1
Q
What are the 7 categories of bacteria based on interaction with humans?
A
- Symbiosis/Commensal: Natural flora
- Persistent colonizers with positive and negative effects
- Opportunists
- Persistent pathogens
- Disease caused by immune response
- Invaders
- Toxinoses
2
Q
What is normal flora also called? 4
A
commensal flora,
indigenous flora,
microflora
microbiome
3
Q
Bacterial genes in the gut outnumber human genes by how much?
A
150 to 1
4
Q
Colonization with normal flora begins when?
What is first?
Where does most of it come from?
A
At birth
Skin
The mother
5
Q
Microflora is affected by what? 7
A
age, anatomic niche, diet, illness, hospitalization, antimicrobial therapy, genetic makeup
6
Q
Is colonization the same as infection?
A
no
7
Q
What system of the body has a lot of normal flora?
A
GI
8
Q
Most of the colon bacteria are what type?
A
Strict anaerobes
9
Q
Skin is heavily colonized where?
A
Moist areas
10
Q
What bacteria dominate the upper respiratory tract?
A
Anaerobes outnumber aerobes 10-100:1
11
Q
What bacteria colonize the cervix and uterus?
A
None, sterile.
12
Q
When does normal vaginal flora begin?
A
Puberty
13
Q
Intestinal cell carbohydrate-metabolizing genes can respond to signals from what?
A
Commensal bacteria
14
Q
Intestinal bacteria can do what 3 things for you?
A
- Synthesize K and B vitamins
- Liberate useable metabolic products from indigestible carbs
- Contribute to lipid metabolism
15
Q
How does the intestinal immune system interact with commensal bacteria? (2)
A
- Keep commensal bacteria from invading across mucosal barrier
- Develop a degree of tolerance to normal flora.
16
Q
Intestinal bacteria affect innate immune response how? 7
A
- Enhance anti-bacterial peptides made by mucosal cells like Paneth.
- Enhance production of anti-inflammatory cytokines
- Decrease pro-inflammatory cytokine production
- Interfere with complement-mediated tissue toxicity
- Maintain integrity of gut epithelium
- stimulate angiogenesis
- Contribute to maintenance of intestinal epithelial homeostasis
17
Q
Intestinal bacteria affect development of adaptive immunity how? 4
A
- Aid development of Peyer’s patches by enhancing T and B cell interactions
- Stimulate production of IgA
- Attract T cells to gut epithelium
- Stimulate development of immune tolerance to themselves and other antigens.
18
Q
What is the value of normal flora in terms of the hygiene hypothesis?
A
Lack of normal flora means your body doesn’t develop tolerance to harmless bacteria which leads to inappropriate harsh immune responses later in life.
19
Q
What is antagonism?
A
Commensal flora inhibit growth of pathogens by
20
Q
How is antagonism accomplished? (4)
A
- Compete for nutrients, oxygen and iron
- Produce toxic substances
- Take up space on mucosal surfaces
- Interfere with cell-to cell communication (quorum sensing)
21
Q
Loss of normal flora from inappropriate or overuse of antibiotics can ead to what?
A
overgrowth of pathogenic organisms
22
Q
Examples of pathogenic bacteria taking over normal flora in antibiotic use? (3)
A
- Candida in mouth or vagina (thrus, candidiasis)
- Bacterial vaginosis
- C-dif or C-perfring in GI tract
23
Q
What are probiotics?
A
Live microorganisms which, when administered in adequate amounts, confer a health benefit on the host
24
Q
Conditions in which probiotics are recommended? 7
A
- Crohn’s
- Antibiotic diarrhea
- Vaginosis
- UTI
- Reforming flora in elderly
- Reducing allergies
- Necrotizing entercolitis of newborns
25
Are all strains of the same organism equally effective as probiotics?
No
26
Is replacing entrenched flora easy?
No
27
Do commercial yogurts have probiotics?
No
28
How has the defining of gut bacteria been accomplished?
Metagenomics
29
What has allowed for detection of non-cultivable human flora? 2
16S rRNA gene sequencing
| Deep sequencing
30
90% of all human normal flora species belong to how many divisions?
