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Immunology Block 1 > Micro Lectures > Flashcards

Micro Lectures Flashcards

1
Q

There are ___X more bacterial cells and ___X more microbial genes than human cells and genes

A

There are 10X more bacterial cells and 300X more microbial genes than human cells and genes

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2
Q

Bacteria are most abundant in the _____ and _____. The area with the highest amount of bacteria is the _______.

A

Bacteria are most abundant in the oral cavity and GI tract. The area with the highest amount of bacteria is the lower GI tract.

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3
Q

Are there more anaerobes or aerobes in our microbiome?

A

anaerobes

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4
Q

Less than 30% of our gut microbes are ______

A

Less than 30% of our gut microbes are CULTIVABLE

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5
Q

Most of our normal flora comes from the phylum of ______ and ______, NOT ______

A

Most of our normal flora comes from the class of FIRMICUTES and BACTEROIDETES, NOT PROTEOBACTERIA

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6
Q

Where do our gut microbes come from?

A

Consider birth methods (some exposure to mom’s bacteria during development, a lot of exposure during vaginal birth and during breast feeding)

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7
Q

Explain the relationship between normal flora and antibiotics:

A

Normal flora occupy gut niches, which makes it more difficult for pathogens to take hold. Antibiotics clear spaces for pathogens.

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8
Q

C. difficile is a ____-forming bacterium. These are not metabolically active and are extremely stable

A

C. difficile is a SPORE-forming bacterium. These are not metabolically active and are extremely stable

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9
Q

What do our gut microbes do for us?

A
  • Help digest food,
  • Produce vitamins B and K,
  • Occupy niches and exclude pathogens,
  • Train our immune systems
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10
Q

Colonization of bacteria:

A

Can happen when organisms simply get a place to stay/get attachment to a host cell or epithelial surface. Doesn’t necessarily mean that something bad will happen, but is a state of being present in the host.

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11
Q

Carrier state of bacteria:

A

A little further along in the pathogenesis process. This is when you have a pathogen that is present that may not be causing disease in that individual, but could cause disease in others.

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12
Q

Location is key in bacterial presence:

A

What’s good in the gut (e.g. C-diff is normally there in healthy people, but if gut is nicked in surgery everything that’s in GI tract gets into peritoneal cavity and then causes problems). Immune status of the host is also an important consideration.

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13
Q

Important normal flora on skin:

A

Staphylococcus epidermidis

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14
Q

Important normal flora of the nose:

A

Staphylococcus aureus

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15
Q

Important normal flora of the vagina:

A

Lactobacillus species

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16
Q

Important normal flora of the GI tract:

A

Bacterioidetes and Firmicutes (gram +); E. coli and Clostridium species

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17
Q

Sessile bacteria:

A

bacteria growing in a biofilm or attached to a surface (most real-life bacteria are sessile)

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18
Q

Planktonic bacteria:

A

Free-floating or motile bacteria not attached to a surface (most bacteria we deal with in lab are planktonic)

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19
Q

A polysaccharide capsule is a bacterial _____ factor

A

A polysaccharide capsule is a bacterial VIRULENCE factor

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20
Q

Characteristics of polysaccharide capsules:

A
  • Extracellular, but attached to gram-positive or gram-negative bacterial surface
  • Organized,
  • Covalently bound bacterial surface
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21
Q

Lipopolysaccharide (LPS or LOS):

A

Lipid A + saccharide core +/- antigen side chains; integral part of gram-negative bacterial outer membrane

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22
Q

Exopolysaccharides:

A

Secreted beyond the bacterial envelope into the environment. Do not remain attached to individual bacteria.

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23
Q

Stages in biofilm formation:

A
  1. Reversible attachment,
  2. Irreversible attachment,
  3. Polysaccharide production,
  4. Growth and formation of 3D structure,
  5. Dispersal (some bacteria become planktonic and are sent off to colonize another area)
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24
Q

In nature, ___% of bacteria live in biofilms and >___% of bacterial infections are thought to be caused by organisms growing as biofilms

A

In nature, 99% of bacteria live in biofilms and >80% of bacterial infections are thought to be caused by organisms growing as biofilms.

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25
Q

Exopolysaccharide casing of biofilm limits ______ of host defenses and antibiotics

A

Exopolysaccharide casing of biofilm limits PENETRATION of host defenses and antibiotics

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26
Q

Bacterial biofilm on an implanted inert surface:

A

“Foreign body infection.”

