Week 1 Flashcards
1
Q
4 classes of microbes
A
- Virus
- Bacteria
- Fungus
- Parasite
2
Q
Morphology of bacteria
A
- Cocci
- Bacilli
- Spirals
- Pleiomorphic
3
Q
Cocci
A
circle
4
Q
Staph
A
cluster
5
Q
Strep
A
string
6
Q
Bacilli
A
rod
7
Q
What is used to look at cell wall?
A
Gram stain
8
Q
Gram +
- color
- peptidoglycan
A
- purple
- thick peptidoglycan, traps 1st dye
9
Q
Gram -
- color
- peptidoglycan
A
- pink
- thin peptidoglycan layer
- has layer of lipopolysaccharide
10
Q
Porins
A
how drug gets into bacteria
11
Q
Function of flagella
A
motility
12
Q
Function of pilli
A
for genetic transmission between bacteria; sexual transfer–importance in antibiotic resistance
13
Q
Function of fimbriae
A
for adhesion
14
Q
Why is morphology important?
A
If taking a sample it will be some of the first information that will clue you in to what organism it is
15
Q
What is Pleiomorphic?
- found?
- what do we get?
A
- varied shapes
- extreme environments
- enzymes to run some of diagnostic testing
16
Q
Cell wall
A
- used for protection
- target of beta-lactamases
17
Q
Layers of cell protection
A
cell membrane, cell wall, capsule
18
Q
Bacteria that will not stain
A
Syphilis, chlamydia
19
Q
Importance of lipopolysaccharide layer in gram -
A
important in virulence of bacteria
20
Q
E. coli
A
-has flagella, pilli, H antigen, O antigen, K antigen
21
Q
Virulence factors of E. coli
A
- pilli
- flagella
- LPS
22
Q
H antigen
A
- flagella
- used for testing in serology
23
Q
O antigen
A
- antigenic variation
- seen in flu
- used for testing in serology
24
Q
K antigen
A
-capsule
25
Importance of capsule
- antiphagocytic property
- can help with adherence
- can help form biofilm
- can dry out quickly
26
Bio-film
-ale to avoid complement/anti-body because it acts as barrier between the bacteria and the immune system
27
1st test when suspecting bacteria
gram stain
28
E. coli gram stain
-gram negative rods
29
How to test for aerobic/anaerobic
- catalase test
| - culture
30
Plates used for E. coli
- Eosine methylene blue: will have metallic green sheen because it ferments lactose very quickly
- MacConkey agar: hazy bright pink
31
What does eosine methylene blue inhibit?
growth of gram + bugs
32
MacConkey agar
- Lactose negative- no color
| - Lactose positive- pink
33
Catalase testing
- tests bacteria for catalase enzyme
| - will add hydrogen peroxide to sample, looking to see if enzyme will cleave hydrogen peroxide into water and gas
34
Cytochrome C oxidase testing
- Cytochrome C oxidase is enzyme used in ETC of aerobic bacteria
- will be positive if the test turns blue
35
What kind of respiration does E. coli use?
- faculatative anaerobe
| - can survive in aerobic environment, but prefers anaerobic respiration
36
Why would bacteria not want to be aerobic?
-Oxygen damages cell with radicals
37
Indole test
- looking for red ring
| - breaks down tryptophan
38
Indole test and e. coli
positive
39
Acid fermentation test
-e. coli is mixed acid fermenter and produces gas
40
VP test
-looks for glucose fermenters
41
VP and E. coli
- negative; because only one substrate added
| - however, E. coli can use glucose in aerobic environment
42
Methyl red test
| - e. coli
- looks for mixed acid fermenters
| - positive
43
Can body naturally degrade bacterial cell wall?
yes; with lysozymes
| -cleaves between NAG/NAM complexes
44
NAG and NAM
- creates chain linked fance formation for cell wall
- always attached to different AA
- building blocks of chain made from NAG-NAM complex which binds to another complex with an AA bridge
45
lysostaphin
- natural body mechanism
- knocks out the cross bridges making the cell wall less stable
- used in gram +
46
How to get rid of lipopolysacharide
-dry it out
47
Things to consider when choosing anti-biotic
1. Disease state of patient
2. Prior adverse reaction
3. Impaired elimination
4. Patient age
5. Pregnancy status
6. Epidemiologic exposure
7. Pharmacologic factors
48
Why is disease state of patient important?
-antibiotics are chemotherapeutic drugs because they are trying to kill/stop growth of living cell
49
Why is disease state of patient important?
- antibiotics are chemotherapeutic drugs because they are trying to kill/stop growth of living cell
- looking out for immuno-compromised individuals
50
Why is impaired elimination important?
-If you cannot get rid of of drug then it could cause toxicity
51
Why is age important?
