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Bio Infectious Diseases > Exam 2: Staphylococci > Flashcards

Exam 2: Staphylococci Flashcards

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Biology 101 flashcards
1
Q

enzymes that can lyse red blood cells

A

hemolysins

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2
Q

for bacteria that can secrete hyemolysins

A

Blood hemolysis plating

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3
Q

inhibits fungal growth

A

cycloheximide

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4
Q

inhibits peptidoglycan synthesis

A

LB

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5
Q

mimic D-ala-D-ala

A

LB+penicillin+cycloheximide

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6
Q

what happens when we are infected with the flu?

A
  • flu penetrates airway epithelium
  • “send help” –> CD8+ T cell
  • cytotoxic response (killing infected cells)
    • decrease phagocytes antimicrobial function
    • decrease phagocytosis
    • decrease ROS production
    • increase susceptibility to bacterial infection
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7
Q

what happened during the 1918 spanish flu H1N1?

A
  • 50% of the world was infected
  • 40-50 million died
  • even healthy young adults died
  • 95% actually died from bacterial pneumonia (secondary ico-infection)
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8
Q

how does the flu infect humans and how does it work?

A
  • endocytosis
    • membrane engulfs flu cell
    • forms endosome (has H+, hydrolytic enzymes, flu cell)
    • virus RNA replicate and go into host cell
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9
Q
  • help degrade H and N proteins

* help with viral-endosomal membrane fusion

A

staph proteases

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10
Q

what does the epidermis consist of?

A
  • keratinocytes
  • hair
  • basal layer
  • Dendritic cells
  • CD8+
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11
Q

what does the dermis consist of?

A
  • SALT

- lymph blood vessels

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12
Q

where does bacteria most likely grow in the skin?

A

most likely grow by hair follicle

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13
Q

what defenses does the skin provide against bacteria?

A
  • hard to penetrate
  • slough off; hard to adhere
  • dry, low pH
  • antimicrobial fatty acids
  • dendritic cells
  • CD8 T cells
  • SALT
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14
Q

what kind of dendritic cells are on the skin?

A

Langerhans cells (antigen presentation)

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15
Q

skin associated lymphoid tissue

A

SALT

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16
Q

how do we also prevent bacterial penetration on our skin?

A
  • handwashing

- skin microbiota

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17
Q

how do our skin microbiota protect us?

A

occupy a nutrient niche and secrete antimicrobial compounds

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18
Q

how can bacteria be classified?

A
  • gram staining (+/-. shape/size)
  • O2 requirement
  • salt
  • temperature
  • pH
  • nutritional (autotroph/heterotroph, etc)
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19
Q

what are the two types of positive bacteria from gram staining?

A

rod shape and cocci

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20
Q

what are the rod shape bacteria?

A
  • Listeria

- clostridium bacillus

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21
Q

what are the divisions of cocci bacteria?

A

*they can either be catalase + (bubbles) or catalase - (H2O2–> O2 + H2O)

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22
Q

if a coccus bacteria is catalase +, what kind of bacteria is it?

A

Staphyloccocus

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23
Q

if a coccus bacteria is catalase -, what kind of bacteria is it?

A

streptococcus

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24
Q

what are the divisions of staphylococcus?

A

coagulase + (clot) and coagulase -

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25
Q

If a staphylococcus bacteria is coagulase +, what specific bacteria is it?

A

staphylococcus aureus (usually beta hemolysis)

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26
Q

if a staphyloccous bacteria is coagulase -, what specific bacteria is it?

A

staphylococcus epidermis

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27
Q

what can streptococcus bacteria perform?

A

hemolysis

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28
Q

can perform beta hemolysis

A

Group A and B streptococcus

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29
Q

can perform alpha hemolysis (partial clearing)

A

streptococcus pneumonia

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30
Q

perform gamma hemolysis, which is no hemolysis

A

enterococcus

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31
Q

what is an example of technology being developed without consulting microbiologists?

A

double absorbing action tampons

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32
Q

what did double absorbing action tampons?

A

toxic shock syndrome

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33
Q

what is toxic shock syndrome caused by?

A

release of poisonous substances from an overgrowth of bacteria called Staphylococcus aureus

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34
Q

what are the characteristics of s. aureus?

A
  • gram +
  • catalase activity +
  • coagulase +
  • very well human adapted pathogen
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35
Q

what are the requirements for infection of s. aureus?

