Q

List important characteristics of arachnids.

A

Nymphs and adults have 4 pairs of legs. Larvae have 3 pairs of legs. Body has cephalo-thorax and abdomen (not segmented body), no antenna but has palps.

123
Q

List common arachnid groups in veterinary medicine.

A

Ticks, mites.

124
Q

List important characteristics of protozoa.

A

Unicellular, eukaryotic. Classified based on mode of locomotion (pseudopodia, flagella, gliding, cilia)

125
Q

Define Innate Response.

A

Functions in normal/healthy host without prior exposure to invading microbes.

126
Q

Define Acquired/Adaptive Response.

A

Specific immune responses that are induced by exposure to antigen(s), the response is specific for the inducing antigen(s) and immunologic memory is generated.

127
Q

What is another term for an antibody response?

A

Humoral response

128
Q

Describe the specificity for innate immunity

A

Specific for molecules and molecular patterns associated with pathogens.

129
Q

Describe the specificity for adaptive immunity

A

Highly specific, discriminated even minor differences in molecular structure; details of microbial or non-microbial structure recognized with high specificied.

130
Q

Describe the diversity of innate immunity.

A

A limited number of germ line-encoded receptors.

131
Q

Describe the diversity for adaptive immunity

A

Highly diverse; very large number of receptors arising from genetic recombination of receptor genes.

132
Q

Describe the response time of innate immunity

A

Minutes/Hours

133
Q

Describe the response time of adaptive immunity

A

Days

134
Q

Describe the memory responses of innate immunity

A

None

135
Q

Describe the memory responses of adaptive immunity

A

Persistent memory with faster response of greater magnitude on subsequent infection

136
Q

Describe the self/non-self discrimination in innate immunity

A

Perfect. No microbe-specific patterns in host.

137
Q

Describe the self/non-self discrimination in adaptive immunity?

A

Very good; occasional failures of self/non-self discrimination results in autoimmune disease.

138
Q

Describe the soluble components of blood or tissue fluids in innate immunity

A

Many antimicrobial peptides and proteins.

139
Q

Describe the soluble components of blood or tissue fluids in adaptive immunity

A

Antibodies

140
Q

Describe the major cell types in innate immunity

A

Phagocytes (monocytes, macrophages, neutrophils), natural killer cells, dendritic cells

141
Q

Describe the major cell types in adaptive immunity

A

T Cells, B Cells, Antigen-presenting cells

142
Q

What is a constitutional factor ? List them.

A

A factor that makes one species innately susceptible and another resistant to certain infections.
Genetic, age, metabolic factors, neuroendocrine factors, environment

143
Q

What are the 3 types of natural barriers in innate immunity?

A

Mechanical, Chemical, Microbiological

144
Q

How do normal flora resist colonization by bacteria (Microbiological natural barrier)?

A

Layer formation by normal flora (compete for attachment sites + nutrients), waster product formation, immune stimulation

145
Q

What are the major functions of Type I interferons?

A

Induce resistance to viral replication in all cells.
Increase MHC Class I expression and antigen presentation in all cells.
Activate NK cells to kill virus-infected cells.

146
Q

What are the 3 types of Type I interferons? Which 2 are most important for antiviral action?

A

Alpha, Beta, and Gamma.

Alpha and Beta.

147
Q

What is the other name for interferon-alpha? What is it produced by? What is it induced by? What is its action?

A

Leukocyte interferon.
Produced by leukocytes, fibroblasts, macrophages, epithelial cells
Induced by viruses, double stranded RNA.
Antiviral action.

148
Q

What is the other name for interferon-beta? What is it produced by? What is it induced by? What is its action?

A

Fibroblast interferon.
Produced by leukocytes, fibroblasts, macrophages, epithelial cell.
Induced by viruses, double stranded RNA.
Antiviral action.

149
Q

When are IFN-alpha, IFN-beta, and IL-12 produced (time after viral infection)? When are NK cells produced? When are T cells produced?

A

Right away; within the first day; after a couple of days

150
Q

List the different cell types involved in the defence against microbes.

