Bailey Flashcards

1
Q

Oligotrophs

A

Can grow with limited nutrients

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2
Q

Microaerophiles

A

Require lower levels of oxygen

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3
Q

Mesophiles

A

Grow well in mild temps (15-45 Celsius/59-113 F)

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4
Q

Gram + bacteria membrane

A

Murein/Peptidoglycan cell wall outside of the cell membrane

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5
Q

Gram - bacteria membrane

A

Thin Murein layer between 2 layers of cell membrane

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6
Q

Structure of Murein

A

Nam & Nag backbone

Nams are connected by cross-linked peptides

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7
Q

Difference in peptide chain bonding in Murein between gram + and -

A

In gram + lysine binds to alanine via pentameric glycine

In gram - DAP binds to alanine

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8
Q

What is a common target for antibiotics?

A

Biosynthesis of Murein

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9
Q

Surface structure of gram + bacteria

A

Teichoic acid

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10
Q

Surface structure of gram - bacteria

A

LPS (Lipopolysaccharide)

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11
Q

Structure of LPS

A

Lipid A
Polysaccharide core
O-antigen (highly variable - defines type of bacteria)

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12
Q

Function of LPS

A

Induces TNF-alpha which leads to septic shock at high levels (shock/organ failure/low bp)

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13
Q

What are PAMPs?

A

Pathogen associated molecular patterns

LPS and Teichoic acid are PAMPs

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14
Q

How do cells of the immune system recognize PAMPs?

A

Using PRRs (pattern recognition receptors)

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15
Q

TLR 4 recognizes what

A

LPS (Gm -)

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16
Q

TLR 2 recognizes what

A

Peptidoglycan (Gm +)

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17
Q

TLR 2+6 recognize what

A

Teichoic acids (Gm +)

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18
Q

TLR 5 recognizes what

A

Flagella

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19
Q

3 additional extracellular structures on bacteria

A

Pili (fimbriae)
Flagella
Glycocalyx

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20
Q

Pili function

A

Attach bacteria to cells & other surfaces

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21
Q

Adhesins definition & function

A

Specialized proteins on tip of fimbriae specifically developed for adherence (major cause of virulence)

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22
Q

Monotrichous bacteria

A

1 flagella

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23
Q

Lophotrichous bacteria

A

A few flagella

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24
Q

Petritrichous bacteria

A

Has flagella everywhere

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25
Q

Which direction of flagella turning results in a run & which makes it tumble?

A
CCW = run (pushes forward)
CW = tumble (goes backward/tangled)
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26
Q

Taxis definition

A

Movement of bacteria that is directed (either toward something good or away from bad)

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27
Q

Glycocalyx definition/types/structure

A

D - Substance that surrounds a cell
T - 1. Capsule- Well organized,firmly attached layer
2. Slime layer- Not well organized or firmly
attached
S - Usually made of polysaccharides, but can include monosaccharides & glycoproteins

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28
Q

Function of capsule

A

Masks LPS/Teichoic acids

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29
Q

Can the immune system ever recognize and encapsulated bacteria?

A

Yes via TLR 5 recognizing flagella or sometimes the capsular polysaccharide

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30
Q

What does the O antigen in a serological designation represent?

A

Presence of LPS

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31
Q

What does the H antigen represent?

A

Flagella

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32
Q

What does the K antigen represent?

33
Q

2 broad classes of bacterial pathogens

A
  1. Opportunistic

2. Primary

34
Q

What are the virulence determinants that make a bacterial pathogen a primary class?

A
  1. Adhere
  2. Colonize
  3. Invade
  4. Induce damage
35
Q

Methods of adherence

A

-Nonspecific
-Specific
~Irreversible
~Anchoring
Via adhesins (often found on fimbriae)
Can also occur by binding to fibronectin in plasma
and associated with mucosal surfaces

36
Q

What is a limiting factor of colonization?

A

Nutrient availibility

37
Q

How do bacteria take up nutrients?

A
  1. Carrier-mediated diffusion (facilitated)
  2. Phosphorylation-linked transport (group translocation)
  3. Active transport (energy dependent)
38
Q

What is the action of hyaluronidase?

A

Degrades hyaluronic acid (which is a common component of the ECM)

39
Q

What is the action of collagenase?

A

Degrades collagen (which is an important component of connective tissue)

40
Q

What does Type I exotoxin do?

A

Membrane acting

Toxins bind surface receptors and stimulate transmembrane signals

41
Q

What does Type II exotoxin do?

A

Membrane damaging

Toxins directly affect host cell membranes (ex. create pores)

42
Q

What does Type III exotoxin do?

A

Intracellular effectors

Get into the host cell and induce enzymatic activity

43
Q

What is the ideal therapeutic index for an antibiotic?

A

A high number

44
Q

What does a therapeutic index of 1 indicate?

A

You need a toxic does in order to eradicate the miccrobe

45
Q

What is therapeutic index?

A

Ratio of toxic dose:effective dose

46
Q

What are the 5 ways that antibiotics inhibit bacteria?

A
  1. Inhibition of cell wall synthesis
  2. Disruption of cell membrane function
  3. Inhibition of protein synthesis
  4. Inhibition of nucleic acid synthesis
  5. Action as antimetabolites (needed for bacterial replication)
47
Q

How does penicillin disrupt cell wall synthesis?

