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microbial pathogenesis Flashcards

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Biology 101 flashcards
1
Q

five steps required for a pathogen to cause disease

A

1- host entry
2- attachment and colonization
3- avoidance of host immunity
4- host damage
5- host exit

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2
Q

virulence factors

A

traits that enhance a pathogen’s ability to cause disease

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3
Q

horizontal gene transfer

A

major mechanism in which bacteria acquire new virulence factors (conjugation, transformation, transduction)

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4
Q

genomic island

A

integration of foreign DNA into the host chromosome

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5
Q

pathogenicity island

A

look different, flanked by phage or plasmid genes, and contain virulence factors

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6
Q

what determines if a particular genomic island is a pathogenicity island?

A

the DNA increases the fitness of a microbe within its host

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7
Q

what virulence factors are required for attachment

A

adhesions

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8
Q

why is attachment required for all microbes to colonize the host?

A

it is step one for successful disease and is required to cause disease. Pathogens must overcome barrier methods that the body has in place to resist pathogens

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9
Q

pilin

A

protein that forms pilus/pili

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10
Q

pilus/pili

A

product of pilin assembly (an adhesion)

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11
Q

which region of the pili is assembled first?

A

the tip

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12
Q

which region of the pili interacts with the host receptors?

A

adhesion protein

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13
Q

type I pili

A

static, hairlike appendages, for attachment adhesion only

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14
Q

type IV pili

A

dynamic, thin, and flexible for twitching adhesion AND motility

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15
Q

pili are an example of adhesion molecules what should we appreciate about them?

A

different adhesions on bacteria will determine host species and cell types that these bacteria will attach to and colonize

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16
Q

how do bacteria colonize the body do so?

A

biofilms

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17
Q

biofilm attach to

A

organic (tissue and organs) and inorganic (implants) materials

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18
Q

biofilms vs planktonic cells

A

cells within biofilms (planktonic cells) have differences in the expression of surface molecules, antibiotic resistance, nutrient use, and virulence factors

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19
Q

quorum sensing

A

the cell to cell communication that occurs between cells in a biofilm

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20
Q

how do biofilms lead to chronic infections and chronic inflammation?

A

their presence chronically activates toll-like receptors and triggers chronic inflammation due to cytokines and the biofilm not clearing up

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21
Q

appreciate the steps of bacterial pathogenesis in order, what type of bacteria does this apply to?

A

1) entry into the body
2) adhesion to host cell surface
3) colonization
4) biofilm development
APPLIES TO: extracellular bacteria

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22
Q

how do intracellular pathogens’ pathogenesis differ?

A

1) adhesion
2) entry
3) colonization
4) biofilm
intracellular pathogens may enter cells after adhesion but before colonization and biofilm development

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23
Q

assume a pathogen gets to the colonization step, is it at risk of being sensed/removed from the immune system?

A

YES! It is after colonization that bacteria will be sensed/removed. pathogens must evade or counteract the immune system to develop disease

24
Q

how do pathogens sense they are in our bodies?

A

by using mechanisms to sense environmental conditions

25
Q

when are virulence factors expressed?

A

when environmental cues are sensed

26
Q

what are the 6 mechanisms extracellular bacteria use to avoid being sensed/removed by the immune response?

A

1- capsule
2- vary antigen structure
3- sequester antibodies
4- secrete fake cytokines
5- manipulate host cytokine production
6- control virulence factor synthesis

27
Q

how does a capsule benefit bacteria?

A

coats bacterial cell walls that mask PAMPS (pathogen-associated molecular patterns) and antigens, prevents phagocytes from binding

28
Q

how does varying antigen structure benefit bacteria?

A

on the cell surface to avoid immune detection

29
Q

how do sequester antibodies benefit bacteria?

A

cell surface proteins like Protein A bind the Fc region

30
Q

how does secreting fake cytokines benefit bacteria?

A

influences the immune system

31
Q

how does manipulating host cytokine production help benefit bacteria?

A

manipulates immune cells

32
Q

virulence factor synthesis is?

A

induced by biofilm quorum sensing

33
Q

what are the two classes of intracellular pathogens? which class would be most likely to spread from person to person?

A

(1) facultative intracellular pathogens- can invade host cells but can also survive outside the cell *** more likely to spread from person to person because more adaptive to different modes of transmission due can survive and replicate outside of the cell

(2) obligate intracellular pathogens- invade and reproduce inside the cell only

34
Q

what is something to appreciate about intracellular bacteria in relation to extracellular bacteria?

