Exam 2: Staphylococci Flashcards
(150 cards)
1
Q
enzymes that can lyse red blood cells
A
hemolysins
2
Q
for bacteria that can secrete hyemolysins
A
Blood hemolysis plating
3
Q
inhibits fungal growth
A
cycloheximide
4
Q
inhibits peptidoglycan synthesis
A
LB
5
Q
mimic D-ala-D-ala
A
LB+penicillin+cycloheximide
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
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)
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
9
Q
- help degrade H and N proteins
* help with viral-endosomal membrane fusion
A
staph proteases
10
Q
what does the epidermis consist of?
A
- keratinocytes
- hair
- basal layer
- Dendritic cells
- CD8+
11
Q
what does the dermis consist of?
A
- SALT
- lymph blood vessels
12
Q
where does bacteria most likely grow in the skin?
A
most likely grow by hair follicle
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
14
Q
what kind of dendritic cells are on the skin?
A
Langerhans cells (antigen presentation)
15
Q
skin associated lymphoid tissue
A
SALT
16
Q
how do we also prevent bacterial penetration on our skin?
A
- handwashing
- skin microbiota
17
Q
how do our skin microbiota protect us?
A
occupy a nutrient niche and secrete antimicrobial compounds
18
Q
how can bacteria be classified?
A
- gram staining (+/-. shape/size)
- O2 requirement
- salt
- temperature
- pH
- nutritional (autotroph/heterotroph, etc)
19
Q
what are the two types of positive bacteria from gram staining?
A
rod shape and cocci
20
Q
what are the rod shape bacteria?
A
- Listeria
- clostridium bacillus
21
Q
what are the divisions of cocci bacteria?
A
*they can either be catalase + (bubbles) or catalase - (H2O2–> O2 + H2O)
22
Q
if a coccus bacteria is catalase +, what kind of bacteria is it?
A
Staphyloccocus
23
Q
if a coccus bacteria is catalase -, what kind of bacteria is it?
A
streptococcus
24
Q
what are the divisions of staphylococcus?
A
coagulase + (clot) and coagulase -
25
If a staphylococcus bacteria is coagulase +, what specific bacteria is it?
staphylococcus aureus (usually beta hemolysis)
26
if a staphyloccous bacteria is coagulase -, what specific bacteria is it?
staphylococcus epidermis
27
what can streptococcus bacteria perform?
hemolysis
28
can perform beta hemolysis
Group A and B streptococcus
29
can perform alpha hemolysis (partial clearing)
streptococcus pneumonia
30
perform gamma hemolysis, which is no hemolysis
enterococcus
31
what is an example of technology being developed without consulting microbiologists?
double absorbing action tampons
32
what did double absorbing action tampons?
toxic shock syndrome
33
what is toxic shock syndrome caused by?
release of poisonous substances from an overgrowth of bacteria called Staphylococcus aureus
34
what are the characteristics of s. aureus?
- gram +
- catalase activity +
- coagulase +
- very well human adapted pathogen
35
what are the requirements for infection of s. aureus?
1. adhesion and survival
2. invasion and damage
3. secrete other toxins (virulence factors)
36
What is involved in adhesion and survival for s. aureus? In other words, how does s.aureus adapt the the challenges of the skin?
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
37
microbial surface components recognizing adhesive matrix molecules
MSCRAMMs
38
what does bacteria add to the membrane of the host and how does it change it?
* *antimicrobial peptides are +
- bacteria adds D alanine to modify the charge
- adds L-lysine
- results in negative charges at surface
39
what does s. aureus do to invade and damage a host?
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
40
what toxins do s. aureus secrete?
* exfoliative toxins
* enterotoxins
* super antigens
41
what is the exfoliative toxin that s. aureus secretes?
serine proteases
42
cleave keratinocyte proteins, which hold the skin together
serine proteases
43
who are more susceptible to serine proteases?
infants/newborns and immunocomprimised adults
44
what do newborns often develop because of serine proteases?
staphylococcal scalded skin syndrome
45
- found in GI
- causes food poisoning in gut
* emetic and diarrheal symptoms
- causes toxic shock syndrome in blood
* acts as superantigen
enterotoxins
46
what is an example of a superantigen?
toxic shock syndrome toxin-1
47
what are the effects of superantigens?