A 
Phagocytic cells (polymorphonuclear neutrophils, mononuclear phagocytes (monocytes in blood, macrophage in tissues), eosinophils)
Lymphocytes (B Cells, T Cells, Large granular lymphocytes (null cells or NK cells))
151
Q

What are the 3 types of phagocytic cells

A
  1. Polymorphonuclear neutrophils
  2. Mononuclear phagocytes
    Monocytes in Blood
    Macrophages in Tissue
  3. Eosinophils
152
Q

What type of cells produce antibodies?

A

Plasma cells.

B-cells become plasma cells that produce antibodies.

153
Q

What do T-cells do?

A

Cell mediated immune response = Help B cells in antibody production.

154
Q

What do large granular lymphocytes (null cells or NK cells) do?

A

Kill other rogue cells in a nonspecific manner

155
Q

What is phagocytosis?

A

Engulfment and digestion of infectious agents or other foreign bodies by phagocytic cells.

156
Q

Describe the steps of phagocytosis.

A
  1. Bacterium becomes attached to pseudopodia.
  2. Bacterium is ingested forming phagosome.
  3. Phagosome fuses with a lysosome –> Phagolysosome
  4. Lysosomal enzymes digest captured material
  5. Digestion products are released from the cell
157
Q

How does the innate immune system distinguish self from non-self?

A 
Pattern Recognition Receptors (PRRs)
        Toll-like Receptors (TLRs)
        Rig-like Receptors (RLRs)
        Complement
Missing/altered self receptors (NK cells)
158
Q

How does the adaptive immune system distinguish self from non-self?

A

Antigen presentation (MHC I)
Antibodies
T-Cell Receptors (TCRs)

159
Q

What do PRRs recognize?

A

PAMP (Pathogen Associated Molecular Patterns)

160
Q

List the mediators of antimicrobial and cytotoxic activity of macrophages/neutrophils.

A

Oxygen Dependent: Reactive oxygen intermediates, reactive nitrogen intermediates
Oxygen Independent: Defensins, tumor necrosis factor (macrophage only!), lysozyme, hydrolytic enzymes

161
Q

What is the purpose of neutrophils?

A

To phagocytize and kill extracellular bacterial and yeast pathogens in acute inflammation.
Bind bacteria, engulf them and destroy them with the toxic contents of the neutrophil granules

162
Q

How long do neutrophils live in tissues?

A

~1 day

163
Q

What cleans up dead neutrophils?

A

Macrophages.

164
Q

Describe the typical scenario for acute inflammatory response involving neutrophils.

A

Leukocytosis (increased # of WBC in blood) more specifically granulocytosis (increased # of granulocytes (specific type of WBC)) because of bacterial infection.
Large reservoirs of neutrophils released to fight infections.
Neutrophils travel to and enter the infected tissue where they engulf and kill the bacteria.
Neutrophils die.

165
Q

Where are neutrophils stored?

A

Bone marrow.

166
Q

What is an important defence against helminths?

A

Eosinophils!

167
Q

What percentage of WBC are eosinophils?

A

1-3% but this increases in parasitic infections and patients with type I hypersensitivities.

168
Q

Describe Natural Killer Cells (NK Cells). How common are they?

A

Large, granular lymphocytes that lack antigen-specific receptors (B-cells and T-cells have antigen-specific receptors).
Abundant lymphocytes - 2% of circulating WBC

169
Q

Are cytokines interferons?

A

No. Interferons are cytokines, but not all cytokines are interferons.

170
Q

What stimulates the increase of NK Cells (stimulates their division)?

A

IFN produced by infected cells and dendritic cells (when infected with virus).

171
Q

How do NK Cells kill cells?

A

Release perforins and granzymes - these perforate the membrane and trigger the release of caspase –> leads to mediated cell death

172
Q

How NK Cells recognize self vs. non-self?

A

There are 2 receptor-binding interactions that are required for discrimination:
1. Virus Infection Associated Ligand = ACTIVATES
2. MHC I Molecules = BLOCKS
Virus infected cells are prime targets because fewer MHC I on surface.

RUSVM Principles of Infectious Disease Orange Semester 2016 (2 decks)

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