A

Cleaves ala bond (cleaves the cross-linking peptides of Murein)

48
Q

Methods of antibacterial inhibition of protein synthesis

A

Prevent 30S or 50S subunits from forming

Prevent ribosomes from recognizing RNA

49
Q

What is one inhibitor of DNA replication that isn’t toxic to human cells

A

Metronidazole
It is inert, but can be converted to an active form by anaerobic microbes
Used for abscesses & periodontitis

50
Q

What are the methods of inhibiting nucleic acid synthesis

A
  • Inhibiting DNA replication (most too toxic though)
  • Affecting DNA gyrase (gyrase relieves strain while DNA is unwound by helicase)
  • Inhibit RNA polymerase
51
Q

Steps in the action of antibiotics

A
  1. Drug penetrates the envelope
  2. Transport into the cell
  3. Drug binds to target
52
Q

Mechanisms of drug resistance

A
  1. Synthesis of enzymes that inactivate the drug
  2. Prevention of access to the target site
    a. Inhibiting uptake
    b. Increasing secretion of the drug
  3. Modification of the target site
53
Q

Example of enzymes that inactivate antibiotics

A

B-lactamases inactivate b-lactin antibiotics like penicillin

54
Q

Example of preventing access of antibiotics to their target site

A

Some bacteria develop efflux pumps to pump antibiotics out of them

55
Q

Example of modification of target site

A

Alteration of metabolic pathway

Modify enzyme affinity

56
Q

How does antibiotic resistance spread?

A
  1. Chromosome associated resistance
  2. Plasmid mediated resistance (most common)
  3. Rapid spread of resistance
57
Q

How do you combat an antibiotic resistant pathogen?

A

Synergism
Antagonism
Indifference (many antibiotics are indifferent)?

58
Q

Are antibiotics effective against all microbes?

A

NO

not against viruses

59
Q

Identifying factors of streptococci

A
Gm +
Chains or diplococci
Non-spore forming
Facultative anaerobes
Catalase negative
Infect humans & animals
60
Q

Methods of classifying streptococci

A
  1. Hemolysis pattern (alpha, beta, gamma)
  2. Lancefield group (Displays A-U antigen on cell wall/+ or - agglutination)
  3. Species
61
Q

Alpha hemolysis in blood agar

A

Partial hemolysis and green discoloration of hemoglobin

62
Q

Beta hemolysis in blood agar

A

Clear zone of complete hemolysis

63
Q

Gamma hemolysis in blood agar

A

No zone of clearing

64
Q

Group A streptococcal diseases

Beta-hemolytic

A
  • Acute pharyngitis (strep throat)
  • Scarlet fever (strep throat + rash)
  • Pyoderma (skin infections)
  • Group A streptococcal pneumonia
  • Necrotizing fasciitis & myositis (hospital gangrene & flesh-eating bacteria)
  • Childbed fever
  • Foodborne outbreaks
65
Q

What is the cause of Group A streptococcal (GAS) infections?

A

S. pyogenes

66
Q

What are the sites of infection for ARF?

A

Acute Rheumatic Fever -

Pharynx is the only site of infection that is followed by ARF

67
Q

How to prevent ARF

A

Acute Rheumatic Fever -
Treating strep throat with full course of penicillin will prevent ARF (cannot treat it with penicillin after it has started)

68
Q

APSGN

A

Acute Post-Streptococcal Glomerulonephritis
Inflammation of glomeruli of kidneys causes smoky urine
Can follow pharyngitis or impetigo infections

69
Q

Where are group A infections encountered?

A
  • Live on skin & mucous membranes (20% of school-aged children carry w/o symptoms)
  • Infected respiratory droplets
  • Hand-to-hand-to-mouth
  • Food
  • Skin/wound infections
    • Towels
    • Shed skin
70
Q

Methods of entry of group A infections

A

Cannot penetrate intact skin
Bacteria bind to epithelial cells via adhesins
-Lipoteichoic acid (LTA) binds fibronectin
-Protein F binds fibronectin
-M protein binds keratinocytes

71
Q

Methods of spread of group A infections

A

Remains localized on skin or mucous membranes

Spreads rapidly in deeper tissue infections

72
Q

Group A bacteria avoid phagocytosis via

A

M protein - binds host serum proteins/inhibits formation of opsonins
Hyaluronic acid capsule - mucoid capsule that makes it slippery, interfering with phagocyte attachment
C5a peptidase - inactivates phagocyte chemotaxin

73
Q

Superantigens

A

Mimic the effects of endotoxins (activated T cells release of cytokines)
Cause toxic shock syndrome

74
Q

GBS

What is it? Where is it? What does it cause?

A
Group B Streptococci
Beta-hemolytic
Has a different polysaccharide capsule
Inhabit lower GI & female genital tracts
Cause cellulitis, arthritis, and meningitis
75
Q

GDS

A

Group D Streptococci
Alpha or Gamma hemolytic
Enterococci and nonenterococci
Normal flora of GI & genitourinary tracts
-Low virulence, usually accompany other bacterial infections

76
Q

Enterococci

A

Worlds toughest pathogenic bacteria
Antibiotic synergism required (penicillin & an aminoglycoside)

VRE
Low virulence but untreatable
Can transfer vancomycin resistance to staphylococci

77
Q

Nonenterococcal group D streptococci

A

S. bovis - most common for human disease
Subacute bacterial endocarditis - abnormal heart valves (most commonly caused by viridians streptococci)
Bacteremia - colonic lesions

Most strains are killed by penicillin, do not grow in high salt

78
Q

Viridans streptococci

A
Alpha hemolytic (greening)
30-60% of orophayngeal flora 
Low virulence
Most common cause of subacute bacterial endocarditis
Responsible for dental caries