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WEEK 11 SEM 4 > Mechanisms of bacterial Infection I > Flashcards

Mechanisms of bacterial Infection I Flashcards

1
Q

What is symbiosis?

A

2 organisms existing together

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2
Q

What are 3 types of symbiosis?

A

commensalism
mutualism
parasitism

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3
Q

What is commensalism?

A

smaller organism takes benefit from host without causing harm
e.g. commensal flora in body

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4
Q

What is mutualism?

A

host and small organism benefit
opportunisitic
usually asymptomatic

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5
Q

What is parasitism?

A

small species harms host
full pathogen
lead to infection

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6
Q

The effect the pathogen has on a host depends on what?

A

balance between pathogenic mechanisms of the bacteria, and defensive mechanisms of the host

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7
Q

What are some pathogenic mechanisms of the pathogen?

A

adhesins:
toxins:
POLYSACCHARIDE capsules:
enzymes:

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8
Q

What do adhesins do?

A

allow the bacteria to adhere to mucosal surfaces which is one of the first steps in any pathogenic process

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9
Q

What do toxins do?

A

can damage the host,
undermine immune response
evades immune response

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10
Q

What are capsules?

A

defense structures on the outside that prevent the

pathogens from being attacked by antibodies and complements

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11
Q

What are host defence mechanisms?

A

natural barriers: skin and mucosal surfaces = elicit mucous and bile in the gut
tight junctions between epithelial cells- cilia on them= allows mucus clearance in lungs
lysozymes = tears and secretions
lactoferrin and acute phase proteins in the blood that chelate iron from bacteria that require it to grow
there are defensive cells, complement proteins and immune responses

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12
Q

According to Koch’s posulates, what criteria must be met to correlate a pathogen to a disease?

A
  1. microbe present in EVERY case of infection
  2. microbe has to be cultured from cases in vitro
  3. microbe must reproduce the disease in animals
  4. microbe must be able to be isolated from the infected animal
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13
Q

Can there be exceptions to koch’s postulates?

A

yes
-cant culture many organisms e.g. leprosy and syphilis

for infections like these, molecular tests e.g. PCR are done to show their presence

for some bacterial disease, you cant find the bacteria causing it-because it’s the product of the organism that is released into the host that
causes the disease
e.g. toxins produced by the organism B, cereus

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14
Q

What does the organism B cereus cause?

A

B cereus= food poisoning bacteria
-contaminates food, and if a person eats part of the food which is contaminated, it will lead to a toxin mediated disease

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15
Q

What is a local infection?

A

spots on skin
cholera
gonnorhea

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16
Q

What does V.cholera do?

A 
lives on the gut
adheres to epithelial cells of gut
doesn't penetrate body but releases toxins
effect on enterocytes
leads to watery perfuse diarrhoea
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17
Q

Where does gonnorhea live?

A

mucosal surface of uroepithelial layers
cause mucosal inflammation
cause localized infections

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18
Q

What is an invasive infection?

A 
enter lymphatics (not just on musocal surfave)
e.g. shigella, staph aureus
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19
Q

What is a systemic infection?

A

spread via blood and lymph
infect other body parts
e.g. s, typhi N. meningitidis

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20
Q

How does tetanus act?

A

releases toxins and enzymes

secreted in one place but have effect on another place

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21
Q

What does shigella do?

A

cause watery diarrhoea

invades tissue causing submucosal tissue damage

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22
Q

What doe S.typhi cause?

A

typhoid

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23
Q

What is N.meningitis?

A

N mengitidis- gram negative bacteria causing meningitis

starts off as commensal organism

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24
Q

What are the stages of of bacteria causing an infection?

A 
ACP MIDTR
acquisition
colonization
penetration
multiply and spread
immune evasion
damage host
transmission and shedding
resolution
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25
Q

What happens in acquisition?

A

get/acquire organism

breathe in, get in on skin- inject in through broken skin wound

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26
Q

What happens in colonization?

A

bacteria needs to ADHERE

IF It cant it gets cleared away in blood

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27
Q

What happens in penetration?

A

once adhered
bacteria release toxins and enzymes
allows them to penetrate into tissue
create an environment where they can survive

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28
Q

What happens with mulptiplication and spreading?

A

bacteria has made niche for itself, it now multiplies
spread locally or through blood

e.g. meningitis normally lives in nasopharynx, but can invade local mucosa and enter blood stream = cause meningitis (because it can evade all the immune attacks)

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29
Q

What happens in immune evasion?

A

if a bacteria cant evade the immune system, then it will get wiped out, but very serious bacterial infections have mechanisms to evade immunity

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30
Q

How can a bacteria cause damage?

A

triggers an inflammatory response

release of inflammatory mediators, toxins, and enzymes)

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31
Q

What happens in transmission and shedding?

A

bacteria damages host to allow bacteria to transmit to next host

e.g. V. cholera produces toxins that result in diarrhea, and as the bacteria are growing and multiplying in the gut, they are released into the environment through the diarrhea−it is worth noting however that the disease is not always required for transmission, there can be asymptomatic shedding

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32
Q

What is resolution?