A

intracellular bacteria will be inherently more hidden from most innate and immune cells than extracellular bacteria are but they can still be detected and removed

35
Q

what are the 3 mechanisms that intracellular bacteria can use to survive within cells when they are endocytosed/phagocytosed consider how these fates benefit the bacteria or hide them from the immune system

A

(1) Survive and replicate within phagolysosomes
(2) prevent lysosome fusion and persist in phagosome
- exocytosis can expel bacteria into extracellular space
-phagocytes can inject pathogens and deliver them to the lymph node
(3) can break out of the phagosome and move throughout the cytoplasm and adjacent cells

35
Q

what is an endotoxin and what types of bacteria express it?

A

an important virulence factor common to all gram-negative cells

35
Q

why is it called an endotoxin?

A

is it within the cell and is toxic once the cell (in this case gram-negative cells) dissinegrate

36
Q

(1) which component of the LPS acts as an endotoxin? (2) In what situation do immune cells recognize it? and (3) what senses it and what is the result?

A

1- Lipid A on the outer membrane
2- when gram-negative cells die they release lipid A and
3- toll-like receptors of the immune system recognize it which leads to a dramatic release of proinflammatory cytokines

37
Q

what is the role of endotoxins in driving sepsis?

A

this release of pro-inflammatory cytokines causes a “cytokine storm” which can contribute to the signs/symptoms of sepsis (fever, activation of clotting factors, activation of complement, vasodilation -> low BP -> shock and death

38
Q

exotoxins

A

secreted by bacteria to alter host cell function, disrupt the immune system, or outright kill the host cell to obtain nutrients, exotoxins are secreted

39
Q

list the 9 exotoxin modes of action

A

1-plasma membrane disruption
2-cytoskeleton alterations
3-protein synthesis disruption
4-cell cycle disruption
5-signal transduction disruption
6-cell-cell adhesion disruption
7-blockage of exocytosis
8-redirection of vesicle traffic
9-superantigens that cause immunopathology
acronym-?

40
Q

which membrane are exotoxins transported across in gram-positive cells? gram-negative?

A

gram-positive: cytoplasmic membrane
gram-negative: both the outer membrane and cytoplasmic membrane (have outer membrane)
BOTH use general secretion systems to transport proteins across the cytoplasmic membrane

41
Q

what type of bacteria uses specialized type II, III, and IV secretion systems?

A

gram-negative

42
Q

mechanisms of the general secretion pathway. secrete outside of the cell or exotoxin directly to target?

A

Gram-positive bacteria use general to transport proteins outside of the cell and into the periplasm
*secrete outside of the cell

43
Q

mechanisms of specialized secretion type II. secrete outside of the cell or exotoxin directly to target?

A

piston mechanism, push proteins out of the cell
*secrete outside of the cell

44
Q

mechanisms of specialized secretion type III, secrete outside of the cell or exotoxin directly to target?

A

needle mechanism, inject proteins into the host cell
*directly to target (cell-cell contact)

45
Q

mechanisms of specialized secretion type IV. secrete outside of the cell or exotoxin directly to target?

A

modified conjunction sex pilus mechanism, transport toxins
*directly to target (cell-cell contact)

46
Q

remember the definition of viruses

A

obligate, intracellular parasites
*all viruses are pathogens in their host and all pathogens are parasites

47
Q

what happens to a virus outside of the host cell

A

it is completely inert (inactive)

48
Q

what are the main ways (3 examples) viruses have immune avoidance (changing the way they look to the immune system)

A

antigenic variation
1-serotypes
2-antigenic drift
3-antigenic shift

49
Q

serotypes

A

same species but antigenically distinct enough to generate a unique immune response

50
Q

antigenic drift

A

small; mutations cause slightly different forms

51
Q

antigenic shift

A

big; reassortment of genome segments from a viral strain with segments that infect one species with strains from a different species

52
Q

why is influenza more pathogenic than rhinovirus?

A

-influenza replicates more easily at body temperature (37 degrees Celsius)
-PAMPs from influenza trigger proinflammatory cytokines in the lower and upper respiratory tracts
-patients from influenza are more likely to have secondary infections due to the immunopathology (damage from disease) in the respiratory tract

53
Q

(1) what strategies of viral pathogenesis are used by HPV and (2) how do the effects on the host cell benefit the virus?

A

1- antigenic variation- 100s of serotypes. Also the proteins expressed during HPV increase host cell division of virus infected cells
2- these transformed host cells become immortal and replicate uncontrollably which can lead to cancer

54
Q

(1) what type of virus infection has a stage that does not cause disease and (2) what process allows these viruses to replicate and cause disease

A

1- Herpres virus has a latency period
2- reactivation

55
Q

In what 3 ways does HIV contribute to immunosuppression

A

1- depletes helper T cells by attachment proteins binding to CD4 and CDR5 on T helper cells
2- inhibits apoptosis of virus-producing cells while also initiating the death of healthy cells
3- HIV downregulates CD4 and MHC-1 to hide from CD8 cytotoxic T lymphocytes

Microbiology (4 decks)

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