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Microbiology > Lecture 4: Colonization, Invasion and Clinical Disease > Flashcards

Lecture 4: Colonization, Invasion and Clinical Disease Flashcards

1
Q

What is mutualism

A

Host and microbe benefit

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2
Q

What is commensalism

A

Microbe benefits, host is neither helped nor harmed

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3
Q

What is parasitism

A

Microbe benefits, host is harmed

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4
Q

What is the normal microbiota

A

Stable polymicrobial communities in skin, conjunctiva, respiratory, urogenital and GI tracts

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5
Q

What symbiotic relationships does the normal microbiota have and what do they do

A

Mutualists and commensals that help prevent colonizations by pathogens

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6
Q

Describe the opportunistic pathogen example of Fusobacterium necrophorum

A

F. Necrophorum is typically a commensal bacteria in the rumen but with lactic acidosis it enters blood stream, travels to liver and causes lesions

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7
Q

What is pathogenicity

A

Ability of a microbe to damage a host- produce disease

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8
Q

What is virulence

A

Relative capacity of a microbe to cause damage in a host

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9
Q

What is transmissibility

A

Relative ease with which an infectious agent spreads between hosts

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10
Q

How far can large infectious droplets travel

A

1-3 ft

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11
Q

How far can small infectious droplets travel

A

3-5ft

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12
Q

How far can infectious droplet nuclei travel

A

5-160+ft

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13
Q

What is infectivity

A

Capacity of a microbe to become established in a host

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14
Q

What is a virulence factor

A

Traits that confer pathogenicity: ex: toxins

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15
Q

What mechanism do genes use to spread virulence factors

A

Horizontal gene transfer
Modes of transmission: natural transformation, transduction, conjugation

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16
Q

What is the consequence of horizontal gene transfer

A

A virulent strains acquire virulent genotype/phenotype

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17
Q

Virulence factors help pathogens to do what things

A

Colonize hosts, evade host defenses, grow, invade, cause damage

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18
Q

What are the 3 major categories of virulence factors

A

Adhesins, capsules, toxins

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19
Q

What are adhesins

A

Macromolecules that bind bacteria to host cells or tissues

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20
Q

Where are adhesins located and what are some examples

A

Located on bacterial surface structures
Ex: fimbriae, glycocalyx

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21
Q

Adhesins bind to ___

A

Complementary receptor molecules found on target host cells/tissues

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22
Q

T or F: adhesins are highly specific receptor-ligand interactions

A

True

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23
Q

Adhesin attachment specificity helps bring about what 2 things

A
  1. Tissue tropism
  2. Host specificity
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24
Q

Describe the example of adhesin host specificity with E. Coli K88

A

E. Coli K88 strain has fimbrial adhesin K88 that binds to specific receptors on brush border of pig enterocytes

E. Coli K88 is limited to pigs

25
What are the functions of capsules
1. Impair phagocytosis 2. Mediate adherence and biofilm formation 3. Prevent desiccation and may serve as nutrient reserve
26
Toxins damage host and cell tissues at what sites
1. Site of colonization and invasion 2. Sites remote from original point of invasion
27
What are the two major types of toxins
1. Exotoxins 2. Endotoxins
28
What are exotoxins
Proteins or enzymes secreted by Gram negative and -positive bacteria that cause highly specific effects on target cells/tissues
29
What are endotoxins
Cell wall components of gram negative bacteria primarily released following cell death, produce generalized inflammation related damage to host
30
Where are endotoxins present
LPS of outer membrane of gram negative bacteria
31
What is the toxic portion of LPS
Lipid A
32
How does lipid A cause a systemic inflammatory response (3)
1. Stimulate leukocytes to release high levels of cytokines 2. Activate complement 3. Activate coagulation cascade
33
What are some results of systemic inflammatory response caused by Lipid A
Fever, chills, weakness, myalgia, hypotension, DIC, shock, death
34
What are the 4 major categories of exotoxins
1. Enzymes that digest ECM 2. Toxins that act on plasma membrane of target cells 3. Toxins that act inside their target cells 4. Toxins that provoke exaggerated immune response
35
How are exotoxins named
1 type of host cell attacked 2. Associated disease 3. Microbe that makes toxin
36
Some exotoxins are inactivated with ____, the resulting toxoid is used for immunization
Formaldehyde
37
What are the 3 basic steps of pathogeneis
1. Colonization 2. Invasion 3. Damage
38
What is colonization
Establishment of pathogen at appropriate portal of entry
39
What are the 3 main portals of entry
1. GI tract 2. Respiratory tract 3. Urogenital tract
40
During colonization, what are some ways the pathogen evades host defenses
1. Impair phagocytosis (capsules, biofilms, leukocidins) 2. Evade complement (capsules, biofilms, modification of LPS) 3. Hydrolysis of IgA 4. Antimicrobial peptides 5. Complement components
41
During colonization how does the pathogen grow
1. Co-opt host nutrients 2. Acquire nutrients by overtly damaging host cells/tissues
42
What do siderophores do
Steal iron from iron binding proteins to promote growth of pathogen
43
What do biofilms do during colonization
1. Enable development of high cell densities 2. Enable quorum sensing, which allows biofilm inhabitants to coordinate their cellular activities (ex: exotoxin production)
44
What is quorum sensing
Allows pathogens to coordinate their cellular activities
45
How does invasion occur via enzymes
Invasins cause local damage to host cells and extra cellular matrix to facilitate spread beyond colonization
46
How does hyaluronidases and collagenages work during invasions
Hyaluronidase splits epithelial cells and pathogen enters Collagenase breaks open basement membrane which allows pathogen to invade deeper tissues and enter blood stream
47
What does it mean for pathogen to invade paracellularly
Between epithelial cells
48
What does it mean for pathogen to invade transcellularly
Passage through epithelial cells
49
How do obligate and facultative organisms invade host
1. Adhesin mediated uptake 2. Growth in host cell 3. Release by intact or lysed cell 4. Invasion of uninfected host cell 5. Repeat
50
Pathogens can also invade via ___ and ___ systems
Circulatory, lymphatics
51
Pathogens can also invade from organ to organ in ___ and ___ cavities
Peritoneal and pleural cavities
52
Pathogens can also invade via mobile ___
Phagocytes
53
What are the 4 ways a pathogen damages a host
1. Use host nutrients 2. Direct damage at sites of colonization/ invasion 3. Pathogens produce toxins that damage sites distant from invasion site 4. Pathogens cause collateral damage due to host inflammatory or immune reactions
54
What are the portals of exit
Pathogenic effects- diarrhea, coughing, skin lesions that facilitate transmission of pathogens to new hosts or other reservoirs
55
What is a passive carrier
Carry/transmit pathogen without having had the disease
56
What is an incubatory carrier
Transmit pathogen during incubation period of the disease when there are no overt signs/ symptoms in the carrier
57
What is a convalescent carrier
Harbor/transmit pathogen while recovering from disease
58
What is an active carrier
Completely recovered from disease but still harbor/ transmit pathogen
59
Describe how Streptoccous equine and equine strangles is an active carrier
1. Upper respiratory tract—> nasal discharge 2. Nasal shedding of S. Equin 1-2 days after fever and persists for 203 weeks 3. Transmission via direct or indirect transfer of S. Equi shed in nasal discharge

Microbiology (31 decks)

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