In terms of all pathogens, how many divisions
4
| 7
31
The oral cavity contains how many species?
Greater than 700
32
The GI tract contains how many species?
greater than 1000
33
How many species are common in 90% of individuals
57
34
What are opportunistic pathogens in layman's terms?
Good bugs gone bad.
35
What causes normal flora to turn bad? (4)
1. Power balance shift
2. Trauma allows normal flora to be toxic in a place they shouldn't exist
3. Acquisition of virulence factors
4. Changes in physiology and nutrition.
36
Requirement for attachment and entry into the body of outside invaders?
Phenomenon this is?
Evade natural protective mechanisms
Entry
37
Requirement for local or general spread in the body?
| Phenomenon?
Evade immediate local defenses
Spread
38
Multiplication of outside invaders requirement?
Increase numbers
39
Evasion of host defenses requirement?
Evade immune defenses long enough for full cycle in host to be completed.
40
Shedding from body requirement?
Leave body at a site and on a scale that ensures fresh hosts.
41
What are the phenomenons in order in the attack of outside invaders? 6
1. Entry
2. Spread
3. Multiplication
4. Microbial answers to host defenses
5. Pathology/Disease
6. Transmission
42
Routes of entry and exit for bacteria naturally?
1. Mouth
2. Conjunctive
3. Respiratory tract
4. Urogenital tract
5. Alimentary tract
6. anus
7. skin
43
Artificial routes of bacteria?
1. IV drug use
2. Surgical incisions
3. Surgical implants
4. catheters and tubes
5. contact lenses
6. IUD
7. Tattoo/Piercing
44
Attachment of bacteria is generally accomplished by what?
bacterial surface proteins with specific affinity for host surface features including carbohydrates and proteins as well as extracellular matrix proteins like collagen and fibronectin
45
Two types of bacterial adherence methods?
1. Using pili with tip adhesins to bind to host cell
| 2. Using adhesins on the bacteria to bind directly to host cell
46
What are bacteria's two options upon adhering?
1. Remain satisfied with surface growth and produce biofilms
| 2. Penetrate cell layers and enter blood and lymph
47
What is passive transfer?
Using the cells own trafficking mechanisms
48
What is active transfer?
Specifically polymerizing actin tails
49
3 steps to evading the immunse system?
1. Avoiding phagocytosis
2. Avoiding complement
3. Avoiding antibody
50
6 ways to avoiding phagocytosis?
1. Toxin release to kill cell
2. Make anti-Opsonization protein
3. Capsule prevents contact with cell
4. Phagolysosome formation inhibited
5. Organism escapes phagolysosome
6. Resistant to killing
51
What are the six ways to avoid complement?
1. Have a capsule
2. Have surface structures prohibit macrophage and C3b from getting too close.
3. Surface structures bind the lytic complex and keep it away
4. Surface proteins are shed and take c3b with them
5. Resistance to outer membrane to surface lytic complex binding.
6. Secretion of decoy molecules.
52
What does immune mimicry lead to?
Damage to host cells.
53
How can a bacteria avoid antibody?
1. Mimic host surface proteins
2. Antigenic variation
3. Use Fc receptors on outside to bind Ab's backwards
54
What are the mechanisms of antigenic variation?
1. Simple genetic inversions
2. Recombination
3. Slipped strand mispairing.
55
Infections with encapsulated bacteria have what severity?
What relative time length?
Recovery requires what?
Acute and severe
Brief
Opsonizing antibodies
56
Infections with intracellular bacteria have what severity?
What relative time length?
Recovery requires what?
Less severe
Chronic
Activation of macrophages by CMI
57
What are some examples of direct assault? 5
1. Lipases against cell membranes
2. Pore forming proteins such as hemolysins and cytolysins
3. Binary A-B toxins
4. Type III Secretion system
5. Immunomodulators
58
The pore forming proteins hemolysin and cytolysin do what?
Polymerize in cell membrane to form pore.
59
What is the B portion of AB toxin?
| What is it used for clinically?