  1. Floating planktonic bacteria
  2. Adherent bacterial cells form biofilm.
  3. Frustrated phagocytosis, release of enzymes.
  4. Enzymes damage tissue around biofilm, planktonic bacteria released, causing dissemination and acute infection in neighboring tissue.
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27
Q

______ placement is a huge source of biofilm-mediated infection in hospitals

A

CATHETER placement is a huge source of biofilm-mediated infection in hospitals

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28
Q

Penetration of antibiotics and host immune defenses into biofilms is ______

A

Penetration of antibiotics and host immune defenses into biofilms is LIMITED.

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29
Q

Pathogen:

A

Organism that can cause disease

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30
Q

Pathogenesis:

A

Process resulting in disease

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31
Q

Pathogenicity:

A

Organism’s ability to cause disease

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32
Q

Virulence:

A

Degree of damage or disease resulting from infection

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33
Q

Infectivity:

A

Likelihood of causing infection and/or disease with exposure to a particular dose

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34
Q

ID50:

A

Infectious Dose - dose that leads to infection in 50% of exposed individuals

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35
Q

LD50:

A

Lethal Dose - dose that leads to death in 50% of exposed individuals

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36
Q

Infectious disease outcomes are influenced by multiple factors:

A

Outcome is dependent on susceptibility of host, pathogen virulence, and environmental factors.

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37
Q

Rhinovirus:

A

ss + RNA, naked virion. Causes common cold.

-High infectivity, low virulence

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38
Q

Influenza:

A

ss - RNA, segmented, enveloped. Causes flu.

-Moderate infectivity, greater virulence, host-dependent

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39
Q

Ebola:

A

ss - RNA, enveloped. Causes hemorrhagic fever.

-High infectivity, high virulence.

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40
Q

Active infection/disease:

A

Can be asymptomatic or symptomatic. Can be acute or chronic.

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41
Q

Asymptomatic vs. symptomatic active infection:

A

This describes the subjective experience of the patient - not a feature necessarily of the organism but depends on relationship with the patient. These are specific outcomes in a specific patient!!! Another patient with that same strain might be highly symptomatic.

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42
Q

Acute vs. chronic active infection:

A

These can be related. Something may start out as acute and asymptomatic. It could eventually become chronic and then also symptomatic. This is dynamic.

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43
Q

Latent infection/disease:

A

Have pathogen present but little or no replication. Nothing is happening right now, and infection is under control by some aspect of the immune system. Little or no replication. But NOT dead.

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44
Q

Endogenous acquisition/transmission of microbial agents:

A

Organism escapes from location where it is part of the normal microbiome

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45
Q

Exogenous acquisition/transmission of microbial agents:

A
  • Person to person (could be horizontal or vertical),
  • Animal to person (zoonoses),
  • Insect to person (vector borne diseases),
  • Environmental (nature, nosocomial, fomite)
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46
Q

Routes of microbial transmission:

A
  • Entry via epithelial surfaces,

- Deeper tissue penetration

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47
Q

Infection from entry via epithelial surfaces (routes):

A
  • Inhalation,
  • Ingestion,
  • Sexual contact,
  • Exposure during vaginal birth
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48
Q

Infection via deeper tissue penetration (routes):

A
  • Spread from epithelia,
  • Insect bites,
  • Cuts and wounds,
  • Organ transplants and blood transfusions
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49
Q

Describe the step-by-step process of host infection:

A
  1. Encounter: Infectious agent meets host,
  2. Entry: agent enters host,
  3. Spread: agent spreads from site of entry,
  4. Multiplication: agent multiplies within host,
  5. Damage: agent, host response, or both, cause tissue damage,
  6. Outcome: agent or host wins, or they learn to coexist
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50
Q

Microbial virulence factors:

A

Factors that promote virulence, generally not required for growth outside the infected host

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51
Q

3 main categories of microbial virulence factors:

A
  1. Structures involved in attachment, adherence, and invasion.
  2. Toxin involved in cell or tissue damage.
  3. Processes involved in immune avoidance.
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52
Q

Bacterial pili/fimbriae:

A

Filamentous structures extending from the bacterial surface. Important role in initial adherence to host cells or extracellular matrix (interactions may be nonspecific or highly specific for individual host receptors)

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53
Q

Polymers of bacterial proteins composing pili are called:

A

Pilins (may be homo- or hetero-polymers)

54
Q

Type IV pili:

A
  • Extend, bind, and retract.