* polyclonal expansion (non-specific)
| * massive T cell activation --> systemic inflammatory responses)
48
how do superantigens achieve polyclonal expansion?
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
49
how does Staphyloccus deal with the immune system?
1. it is a well adapted human pathogen
2. opportunisitic pathogen - always comes down to neutrophils vs staph
3. LD50
50
how do the levels of LD 50 compare in a healthy and weak host?
* takes more LD50 to kill a healthy host
| * takes less LD50 to kill a weak host
51
how do the levels of LD50 compare in a virulent staph and an attenuated host?
* less LD50 in a virulent staph
| * more LD50 in an attenuated staph
52
How does staph react to the host immune response?
*staph has proteins that bind to Fc
53
what are staphs proteins that bind to Fc?
- protein A
- protein Sbi
- SSL7
- SSL10
54
binds to IgG
protein A
55
second binding protein of immunoglobulin
protein Sbi
56
staphyloccocal superantigen like protein 7
SSL7
57
binds to IgG
SSL10
58
what happens when staph proteins bind to Fc?
the cell is not available for phagocytosis
59
what happens in the complement system?
C3-------> C3a + C3b
60
chemoattractant
C3a
61
acts as a label for opsonization
C3b
62
* enzyme that cleaves C3
| * pathogen activates this enzyme
C3 convertase
63
**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
opsonization
64
how does staph react to the complement system?
1. SCIN
2. staphylokinase
3. Efb
65
* staphylococcal complement inhibitor
| * inhibits C3 convertase
SCIN
66
*activates human protease--->degradation of C3b
staphylokinase
67
* extracellular fibrinogen binding protein
| * binds C3 to prevent cleavage
Efb
68
what are the receptors of chemoattractants?
* **chemokines
1. C3a
2. CXC#
3. CXCL #
69
What does Staph do to inhibit chemoattractants?
1. CHIPS
2. FLIPr
3. Staphopain A
70
* chemotaxis inhibitory proteins of S. aureus
| * binds to receptor of chemoattractants
CHIPS
71
binds to receptors of chemoattractants
FLIPr
72
cleaves CXCR2 (protease)
staphopain A
73
needed to bind to adhesion molecules on endothelium for chemotaxis
neutrophils
74
What does staph do to inhibit adhesion molecules on the endothelium to prevent chemotaxis of neutrophils?
1. SEIX
| 2. SSL5
75
* staphyloccocal enterotoxin like toxin X
| * bind to neutrophils receptors for adhesion molecules
SEIX
76
bind to neutrophills receptors for adhesion molecules
SSL5
77
recognizes lipoproteins---->inflammation
TLR2
78
what does staph do to inhibit TLR2?
1. staphylococcal iron transporter C (SITC)
| 2. SSL3
79
binds to TLR2 and blocks it from TLR2 signaling
SSL3
80
what does staph do to inhibit antimicrobial peptides (AMP+)?
1. DLT
2. MprF
3. staphylokinase
4. aureolysin
5. forms biofilm
81
add D-alanine + to teichoic acid -, which increases electrostatic repulsion
DLT
82
add L-lysine + to phospholipid -, which increases electrostatic repulsion
MprF
83
binds AMP
staphylokinase
84
degrades AMP
aureolysin
85
secretes hydrolytic enzymes (degrade) and NETs (trap)
neutrophils
86
what does staph do to inhibit neutrophils?
1. DNase
| 2. Eap
87
deal with NETs
DNase
88
* extracellular adherence protein
| * inhibit proteases from neutrophils
Eap
89
what does staph do to inhibit neutrophils and ROS?
1. superoxide dismutase
2. catalase
3. staphyloxanthin
4. methionine sulfoxide
90
OH---> H2O2 + O2
superoxide dismutase
91
H2O2----> O2 + H2O
catalase
92
* yellow pigment/cartenoid
| * acts as antioxidant for staph
staphyloxanthin
93
reductase
methionine sulfoxide
94
* transmitted without awareness
* is everywhere
* multiple drug resistance
antibiotic resistance (Abx^R)
95
what was the earliest antibiotic?
tetracycline 350-500 BC
96
what was tetracylcine made by?
bacteria streptomyces in soil
97
enzyme that can cleave penicillin
B-lactamase
98
developed because B-lactamase cant cleave it
methicillin
99
where is MRSA commonly found?