A
  1. adhesion and survival
  2. invasion and damage
  3. secrete other toxins (virulence factors)
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36
Q

What is involved in adhesion and survival for s. aureus? In other words, how does s.aureus adapt the the challenges of the skin?

A
  1. s. aureus can survive on dry inanimate objects
  2. has wide ranges of pH survival (4-10)
  3. expresses lipases which cleave fatty acids and use smaller parts for carbon source
  4. express MSCRAMMs (adhesion molecules)
  5. adheres to our collagen
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37
Q

microbial surface components recognizing adhesive matrix molecules

A

MSCRAMMs

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38
Q

what does bacteria add to the membrane of the host and how does it change it?

A
  • *antimicrobial peptides are +
    • bacteria adds D alanine to modify the charge
    • adds L-lysine
    • results in negative charges at surface
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39
Q

what does s. aureus do to invade and damage a host?

A
  1. Hydrolytic enzymes
    • lipases
    • proteases (degrade host proteins + antimicrobial peptides)
    • DNases (degrade DNA; effective against NETs)
  2. cuts, burns, insect bites, or wounds make it easier for invasion
  3. pore forming toxin
    • alpha toxin—> Beta hemolysis
    • leukocidins—> form pores on leukocytes
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40
Q

what toxins do s. aureus secrete?

A
  • exfoliative toxins
  • enterotoxins
  • super antigens
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41
Q

what is the exfoliative toxin that s. aureus secretes?

A

serine proteases

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42
Q

cleave keratinocyte proteins, which hold the skin together

A

serine proteases

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43
Q

who are more susceptible to serine proteases?

A

infants/newborns and immunocomprimised adults

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44
Q

what do newborns often develop because of serine proteases?

A

staphylococcal scalded skin syndrome

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45
Q
  • found in GI
  • causes food poisoning in gut
    • emetic and diarrheal symptoms
  • causes toxic shock syndrome in blood
    • acts as superantigen
A

enterotoxins

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46
Q

what is an example of a superantigen?

A

toxic shock syndrome toxin-1

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47
Q

what are the effects of superantigens?

A
  • polyclonal expansion (non-specific)

* massive T cell activation –> systemic inflammatory responses)

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48
Q

how do superantigens achieve polyclonal expansion?

A

the superantigens are present when the antigen on the antigen presenting cell, with the MHC II, binds with the toll like receptors on the T cell

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49
Q

how does Staphyloccus deal with the immune system?

A
  1. it is a well adapted human pathogen
  2. opportunisitic pathogen - always comes down to neutrophils vs staph
  3. LD50
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50
Q

how do the levels of LD 50 compare in a healthy and weak host?

A
  • takes more LD50 to kill a healthy host

* takes less LD50 to kill a weak host

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51
Q

how do the levels of LD50 compare in a virulent staph and an attenuated host?

A
  • less LD50 in a virulent staph

* more LD50 in an attenuated staph

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52
Q

How does staph react to the host immune response?

A

*staph has proteins that bind to Fc

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53
Q

what are staphs proteins that bind to Fc?

A
  • protein A
  • protein Sbi
  • SSL7
  • SSL10
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54
Q

binds to IgG

A

protein A

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55
Q

second binding protein of immunoglobulin

A

protein Sbi

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56
Q

staphyloccocal superantigen like protein 7

A

SSL7

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57
Q

binds to IgG

A

SSL10

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58
Q

what happens when staph proteins bind to Fc?

A

the cell is not available for phagocytosis

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59
Q

what happens in the complement system?

A

C3——-> C3a + C3b

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60
Q

chemoattractant

A

C3a

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61
Q

acts as a label for opsonization

A

C3b

62
Q
  • enzyme that cleaves C3

* pathogen activates this enzyme

A

C3 convertase

63
Q

**refers to an immune process where particles such as bacteria are targeted for destruction by an immune cell known as a phagocyte
a means of identifying the invading particle to the phagocyte

A

opsonization

64
Q

how does staph react to the complement system?

A
  1. SCIN
  2. staphylokinase
  3. Efb
65
Q
  • staphylococcal complement inhibitor

* inhibits C3 convertase

A

SCIN

66
Q

*activates human protease—>degradation of C3b

A

staphylokinase

67
Q
  • extracellular fibrinogen binding protein

* binds C3 to prevent cleavage

A

Efb

68
Q

what are the receptors of chemoattractants?

A
  • **chemokines
    1. C3a
    2. CXC#
    3. CXCL #
69
Q

What does Staph do to inhibit chemoattractants?