Heavy chain that binds the toxin molecule to a specific receptor
Vaccines
60
What is the A portion of the AB toxin?
| What does it interfere with? 3
Light or Active chain that enters host cell and enzymatically interferes with essential host function
1. Protein synthesis
2. signal tranduction
3. Messes with NT's.
61
Type III Secretion systems are what?
| What are they similar to?
nanostructure for delivering bacterial toxins to a host cytoplasm
to flagellar systems
62
The proteins Type III secretion systems deliver are called what?
What is their effect? (2)
effectors
| promotion of uptake, interference with signal transduction, and induction of apoptosis
63
What makes superantigens? (2)
Bacteria
| Viruses
64
What do superantigens do?
Crosslink the MHC and TCR to activate up to 20% of T cells with no antigen.
65
How do exotoxins and endotoxins differ in terms of what bacteria make them?
Exo: Gram + and Gram -
Endo: Only Gram -
66
How do exotoxins and endotoxins differ in terms of where they do their action?
Exo: Secreted
Endo: In membrane
67
How do exotoxins and endotoxins differ in terms of where their genetic material is located?
Exo: Phage and plasmids
Endo: Chromosome
68
How do exotoxins and endotoxins differ in terms of ability to withstand heat?
Exo: Don't withstand heat
Endo: Stable at 100 C
69
What are the five routes of transmission?
1. Aerosol/Saliva
2. Fecal/Oral
3. Sexually transmitted
4. Vector-borne
5. Zoonotic
70
What are the five stages of evolution of transmission?
1. Agent only animals
2. Primary infection: only get infection from animal
3. Limited outbreak: From animals and a few humans
4. Long outbreak: From animals and many humans
5. Exclusive human agent: Only from humans
71
All pathogens are originally acquired as what?
Zoonoses
72
In the standard view, when is a pathogen most pathogenic to a host?
What causes it to decrease?
1. Initially
Time causes the pathogen to adapt to new host
73
What causes a pathogen's disease to be more severe initially in standard view?
imbalance between the need of the pathogen to replicate and the need to be transmitted to the next host.
74
Why does the pathogen choose to adapt to the host?
it is in the best interest of the pathogen to evolve toward lower virulence or even symbiosis because it can continue to replicate within its host without the necessity of finding a new one.
75
What is wrong with the standard view of pathogen evolution?
Presumes rate limiting step in pathogenesis is transmission.
76
What is the evolution of a pathogen with high transmission rates?
Increasing pathogenesis because they have no concern for keeping the host alive.
77
How does gene transfer complicate pathogen evolution? 2
1, Acquisition of a new virulence factor into a pathogen that is adapting to its host
may temporarily increase its pathogenicity
2. Acquisition of a factor increasing transmissibility may permanently increase
its pathogenicity
78
Virulence is actually a factor of what?
Transmissibility
79
Is there any evolutionary course for bacterial pathogens?
no
80
H. pylori is in how many humans?
80 percent
MICRO
flashcards
Decks in class (22)
# Cards
-
Ch2: Innate Immunity247
-
Ch3: Lymph, MHC, Antigen Presentation135
-
Ch4: B Cells240
-
Ch5: T Cells162
-
Ch6: Host Response to Infection106
-
BRS Immunology228
-
Ch7: Hypersensitivity and Autoimmunity129
-
Ch8: Immunodeficiency and Transplantation86
-
L1: Phylogeny and Morphology of Bacteria153
-
L2: Antimicrobial Agents144
-
L3: Bacterial Genetics82
-
L4: Pathogenesis80
-
L5: Laboratory Diagnosis0
-
L6; Introduction to Pathogens0
-
L7: Introduction to Mycology90
-
L8: Introduction to Parasites104
-
L9: Introduction to Virology83
-
Ch1: Skin276
-
Ch2: Skin, Musculoskeletal, Blood and Lymph Part I70
-
Ch4: Skin, Musculoskeletal, Blood, and Lymph Part II289
-
Ch5: URT Chaussee104
-
Parasitology71