- Promote surface motility, microcolony and biofilm formation, and adherence to host cells and immune system

55
Q

Type IV pili are expressed by:

A
  • Neisseria meningitidis and N. gonorrhoeae,
  • Pseudomonas aeruginosa (esp. problem in CF pts.)
  • Haemophilus influenzae,
  • Vibrio cholerae
56
Q

Pili vs. Flagella:

A
  • Both are filamentous appendages,

- Pili are shorter, thinner, and usually more numerous. Flagella are longer, thicker, and usually fewer.

57
Q

Flagella are usually ______. Their primary function is _____.

A

Flagella are usually POLAR. Their primary function is LOCOMOTION.

58
Q

What is flagella composed of?

A

Flagellin, aka H-antigen, e.g. E. coli O157:H7

59
Q

Gram negative bacteria can use type III, IV, and V systems to:

A

inject substrates into other cells (bugs or host). Type III are “bacterial nanomachines”

60
Q

Translocated substrates are called WHAT. Give 2 examples/categories.

A

Translocated substrates are VIRULENCE FACTORS. e.g. toxins and receptors.

61
Q

What is viral attachment mediated by?

A

Proteins on the surface of the virion.

62
Q

How do naked viruses attach to host cell?

A

Capsid proteins on naked viruses engage receptor on host cell. Virus enters by endocytosis.

63
Q

How do enveloped viruses attach to host cell?

A

Glycoprotein spikes on enveloped viruses engage receptor on host cell. Virus enters via membrane fusion or endocytosis.

64
Q

Describe HIV attachment to host cells:

A
  • two-part glycoprotein (GP) spike in viral envelope (GP120 and GP41).
  • GP120 binds first to CD4 on human T-cell.
  • Conformational change allows contact with co-receptor.
  • GP41 binding initiates viral envelope fusion with T-cell membrane.
65
Q

LPS toxicity:

A
  • LPS is an endotoxin, because it is an integral part of gram-negative outer membrane.
  • O-antigens can define serotypes (e.g. E. coli O157:H7)
  • Lipid A is toxic moiety (saccharide portion is helpful to identify strain, but isn’t the toxic part).
  • Potent stimulator of innate immune responses.
  • Important cause of septic shock.
66
Q

Pathogen-Associated Molecular Patterns (PAMPs):

A

Molecules on the surface of the pathogen that are recognized by the innate immune system. Part of the pathogen.
Recognized by the TLRs.

67
Q

Exotoxins:

A

-Secreted toxins by Gram positive and gram negative. Toxin genes are frequently encoded on plasmids or bacteriophage (rarely on chromosomes)

68
Q

Exotoxin classification is based on:

A

-Structure/function (e.g A+B toxins, pore-forming, superantigen)
-Site of action (e.g. neurotoxin)
[The same toxin can be named based on either]

69
Q

A+B Toxins:

A

Exotoxin. A = active. B = binding.

70
Q

Cholera toxin A+5B:

A

A subunit activates adenylate cyclase; increases cAMP; promotes secretion of electrolytes and fluid by intestinal epithelial cells = profuse watery diarrhea.

71
Q

Anthrax toxin 2A+B

A

A subunits Edema Factor (EF) and Lethal Factor (LF)
EF activates adenylate cyclase
LF cleaves cellular kinases and leads to altered signaling and cell death.

72
Q

A+B Toxin-mediated diseases

A
  1. Diptheria caused by Corynebacterium diptheriae
  2. Tetanus caused by Clostridium tetani
  3. Pertussis caused by Bordatella pertussis
73
Q

Toxoid:

A

Inactivated toxins - still immunogenic but no longer toxic (important for vaccination)

74
Q

Pore-forming toxins:

A

Generate structures that create pores in the host cell surface

75
Q

Superantigens:

A

e.g. Staphylococcal and Streptococcal Toxic Shock toxins.
Unlike normal antigen presentation, which stimulates a small number of T-cells, Superantigens stimulate massive polyclonal expansion of many T-cells (cytokine storm). Bypasses antigen specificity.

