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Micro > 1/2 bacterial structure and pathogenesis > Flashcards

1/2 bacterial structure and pathogenesis Flashcards

1
Q

what organelle do prokaryotes have

A
  • ribosome, just free in cytoplasm
  • no other organelle
  • nothing membrane bound except cell itself
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2
Q

cocci

A

round

ex: streptococci

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3
Q

diplococci

A

two round cells

ex: Neisseria

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4
Q

Baccili

A

rod shape

ex: bacillus

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5
Q

spirilla

A

spiral
ex: campylobacter

**spirochetes = true spiral, corkscrew, oral treponemes

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6
Q

pleomorphic

A

morphology can vary depending on environment (fusobacteria)

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7
Q

Gram stain - 3 groups

A

G pos = purple
G neg = pink
acid fast = myobacteria (tuberculosis) – MYCOLIC ACID

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8
Q

why do acid fast not stain?

A

mycolic acid

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9
Q

cell envelope

A

multiple functionally adn chemically distinct layers

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10
Q

describe G neg

A

(stains pink)

  • inner membrane
  • periplasmic space with peptidoglycan
  • outer membrane with LPS outer leaflet
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11
Q

describe G pos

A

(stains purple)

  • thick peptidoglycan layer
  • *peptidoglycan later gas teichoic acid and lipoteichoic acid
  • over membrane
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12
Q

what is only found in G pos adn only in G neg

A

G pos - only cells with teichoic adn lipoteichoic acids

G neg - only cells with LPS (outer leaflet of outer membrane)

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13
Q

spetic shock cause

A

LPS, Lipid A (G neg)

teichoic/lipoteichoic acids (G pos)

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14
Q

variable components = flagella, pilus, capsule

A
  • flagella, G neg its anchored in many places
  • pilus = fimbria
  • capsule = optional; also can be induced in some when env conditions call for it
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15
Q

LPS components

A

(LPS is outer leaflet of G neg and renders outer membrane)

  • O antigen: external, highly variable, connects to core
  • core region: inner core (heptose sugars adn KDO0 and outer core (hexose sugars)
  • lipid A: membrane anchoring, toxic component
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16
Q

LPS can cause what and how

A

septic shock, MSOF – Lipid A is released when cells are lysed. normally lipid A buried deep

lipid A: fatty acid attached to sugar component - when this is altered slightly, you affect the potentcy. **AA in D configuration

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17
Q

teichoic and lipoteichoic acids

A
  • only in G pos
  • polymer of modified ribose phosphate or glycerol phosphate
  • lipoteichoic acids are anchored to cell membrane by FA
  • Teichoic acids are covalentyly linked to peptidoglycan
  • can trigger septic shock adn MSOF
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18
Q

peptidoglycan (murein)

A
  • in G pos (very thick) and G neg (thin, periplasmic space)
  • alternating units of NAM and NAG
  • strands linked by peptides of D and L-aa’s
  • forms rigid mesh that maintains cell rigidity
  • can be cleaved by lysozyme
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19
Q

what can tear peptidoglycan apart

A

lysozyme

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20
Q

bacterial capsule aka glycocalyx aka slime layer

A
  • polysaccharide or AA network
  • made by some G pos and some G neg
  • promotes adherence (to teeth)
  • protect from our immune system: anti-phagocytic (harder to engulf) and inhibits complement
  • production is regulated, many only produce when needed
  • increase virulence
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21
Q

how does capsule protect & how is it functional

A
  • anti phagocytic (harder to engulf)
  • inhibits complement

-helps bacteria adhere to teeth

^^increaes virulence

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22
Q

pathogenic

A

yes or no question. does it cause diseae? yes or no.

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23
Q

pili and fimbrae

A
  • hollow protein cylinders
  • in most G NEG adn only a few G pos
  • overcome electrostatic repulsion adn help with cell to cell contact adn adhesion
  • pili can do DNA transfer
  • fimbreae shorter adn more numerous
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24
Q

pili in fimbrae found more in which bacteria

A

G neg

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25
Q

pili vs fimbrae

A
  • fimbrae are shorter and more numerous
  • pili can fxn in DNA trasnfer
  • BOTH are hollow protein cylinders that play a role in adherence and cell to cell contact (overcome electrostatic repulsion)
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26
Q

afimbrial adhesins

A

clusters of protein that are not organized in a defined structure that mediate cell to cell binding

  • do not form hollow tube
  • just embedded in membrane
  • lock and key interaction, like pili, but stronger
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27
Q

what proteins are located at pilus tip?