- older: side effects of dizziness- can cause falls
| - neonates: increased bili
52
Epidemiologic exposure
If patient lives in close contact with someone else and is infected with highly contagious organism then the people they live with need to be tested
53
Bacteriacidal
Kills the cell
54
Bacteriacidal
- Kills the cell
| - targets the cell wall
55
Bacteriostatic
- Stops cell growth
| - targets proteins
56
Post antibiotic effect
- in absence of anti-biotic there is still anti-biotic effect, lasts 1.5 hours to 6 hours
- can occur because as medication is excreted as long as concentration stays above MIC there is still antibacteria like effect
57
Minimal inhibitory concentration
Minimum amount of drug that will stop visible growth of bug
58
Minimal bacteriocidal concentration
Minimum concentration of drug that will kill the bug
59
How to choose proper drug
-empirically treat and then
60
Antimicrobials with activity against e coli
```
• Penicillin: Most commonly given
• Cephalosporin: Most commonly given
• Aminoglycosides: It’s a synergistic drug
• Sulfonamides
• Trimethoprim
-fluoroquinolones
```
61
Physical barriers to infection
-mechanical, chemical, microbiological
62
Skin barriers
- m: epi cells are joined by tight junction, longitudinal flor of air/fluid
- c: fatty acids, antimicrobial peptides
- M: normal flora
63
Gut barriers
- m: epi cells are joined by tight junction, longitudinal flor of air/fluid
- c: low pH, antimicrobial enzymes, antimicrobial peptides
- M: normal flora
64
Lungs
- m: epi cells are joined by tight junction, movement of mucus by cilia
- c: pulmonary surfactant, antimicrobial peptides
- M: normal flora
65
Eye, nose, oral cavity
- m: epi cells are joined by tight junction,tears, nasal cilia
- c: antimicrobial enzymes in tears and saliva
- M: normal flora
66
How do antimicrobial peptides kill?
Disrupting pathogen membranes
67
Function of pentraxins
bind microbes and target them to phagocytes
68
Cells of innate immune system
-eosinophil, basophil, neutrophil, NK, T cell, mast cell, monocyte, macrophage, dendritic cell
69
Granulocytes
Eosinophil, basophil, neutrophil, NK cell
70
Phagocytic cells
-neutrophil, monocyte, dendritic cell, macrophage
71
Tissue resident cells
dendritic cell, macrophages, mast cell, plasma cell
72
lymphocytes
T cell, B cell
73
recognition mech of innate immunity
-rapid response, fixed, limited # of specificity, constant during response, multiple cell types
74
recognition mech of adaptive immunity
-slow response, variable, numerous highly selective specificities, improve during response, lymphocytes only
75
complement role in first line defense
Complement coats the surface of bacteria and extracellular virus particles and makes them more easily phagocytosed. Without such a coating, many bacteria resist phagocytosis, especially those that are enclosed in thick polysaccharide capsules.
76
Complement pathways
- alternative, lectin, classical
| - all lead to activation of C3
77
Alternative pathway
- works at start of infection
| - innate immunity
78
Lectin pathway
- innate immunity
| - requires time
79
Classical pathway
- part of both innate and adaptive immunity
- requires the binding of either antibody or an innate immune-system protein called C-reactive protein to the pathogen’s surface.
80
Macrophage effector functions
- bacteria binding to macrophage
- bacterial component binding to macrophage
- induces engulfment and degradation
| - induces the synthesis of inflammatory cytokines
81
Neutrophils moving to infection
| -steps
- rolling adhesions, tight binding, diapedesis, migration
- Neutrophils have CXCL8 receptors and endothelial cells of vasculature near site of infection will express CXCL* so the neutrophils can bind to that site and then move though the vessel to get to the infection
82
TLR-4
- binds to?
- cells carrying receptor
- location
- binds to LPS of gam - bacteria
- macrophage, dendritic cell, mast cells, eosinophils
- plasma membrane
83
NF Kappa B
- used in
- function
- what occurs when non function
- TLR's and NLR
- transcription factor that transcribes proinflammatory cytokines
- non function then you cannot combat against bacterial agents because you cannot produce defensins and cannot recruit WBC to help with fighting bacteria
84
NLR
-important for activation of the inflammasome and very important in transcribing definsins
85
NEMO disease
- A subunit of one of the IkB kinases in the NF-kB pathway is missing therefore
NF Kappa B cannot be released from inhibitory marker to induce transcription
-leads to abnormality in skin, hair, teeth and makes patient susceptible to bacterial infections
86
Neutrophils
-express many bacterial and fungal receptors making them super phagocytes
87
Dendritic cells and NK cells
- activate NK cells and help them to proliferate
- once NK cells are abundant and outnumber dendritic cells then they kill dendritic to regulate further activation of NK cells
- once NK cells are scarce and are outnumbered by the dendritic cells they drive the dendritic cells to mature into the form that initiates adaptive immunity
88
Netosis
unique form of cell death that is characterized by the release of decondensed chromatin and granular contents to the extracellular space.
89
Absence of --- would prevent complement cascade from amplification?
cleavage of C3 by C3bBb
90
What molecule directly prevents formation of C3 convertase?