76
Q

Structures that allow for immune avoidance by microbial pathogens:

A
  • Bacterial and fungal polysaccharide capsules,
  • Antigens that induce blocking antibodies,
  • Molecules that inactivate antibodies,
  • Molecules that mimic host structures and are not recognized as foreign.
77
Q

Processes that allow for immune avoidance by microbial pathogens:

A
  • Antigenic variation,
  • Avoiding immune surveillance,
  • Suppressing immune responses.
78
Q

Polysaccharide capsules:

A

-Avoid phagocytosis, immune recognition (complement and antibody), and are a common feature of pathogens that can disseminate via bloodstream to CNS.

79
Q

Neisseria meningitidis:

A
  • Rmp protein is highly immunogenic, but antibodies don’t protect and block binding to other targets.
  • Serogroup B polysaccharide capsule is polysialic acid – mimics human antigens and is poorly immunogenic.
  • Produces IgA protease that can cleave human IgA antibodies.
80
Q

Antigenic variation:

A

During infection, pathogens express different versions of key antigens. Antibodies made against one version do not recognize later versions.

81
Q

Examples of antigenic variation:

A
  • Trypanosoma brucei protozoan cause of sleeping sickness.
  • Neisseria meningitidis and N. gonorrhoeae bacterial pathogens.
  • RNA viruses e.g. HIV, HCV, influenza virus.
82
Q

Mycobacterium tuberculosis induces formation of _____. (explain)

A

Mycobacterium tuberculosis induces formation of GRANULOMAS. Aggregates of dead cells and extracellular material that ‘wall off’ slowly replicating bacteria allowing persistence of Tb.

83
Q

Herpes virus avoids immune surveillance by:

A

Traveling from periphery to dorsal root ganglia and are latent in sensory neurons.

84
Q

Treponema pallidum expresses very few _______ – teflon pathogen of syphilis

A

Treponema pallidum expresses very few SURFACE PROTEINS – teflon pathogen of syphilis.

85
Q

HIV destroys CD4+ cells resulting in profound ________.

A

HIV destroys CD4+ cells resulting in profound immunodeficiency.

86
Q

M. tuberculosis prevents fusion of _____ and ______ in macrophages.

A

M. tuberculosis prevents fusion of phagosomes and lysosomes in macrophages.

87
Q

Classes of protein synthesis inhibitors that target the 30S ribosome:

A

Aminoglycosides and Tetracyclines

88
Q

Classes of protein synthesis inhibitors that target 50S ribosome:

A

Chloramphenicol, Macrolides, Lincosamides, Streptogramins, Oxazolidinones

89
Q

Aminoglycosides bind the ____ subunit

A

30S

90
Q

Describe the targets/effects of aminoglycosides:

A

Bactericidal, used mainly against gram - rods.

Initially penetrate bacterial envelope by disrupting LPS in outer membrane. Anaerobes are intrinsically resistant.

91
Q

Aminoglycosides are primarily used against gram negative rods, but also work against ______

A

Mycobacterium

92
Q

What bacteria produces aminoglycosides?

A

Streptomyces spp.

93
Q

Key examples of aminoglycosides:

A

Streptomycin and gentamicin

94
Q

Aminoglycosides have reduced activity at low/high pH

A

low

95
Q

What is intrinsically resistant to aminoglycosides?

A

Anaerobes

96
Q

Resistance to aminoglycosides:

A
  • Enzymatically Inactivate Drug (modification by phosphorylation, adenylation or acetylation. Enzymes encoded on mobile genetic elements).
  • Alter Drug Target (Methylation of rRNA; Mutation of ribosomal protein)
  • Alter Drug Exposure [Decreased uptake - non-specific; Increased efflux (esp. Pseudomonas aeruginosa)]
97
Q

Aminoglycosides can work synergistically with _____ (explain):

A

Can co-treat with antibacterials that target the cell envelope and PG synthesis, esp. B-lactams. This pre-weakens the structure of the envelope, allowing the aminoglycoside to get in.

98
Q

Tetracyclines bind the ___ subunit

A

30S

99
Q

Describe the general targets/effects of Tetracyclines:

A

Bacteriostatic; active against G-, G+, mycoplasma, and intracellular bacteria.