A

adhesin proteins that mediate initial binding are at tip of pilus….lock adn key receptor (explains why E coli causes UTI)

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28
Q

what does pili mediated adherence have to do with location of germ

A
  • adhesin protein at tip of pilus = lock adn key type combo with host cell
  • so where you find bacteria is determined by env.condiitions AND where there are cells it can interact with, adhere to
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29
Q

specialized pili

A

fxns: adherence, DNA uptake and exchange, important role in motility

**type 4: extend and attach to surface and then retract to pull bacteria forward, allows for movement along surface

**F pili = sex pili = conjugation, DNA transfer

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30
Q

type 4 pili

F pili

A

type 4 - movement along surface (extend to surface and then retract to pull bacteria to surface)

F pili = sex pili = conjugation = DNA transfer

(general fxn = adherence, DNA uptake, motility)

31
Q

flagella

A
  1. monotrichious = single flagella at one end
  2. lophotrichois = many flagella, all at same end
  3. amphutrichous = bundles at both ends, one set for one way and one for another
  4. peritrichous = extend all directions

**spirochetes – endoflagella

32
Q

monotrichous

A

1 flagella frmo 1 end

33
Q

lophotrichous

A

multiple flagella, from one end

34
Q

amphithrichous

A

bundles of flagella at each end

35
Q

peritrichous

A

flagella extend all directions

36
Q

spirochete flagella type

A

endoflagella – use like cork to drill in tissue, (perio disease!), periplasmic flagellum on inside of cell, localized between inner and outer membranes, many from each end, can reverse direction

37
Q

what do we need to know about flagella structure?

A

very defined portions of the motor

G neg has more anchor sites since more layers

38
Q

bacterial injectisome

A
  • type 3 secretion system
  • structural similarity to flagella
  • directly injects effector protein into host cell

**important in pathogenesis for many G neg cells!

39
Q

what is important to the pathogenesis of many G neg cells

A

injectisome, type 3 secretion system – like a flagella that injects effector protein into host cell

40
Q

bacterial spores

A
  • produced by some G pos
  • resistant to heat/desication
  • have a chromosome copy
  • metabolicaly inactive
  • can persist for YEARS
  • germinate to form a new vegetative cell
  • anthrax
41
Q

what happens to inactive spore when conditions are right

A

it GERMINATES to form a new vegetative cell that can thrive

42
Q

infection

A

signs and symptoms of disease occur

43
Q

pathogenic

A

can cause disease

44
Q

virulence

A

quantitative term for disease causing capacity

45
Q

ID 50

A

dose required to INFECT 50% test population

46
Q

LD 50

A

lethal dose required for killing 50% test population

47
Q

opportunistic pathogen

A

usually not a problem, buut under certain conditions causes disease

48
Q

LD 50 vs ID 50

A

lethal vs infect

-minimum dose to either kill (LD) or infet (ID)

49
Q

gnotobiotic

A

animals devoid of microflora (survive, but do not thrive)

  • less healthy
  • less developed lymphoid tisues & low Ab titers
  • thin intestinal walls
  • low metabolism rate
  • prone to infections
  • require dietary supplements
50
Q

benefits of normal flora

A
  • food metabolism (proteolytic enzymes facilitate absorption –> malabsorption)
  • vitamin production: biotin, panthotenic acid, pyridoxine, riboflavin, vitamin K
  • protective effects: competition, antibacterial production, immune stimulation
51
Q

vitamins produced by normal flora

A

biotin, panthothenic acid, pyridoxine, riboflavin, vitamin K

52
Q

protective effects of normal flora

A
  • competetion for nutrients/space
  • production of antibacterials: metabloic by products are non specific, bacteriocins are specific
  • immune response stimulation (example of M cell, bacterial antigen stimulates IgA antibody production)
53
Q

study of M cells that showed immune stimulation by normal flora

A
  • bacteria taken up by M cell and pass through
  • presented to macrophage that takes it up adn degrades it
  • macrophage presents to cells that make Ag’s which then interact with T cells adn B cells to make ANTIBODIES
  • IgA = antibody in lumen that protects mucosa
54
Q