* hospitals
| * pigs/farms
100
what is B-lactamase encoded by?
gene blaZ
101
how many types of B-lactamase are there?
more than 100
102
resistance mechanism encoded by gene MecA
methicillin
103
encodes penicillin binding protein 2a (PBP2a)
gene MecA
104
has poor methicillin binding
transpeptidase
105
normal PBP vs. MecA PBP2a
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
why can MRSA spread fast?
because MecA is found in the mobile genetic element
107
mobile genetic element of MRSA
staphyloccocal casette chromosome (SCC)
108
when does SCC have a higher expression?
if it is close to the origin of replication
109
allow multiple casettes to come together----> resistance to multiple drugs
direct repeats
110
* binds to transpeptidase substrate--- binds D-ala-D-ala
| * no transpeptidation
vancomycin
111
* came from enterococcus
| * resistance is on plasmid that can facilitate conjugation
Van^R
112
transfer plasmid to another bacteria
conjugation
113
* plasmid DNA
| * jump to recipient and integrate to host DNA
transposon
114
what are the multiple gene products of Vancomycin?
1. Van^R
2. Van^x
3. VanH
4. VanA
115
cleaves D-ala-D-ala
Van^x
116
pyruvate---->D-lactate
VanH
117
synthesize D-ala-D-lactate
VanA
118
what are the antibiotic resistance mechanisms?
1. alter Abx
2. alter abx target
3. decrease intracellular abx accumulation
4. form biofilm
119
what does decreasing the intracellular abx accumulation involve?
* decrease porin (channels on outer membrane) expression
| * increase eflux pump expression (transfer intracellular stuff to the outside)
120
How is antibiotic resistance being combatted?
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
B lactam drug and B lactamase inhibitors
combination drug
122
what does rethinking antibiotic susceptibility testing?
MIC in artificial media
123
ihibits s.aureus and types of gram + bacteria
lugdunin
124
what happened when a human survey on lugdunin was conducted?
people positive for lugdunin have less s. aureus
125
Which of the following terms is most related/similar to "virulence"?
pathogenicity
126
Which of the following surface features of microbes can be used as tools for adhesion?
flagella
pili
capsule
127
True or False: Infection refers to a situation where foreign organisms have cause damages inside a host.
false
128
True or false: An opportunistic pathogen causes diseases when the host resistance is compromised.
true
129
A pathogen is more virulent if the LD50 is a larger number.
false
130
true or false: Dental plaque contains multiple species of microbes.
true
131
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?
less virulent
132
Pathogenicity islands can be mobile genetic elements and be transffered to a non-pathogen to make it become a pathogen.
true
133
True or false: Attenuated bacteria are dead bacteria
false
134
True or false: Pathogens may have a very specific host target that they bind to during infections.
true
135
true or false: Staphylococcus can cause infections in multiple sites of our bodies.
true
136
* 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
coagulase
137
true or false: Toxic shock syndrome is only caused by Staphylococcus aureus.
false
138
what is the purpose for including phenol red in mannitol-salt agar?
to indicate a reduction in pH
139
true or false: If a patient sample is positive for the presence of mecA gene, then methicillin should not be prescribed to that patient.
true
140
which of the following is NOT a function of neutrophils?
A. Chemotaxis
B. Secretion of antibodies
C. Phagocytosis
D. Production of reactive oxygen species
B secretion of antibodies
141
true or false: Macrophages are involved in cleaning up after neutrophils.
true
142
A Staphylococcus aureus mutant lacking catalase will not be able to?
survive through reactive oxygen species
143
true or false: Adding alanine to cell wall teichoic acids makes the bacteria have more negative charges at the surface.
false
144
**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. neutrophil extracellular traps
145
What evidence did the authors show to suggest that the genes encoding the synthesis of lugdunin are likely from other organisms?
GC content
146
How did the authors manage to purify lugdunin for in-depth chemical analysis?
Over-express the genes with a strong, inducible promoter
147
How did the authors test whether or not lugdunin has a toxic effect on mammalian cells
Lactate dehydrogenase release assay
148
True or false: An antibiotic is more potent if it has a high MIC
false
149
What is the specific molecular target of lugdunin?
it is unknown
150
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?
S. aureus growth is not inhibited