100
Q

Key examples of tetracyclines:

A

Tetracycline and doxycycline

101
Q

Absorption of tetracycline is inhibited by WHAT

A

Divalent cations (calcium and magnesium) inhibit absorption in GI tract (so avoid antacids and milk)

102
Q

Tetracycline is contraindicated in what patient populations?

A

Contraindicated in pregnancy and young children due to inhibition of bone growth and discoloration of teeth

103
Q

Why aren’t penicillins and tetracyclines given together?

A

In general, don’t combine bacteriostatic (tetracycline) and bacteriocidal (penicillin) because bacteriocidal agents require bacteria to be growing to work, and bacteriostatic inhibits the growth. (there are exceptions to this rule)

104
Q

Resistance to tetracyclines:

A
  • Alter Drug Exposure (>28 classes of efflux pumps. Most are effective against tetracycline itself, but less so against newer generations).
  • Alter Drug Target (Ribosome protection proteins. Bind to ribosome and displace drug from binding site)
105
Q

Chloramphenicol binds the ____ subunit

A

50S

106
Q

Is chloramphenicol bacteriostatic or cidal?

A

Bacteriostatic (but cidal aginst important encapsulated organisms - really depends on the combo of bugs and drugs)

107
Q

What type of bacteria does chloramphenicol work against?

A

Broad-spectrum.

108
Q

Resistance to chloramphenicol:

A

Enzymatically inactivate drug (modified by acetyl transferases; drug can’t function when acetylated)

109
Q

Why are macrolides generally only used to treat G+ and not G-?

A

Macrolides are large hydrophobic molecules and don’t easily penetrate the inner and outer membranes of Gram-negative bacteria.
[key exception is Chlamydia]

110
Q

Macrolides bind to the ___ subunit.

A

50S

111
Q

What bacteria produce macrolides?

A

Streptomyces spp.

112
Q

Key examples of macrolides:

A

Erythromycin and azithromycin

113
Q

What bacteria produce chloramphenicol?

A

None. This is synthetic.

114
Q

Lincosamides bind the ___ subunit

A

50S

115
Q

Are lincosamides bacteriostatic or cidal?

A

Bacteriostatic

116
Q

Lincosamides are used to treat which types of bacteria?

A

G+ and G- ANAEROBES

117
Q

What bacteria produce lincosamides?

A

Streptomyces lincolnensis

118
Q

Key example of lincosamide:

A

clindamycin

119
Q

Lincosamides are associated with what disease?

A

Highly associated with C. difficile-associated pseudomembranous colitis.

120
Q

Streptogramins A & B:

A

Individually bacteriostatic, bactericidal together. Each part works in a different area of elongation (initial bond formation and then addition of the next amino acid).

121
Q

Streptogramins are produced by what bacteria?

A

Streptomyces spp.

122
Q

Examples of Streptogramins:

A
  • Many individual drugs
  • Older names end in -mycin
  • Newer end in -pristins
123
Q

MLS-B resistance:

A

Resistance to Macrolides, Lincosamids, and Streptogramins B.
-Ribosome methylation by over 40 different erm (erythromycin ribosome methylation) genes.
-Some (but not all) erm genes confer cross-resistance
erm expression can be constitutive or inducible in staphylococci.
-Inducible clindamycin resistance (clinically relevant) is detected using the D-test.

124
Q

Oxaloidinones bind ___ subunit

A

50S (Relatively new class of synthetic antimicrobials, bind to 23S RNA in 50S subunit, no cross-resistance with other protein-synthesis inhibitors)

125
Q

Are Oxaloidinones bacteriocidal or static? What kind of bacteria are they used against?

A

Bacteriostatic; works against many G+ that are resistant to other antibiotics

126
Q

Example of Oxalidinone:

A

Linezolid

127
Q

Resistance to Oxalidinones

A

Alter drug target - mutations in 23S rRNA gene

128
Q

Two mechanisms of vancomycin resistance have been described in enterococci and/or staphylococci:

A

Van A locus & Van B locus

129
Q

Van A locus:

A

constitutive resistance to vancomycin resulting constant expression of D-Ala, D-Lac in the peptide side chain of PG [higher fitness cost than inducible]

130
Q

Van B locus:

A

inducible resistance resulting from temporary expression of D-Ala, D-Lac in the peptide side chain of PG [lower fitness cost than constitutive]

Immunology Block 1 (8 decks)

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