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

Lecture 4: Colonization, Invasion and Clinical Disease Flashcards

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Biology 101 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
Q

What are the functions of capsules

A
  1. Impair phagocytosis
  2. Mediate adherence and biofilm formation
  3. Prevent desiccation and may serve as nutrient reserve
26
Q

Toxins damage host and cell tissues at what sites

A
  1. Site of colonization and invasion
  2. Sites remote from original point of invasion
27
Q

What are the two major types of toxins

A
  1. Exotoxins
  2. Endotoxins
28
Q

What are exotoxins

A

Proteins or enzymes secreted by Gram negative and -positive bacteria that cause highly specific effects on target cells/tissues

29
Q

What are endotoxins

A

Cell wall components of gram negative bacteria primarily released following cell death, produce generalized inflammation related damage to host

30
Q

Where are endotoxins present

A

LPS of outer membrane of gram negative bacteria

31
Q

What is the toxic portion of LPS

A

Lipid A

32
Q

How does lipid A cause a systemic inflammatory response (3)

A
  1. Stimulate leukocytes to release high levels of cytokines
  2. Activate complement
  3. Activate coagulation cascade
33
Q

What are some results of systemic inflammatory response caused by Lipid A

A

Fever, chills, weakness, myalgia, hypotension, DIC, shock, death

34
Q

What are the 4 major categories of exotoxins

A
  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
Q

How are exotoxins named

A

1 type of host cell attacked
2. Associated disease
3. Microbe that makes toxin

36
Q

Some exotoxins are inactivated with ____, the resulting toxoid is used for immunization

A

Formaldehyde

37
Q

What are the 3 basic steps of pathogeneis

A
  1. Colonization
  2. Invasion
  3. Damage
38
Q

What is colonization

A

Establishment of pathogen at appropriate portal of entry

39
Q

What are the 3 main portals of entry

A
  1. GI tract
  2. Respiratory tract
  3. Urogenital tract
40
Q

During colonization, what are some ways the pathogen evades host defenses

A
  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
Q

During colonization how does the pathogen grow

A
  1. Co-opt host nutrients
  2. Acquire nutrients by overtly damaging host cells/tissues
42
Q

What do siderophores do

A

Steal iron from iron binding proteins to promote growth of pathogen

43
Q

What do biofilms do during colonization

A
  1. Enable development of high cell densities
  2. Enable quorum sensing, which allows biofilm inhabitants to coordinate their cellular activities (ex: exotoxin production)
44
Q

What is quorum sensing

A

Allows pathogens to coordinate their cellular activities

45
Q

How does invasion occur via enzymes

A

Invasins cause local damage to host cells and extra cellular matrix to facilitate spread beyond colonization

46
Q

How does hyaluronidases and collagenages work during invasions

A

Hyaluronidase splits epithelial cells and pathogen enters

Collagenase breaks open basement membrane which allows pathogen to invade deeper tissues and enter blood stream

47
Q

What does it mean for pathogen to invade paracellularly

A

Between epithelial cells

48
Q

What does it mean for pathogen to invade transcellularly

A

Passage through epithelial cells

49
Q

How do obligate and facultative organisms invade host

A
  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
Q

Pathogens can also invade via ___ and ___ systems

A

Circulatory, lymphatics

51
Q

Pathogens can also invade from organ to organ in ___ and ___ cavities

A

Peritoneal and pleural cavities

52
Q

Pathogens can also invade via mobile ___

A

Phagocytes

53
Q

What are the 4 ways a pathogen damages a host

A
  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
Q

What are the portals of exit

A

Pathogenic effects- diarrhea, coughing, skin lesions that facilitate transmission of pathogens to new hosts or other reservoirs

55
Q

What is a passive carrier

A

Carry/transmit pathogen without having had the disease

56
Q

What is an incubatory carrier

A

Transmit pathogen during incubation period of the disease when there are no overt signs/ symptoms in the carrier

57
Q

What is a convalescent carrier

A

Harbor/transmit pathogen while recovering from disease

58
Q

What is an active carrier

A

Completely recovered from disease but still harbor/ transmit pathogen

59
Q

Describe how Streptoccous equine and equine strangles is an active carrier

A
  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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