A
  1. CHIPS
  2. FLIPr
  3. Staphopain A
70
Q
  • chemotaxis inhibitory proteins of S. aureus

* binds to receptor of chemoattractants

A

CHIPS

71
Q

binds to receptors of chemoattractants

A

FLIPr

72
Q

cleaves CXCR2 (protease)

A

staphopain A

73
Q

needed to bind to adhesion molecules on endothelium for chemotaxis

A

neutrophils

74
Q

What does staph do to inhibit adhesion molecules on the endothelium to prevent chemotaxis of neutrophils?

A
  1. SEIX

2. SSL5

75
Q
  • staphyloccocal enterotoxin like toxin X

* bind to neutrophils receptors for adhesion molecules

A

SEIX

76
Q

bind to neutrophills receptors for adhesion molecules

A

SSL5

77
Q

recognizes lipoproteins—->inflammation

A

TLR2

78
Q

what does staph do to inhibit TLR2?

A
  1. staphylococcal iron transporter C (SITC)

2. SSL3

79
Q

binds to TLR2 and blocks it from TLR2 signaling

A

SSL3

80
Q

what does staph do to inhibit antimicrobial peptides (AMP+)?

A
  1. DLT
  2. MprF
  3. staphylokinase
  4. aureolysin
  5. forms biofilm
81
Q

add D-alanine + to teichoic acid -, which increases electrostatic repulsion

A

DLT

82
Q

add L-lysine + to phospholipid -, which increases electrostatic repulsion

A

MprF

83
Q

binds AMP

A

staphylokinase

84
Q

degrades AMP

A

aureolysin

85
Q

secretes hydrolytic enzymes (degrade) and NETs (trap)

A

neutrophils

86
Q

what does staph do to inhibit neutrophils?

A
  1. DNase

2. Eap

87
Q

deal with NETs

A

DNase

88
Q
  • extracellular adherence protein

* inhibit proteases from neutrophils

A

Eap

89
Q

what does staph do to inhibit neutrophils and ROS?

A
  1. superoxide dismutase
  2. catalase
  3. staphyloxanthin
  4. methionine sulfoxide
90
Q

OH—> H2O2 + O2

A

superoxide dismutase

91
Q

H2O2—-> O2 + H2O

A

catalase

92
Q
  • yellow pigment/cartenoid

* acts as antioxidant for staph

A

staphyloxanthin

93
Q

reductase

A

methionine sulfoxide

94
Q
  • transmitted without awareness
  • is everywhere
  • multiple drug resistance
A

antibiotic resistance (Abx^R)

95
Q

what was the earliest antibiotic?

A

tetracycline 350-500 BC

96
Q

what was tetracylcine made by?

A

bacteria streptomyces in soil

97
Q

enzyme that can cleave penicillin

A

B-lactamase

98
Q

developed because B-lactamase cant cleave it

A

methicillin

99
Q

where is MRSA commonly found?

A
  • hospitals

* pigs/farms

100
Q

what is B-lactamase encoded by?

A

gene blaZ

101
Q

how many types of B-lactamase are there?

A

more than 100

102
Q

resistance mechanism encoded by gene MecA

A

methicillin

103
Q

encodes penicillin binding protein 2a (PBP2a)

A

gene MecA

104
Q

has poor methicillin binding

A

transpeptidase

105
Q

normal PBP vs. MecA PBP2a

A
  1. if you put two cultures together, normal PBP will grow faster
  2. If there is methicillin, normal PBP will be inhibited and MecA will grow faster
106
Q

why can MRSA spread fast?

A

because MecA is found in the mobile genetic element

107
Q

mobile genetic element of MRSA

A

staphyloccocal casette chromosome (SCC)

108
Q

when does SCC have a higher expression?

A

if it is close to the origin of replication

109
Q

allow multiple casettes to come together—-> resistance to multiple drugs

A

direct repeats

110
Q
  • binds to transpeptidase substrate— binds D-ala-D-ala

* no transpeptidation

A

vancomycin

111
Q
  • came from enterococcus

* resistance is on plasmid that can facilitate conjugation

A

Van^R

112
Q

transfer plasmid to another bacteria

A

conjugation

113
Q
  • plasmid DNA

* jump to recipient and integrate to host DNA

A

transposon

114
Q

what are the multiple gene products of Vancomycin?

A
  1. Van^R
  2. Van^x
  3. VanH
  4. VanA
115
Q

cleaves D-ala-D-ala

A

Van^x

116
Q

pyruvate—->D-lactate

A

VanH

117
Q

synthesize D-ala-D-lactate

A

VanA

118
Q

what are the antibiotic resistance mechanisms?