IgA

A

antibody that protects mucosa of lumen of GI tract, protects against establishment of salmonella and shigella and otehr mucosal pathogens

IgA production is due to normal flora

55
Q

number bacteria in large intestine vs oral mucosa

A

lg intestine- 10^14 per gram tissue

oral mucos- 10^10

56
Q

oxygen levels in air, mouth, subgingiva

A

21%

12% mouth

2% subgingiva

57
Q

what enzymes to anaerobic bacteria lack?

A

catalase and superoxide dismutase

58
Q

environmental variables that affect flora

A
  • oxygen
  • Temp
  • pH
  • diet
  • age
  • hormonal state
59
Q

how are normal floar harmful?

A

-leading cause of infection in…
dental caries, perio disease, UTI

-bacteria capitalize on trauma, weak immune systems, or altered health – and then cause disease

60
Q

5 steps to infection

A
  1. relocation of normal flora or entry of pathogens
  2. adherence and colonization
  3. establishment of porductive population
  4. dissemination (NOT ALL SPREAD)
  5. outcome = disease and host damage
61
Q

what constitutes infection

A

host damage adn disease

62
Q

how can pathogens be transmitted

A
  • aerosols (whooping cough)
  • fecal/oral (cholera)
  • contact (conjunctiva): pink eye
  • arthropods/insect (lymes)
  • transplacental (gonorhea)
  • blood (Hep)
63
Q

arthropod vectors

A

mosquito = west nile, malaria, yellow fever

ticks = lyme, relasping fever, CO tick feevr

assasin bug = chagas disease (trypanosomiasis)

64
Q

adherence and colonization - point adn example

A

ACTIVE, not passive process

ex: E.coli induces cytoskeleton rearrangement in the host, resulting in pedestal formaation (EFFACING)
- -germ can bind pedestal v tightly

65
Q

capsules and host defense evasion

A
  • anti phagocytic: cells hard to engulf, capsule pulls away when grabbed
  • capsule binds protein that inhibits Ab binding and complement
  • molecular mimicry: capsules sometimes made of material that resembles the host
66
Q

host evasion bia antigenic variation

A
  • switch surface antigens
  • ex: relapsing fever–borrelia hermsii–high density in blood, 40vmp genes but only 1 expressed so when host makes Ab to 1, just switch to another
  • -cyclic fevers
67
Q

borrelia hermsii

A
  • relapsing fever
  • 40 vmp genes but only 1 expressed
  • example of antigenic variation in bacteria to evade host defense
68
Q

evasion of host via intracellular localization

A
  • some intracellular pathogens are obligate while others are facultative
  • nutrient rich environment
  • protection from Ab adn complement
69
Q

direct pathogen induced damage

A
  1. destructuve enzymes (proteases, callagenases) = PERIPATHOGENS
  2. toxic metabolic by products
  3. exotoxins – cholera, tetanus
  4. release cellular components
70
Q

LPS has host dirven damage

A
  • LPS has separable toxic and immunostimulatory activities
  • endotoxin = lipid A
  • endotoxic effects only occur upon cell lysis bc lipid A normally buried in membrane
71
Q

physio response to LPS –> all leads to septic short (vascular collapse) and MOSF (multi system organ failure)

A
  1. Fever – cytokines
  2. neutropenia – neutrophils sequestered in organs, transient decrease in circulating n.phils results
  3. DIC = disseminated intravascular coagulation: platelets adhere to and occlude small blood vessels (form clots)
  4. hypotension: vacular leakage causes low BP
  5. lysozymal enyzmes relaesed, damage endothelium
72
Q

DIC (LPS respons)

A

disseminated intravascular coagulation = platelets adhere to and occlude small vessels (form clots)

73
Q

LPS response - hypotension

A
  • low BP bc of vascular leakage

- complement proteins C3a adn C5a attract PMNs (polymorphonuclear leukocytes) which adhere to endothelial cells

74
Q

LPS response - neutropenia

A

neutrophils get sequested in organs causing a transient decrease in circulating neutrophil count

Micro (7 decks)

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