Factor I
91
Molecule that most directly stimulates migration of neutrophils from blood to tissues
C5a
92
Molecule that directly mediates destruction of complement-coated microbes
C3b
93
C3 deficiency
- When you don't have C3, you don't opsonize bacteria as well, so phagocytes are not phagocytizing as well. This leads to increased susceptibility of infection
- lack of opsonization and inability to utilizr the membrane attack pathway
94
Factor H/I deficiency
-causes uncontrolled activation of C3 via the alternative pathway resulting in depletion of C3 and causing C3 deficiency and susceptibility to bacterial infection
95
What is mechanism of joint pain in C3 deficiency?
stems from buildup of immune complexes in the joint
96
Factor D deficiency
Factor D cleaves factor B, so a deficiency in this factor would lead to factor B not being cleaved, and you can't make C3 convertase. If you can't make C3 convertase, you can't cleave C3 which results in decreased opsonization because you can't place C3b on pathogen's surface. Pts with Factor D deficiency are at risk for serious infections.
97
Factor P deficiency
the factor 3 convertase from alternative pathway will not be stabilized so it will disintegrate very quickly and opsinozation will not work effectively
98
lymph capillary
- other name
- description
- role
- initial terminal capillaries
- discontinuous, anchored to the ECM, single layer of epithelial cells,
- role is the formation of the lymph.
99
collectine lymphatics
-contain smooth muscles so they are able to propel the lymph from one portion to the other.
100
lymph node
capsulated, it filters and it’s a reservoir for WBC.
101
lymphatic trunks
drain from the nodes to the ducts
102
lymphatic ducts
where the lymphatic is entering back into the venous system
103
What contributes to net flow rate in lymphatics
Formation and propulsion.
104
driving forces of lymphatic formation
Oncotic pressure and hydrostatic pressure. They help to move the fluid into the interstitial space and then from the interstitial space to the lymphatics.
105
driving forces of lymphatic propulsion
Systemic forces like blood pressure, respiration, exercise and massage. These systemic forces create a change in pressure which is important because fluid moves from high pressure to low pressure.
106
arteries and lymphatics
Lymphatic vessels are next to arteries which pulsate and that pulsating causes the lymphatic vessels and collecting vessels to continue to move.
107
Importance of GAGS in lymph formation
- highly negatively charged so they repel each other and because of that they are able to establish interstitial volume and neutrality which helps to create osmotic gradient leading to lymphatic formation so that the lymphatics can pick up the fluid.
- if disrupted there is less lymphatic formation in the interstitial terminal lymphatics.
108
anchoring filaments
- anchoring filaments pull open the terminal lymphatic capillaries and help to create a tissue pump or a second valve, increasing the luminal volume, causing the fluid to get in and forming the lymph and then sending them to the collecting lymphatics
- if damaged edema can be formed
109
sterling forces
needed to get the fluid from the capillaries into the interstitial space are hydrostatic and oncotic pressures
110
net filtration
- hydrostatic forces are greater than the oncotic forces
| - hyrdostatic pressure is pushing pressure and will push the liquid from the capillaries to the interstitial space
111
net resorption
- oncotic forces are greater than hydrostatic forces
| - oncotic pressure is pulling pressure and will pull the liquid from the interstitial space back to the capillary
112
venous insufficiency effect on lymph
- why?
- treatment
- Venous insufficiency means she's cant move blood back to the heart so there is increased hydrostatic pressure in capillary on venous end, therefore less liquid from interstitum can be pulled back into the capillary and the fluid in interstitum is too much from lymph to completely drain which creates edema
- Also has fibrotic tissue which is leading to remolding of her ECM which could be affecting her Gags and anchoring filaments that affects lymphatic formation
- exercise and compression socks
113
thymus
-primary lymphoid tissue where the T-cells originate
114
activation of adaptive immune response
-dendritic cell will follow lymphatics from tissue to nearest lymph node, then present the antigen from the bacteria to the t-cells, t-cells will activate b cells which will turn into plasma calls and being making anti-bodies to bind antigen
115
what happens if antigen/pathogen is inserted directly in blood?
-it will travel to spleen first and be filtered out there since the spleen is abundant in lymphocytes (specifically T cells)
116
what cells are located in the peri-articular sheath of the spleen?
-t-cells
117
effect of Wuchereria bancrofti
-live in efferent lymphatics which causes a mechanical obstruction in those vessels, so there is a build up and no forward flow in the collecting lymphatics, the smooth muscles get stretched out further and stop working, the pressure builds up, the collecting lymphatics starts to distend. hydrostatic pressure in the lymphatics increases so fluid goes into the tissues instead of being moved through lymph vessels
118
what is primary cause of edema?
-genetic defect, specifically one in VEGF formation which will usually stimulates the formation of new capillaries (both arterial/venous and lymph) so a mutation will lead to absence of terminal lymphatics and absence of lymph formation, causing build up of fluid in interstitum