A
  1. alter Abx
  2. alter abx target
  3. decrease intracellular abx accumulation
  4. form biofilm
119
Q

what does decreasing the intracellular abx accumulation involve?

A
  • decrease porin (channels on outer membrane) expression

* increase eflux pump expression (transfer intracellular stuff to the outside)

120
Q

How is antibiotic resistance being combatted?

A
  1. drug repurposing
  2. combination drug
  3. making derivatives of exhisting drugs/antibiotics
  4. rethinking antibiotic susceptibility testing
  5. discover new drugs
  6. random chemical sensing (targeted screening) microbiota
121
Q

B lactam drug and B lactamase inhibitors

A

combination drug

122
Q

what does rethinking antibiotic susceptibility testing?

A

MIC in artificial media

123
Q

ihibits s.aureus and types of gram + bacteria

A

lugdunin

124
Q

what happened when a human survey on lugdunin was conducted?

A

people positive for lugdunin have less s. aureus

125
Q

Which of the following terms is most related/similar to “virulence”?

A

pathogenicity

126
Q

Which of the following surface features of microbes can be used as tools for adhesion?

A

flagella
pili
capsule

127
Q

True or False: Infection refers to a situation where foreign organisms have cause damages inside a host.

A

false

128
Q

True or false: An opportunistic pathogen causes diseases when the host resistance is compromised.

A

true

129
Q

A pathogen is more virulent if the LD50 is a larger number.

A

false

130
Q

true or false: Dental plaque contains multiple species of microbes.

A

true

131
Q

If you get rid of both of the pathogenicity islands in Salmonella, would the resulting mutant be less or more virulent than the wildtype bacteria?

A

less virulent

132
Q

Pathogenicity islands can be mobile genetic elements and be transffered to a non-pathogen to make it become a pathogen.

A

true

133
Q

True or false: Attenuated bacteria are dead bacteria

A

false

134
Q

True or false: Pathogens may have a very specific host target that they bind to during infections.

A

true

135
Q

true or false: Staphylococcus can cause infections in multiple sites of our bodies.

A

true

136
Q
  • a virulence factor produced by Staphylococcus aureus
  • a bacterial enzyme with a human substrate
  • the cause of fibrin accumulation around Staphylococcus aureus cells during infections
A

coagulase

137
Q

true or false: Toxic shock syndrome is only caused by Staphylococcus aureus.

A

false

138
Q

what is the purpose for including phenol red in mannitol-salt agar?

A

to indicate a reduction in pH

139
Q

true or false: If a patient sample is positive for the presence of mecA gene, then methicillin should not be prescribed to that patient.

A

true

140
Q

which of the following is NOT a function of neutrophils?
A. Chemotaxis
B. Secretion of antibodies
C. Phagocytosis
D. Production of reactive oxygen species

A

B secretion of antibodies

141
Q

true or false: Macrophages are involved in cleaning up after neutrophils.

A

true

142
Q

A Staphylococcus aureus mutant lacking catalase will not be able to?

A

survive through reactive oxygen species

143
Q

true or false: Adding alanine to cell wall teichoic acids makes the bacteria have more negative charges at the surface.

A

false

144
Q

**Staphyloccocus aureus also produces DNase to help evade immune defense mechanisms. Which of the following immune responses is most likely to be rendered ineffective by DNase?
A. Neutrophil extracellular traps
B. Antigen presentation
C. Production of reactive oxygen species
D. Phagocytosis

A

A. neutrophil extracellular traps

145
Q

What evidence did the authors show to suggest that the genes encoding the synthesis of lugdunin are likely from other organisms?

A

GC content

146
Q

How did the authors manage to purify lugdunin for in-depth chemical analysis?

A

Over-express the genes with a strong, inducible promoter

147
Q

How did the authors test whether or not lugdunin has a toxic effect on mammalian cells

A

Lactate dehydrogenase release assay

148
Q

True or false: An antibiotic is more potent if it has a high MIC

A

false

149
Q

What is the specific molecular target of lugdunin?

A

it is unknown

150
Q

Consider the fact that lugdunin is not produced when the bacteria are grown in liquid culture, what is the most likely outcome if you co-culture S. lugdunesis and S. aureus in liquid culture?

A

S. aureus growth is not inhibited

Bio Infectious Diseases (10 decks)

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