A

driven by an antigen specific adaptive immunity - can clear infections
sometimes damage can lead to death even after resolution

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33
Q

Virulence factors are produced by bacteria to help with 3 main functions. What are they?

A
  1. promote colonization and adhesion
  2. to evade host defenses (to block complements, block neutrophils, hide their antigens etc)
  3. to promote tissue damage = necessary for the bacteria to grow and transmit itself eg toxins (exotoxins are secreted by the bacteria and have a mode of action away from the site of secretion)
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34
Q

What are the virulence factors?

A 
adherence factors
invasion factors
capsules
endotoxins
exotoxins
siderophores
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35
Q

What are adherence factors?

A

need for bac to adhere to mucosal surface

−contain pili, fimbraie (proteins with long fibrous nature- allow them to attach to epithelial cells)

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36
Q

What is a capsule?

A

outer surface polysaccharide capsules

prevent them from being opsonized by antibodies or binding complement proteins (the polysaccharide nature stops this from happening)

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37
Q

What are exotoxins?

A

proteins and enzyme released from a bacteria that have a different site of effect (can be cytotoxic, neurotoxic, enterotoxic etc)

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38
Q

What are siderophores?

A

whole series of proteins and binding proteins that bacteria release to compete for micronutrients from hosts

transferrin, lactoferrin and acute phase proteins produced by the liver (these reduce the amount of iron available for the pathogen to grow)

released by the bacteria to bind iron and they have iron binding capacities massively more than lactoferrin and our own iron binding proteins

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39
Q

What are endotoxins?

A

lipolysaccharides on gram negative

cause fever, change in bp, inflammation, lethal shock

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40
Q

What mechanisms drive tissue damage?

A

direct
innate
adaptive

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41
Q

What is the direct method of tissue damage?

A

microorganisms invade cells and cause cell lysis

microorganisms also release exotoxins that cause tissue damage

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42
Q

What is the innate method of tissue damage?

A

microorganisms release endotoxins = activate all components of the immune response that lead to macrophage activation, mast cell degranulation, neutrophil acquisition, clotting activation−these all lead to tissue damage

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43
Q

What are the adaptive immune mechanisms?

A

the generations of granulomas in diseases like Tb which cause necrosis (chronic inflammatory response to bacteria that cannot be killed by innate or adaptive immunity
T and B cells can be activated = cause direct damage to tissue (TCELLS)
OR create antibodies (BCELLS)

44
Q

What does Bordetella pertussis cause?

A

whooping cough- can be mortal in children
now vaccines
not invasive- stays on mucosal surface of upper respiratory tract

45
Q

How does Bordetella pertussis act?

A
  • toxins cause damage
  • cough and localized inflammation (last 3 months)
  • toxins released to stop immune system clearing it
  • toxins- cause inflammation- whoop sound when breathing
46
Q

What is Vibrio cholerae?

A

non invasive bacteria in the gut lumen
attaches to enterocytes
releases toxins which affect the enterocytes
leads to watery diarrhea

47
Q

What happens in Neisseria meningitidis?

A
  • organism= lives in the nasopharyngeal cavities (normal commensal organism in quite a few people)
    GRAM NEGATIVE
    CUASED MAINLY BY ENDOTOXINS
  • occasionally invades
  • causes bacteremia (bacteria in blood), septicemia, endocarditis (inflammation of the endocardium inner layer of heart), meningitis, endotoxemia (endotoxins in the blood)
48
Q

What happens in Staphylococcus aureus?

A
  • locally invasive bacteria
  • produces a lot of toxins
  • cause skin and wound infections
  • very difficult to clear
  • overcomes immunity
49
Q

What happens in myobacterium tuberculosis?

A
  • invasive pathogen
  • starts in lungs
  • gets phagocytosed by macrophages
  • migrate to lymph nodes
  • spread around body
  • cause infection in bones, brain, lungs= miliary Tb (infection caused in every major organ)
50
Q

What is the key pathological process in Tb?

A

Drive chronic granulomatous inflammation

51
Q

What happens in Streptococcus pneumoniae?

A
  • organism causes lobar pneuomina, bone infections, septicemia, meningitis
  • part of childrne’s vaccine
52
Q

What does Streptococcus pneumoniae have?

A
  • outer capsule
  • endotoxin like molecules = drive and dysregulate immune responses
  • toxins that cause damage and local inflammatory responses
  • mechanisms to evade immunity
53
Q

What is streptococcus pyogenes?

A

group A strep
tonsilitis
sore throat
wound infections

54
Q

How does streptococcus pyogenes adhere to host?

A

one of its adhesion molecules is structural component of cell wall called M protein fibrils

55
Q

What are M protein fibrils?

A

adhesion molecules for streptococcus pyogenes

long polymeric proteins, and at the tip they have a very specific protein called an adhesin subunit that allows it to interact with very specific receptors on cells

56
Q

What type of bacteria is Neisseria gonorrhoea?

A

gram negative diplococci
has huge long fibriae all over bacteria
can adhere to uroepithelial surfaces

57
Q

What is the body defence against neisseria gonnorhoea?

A

flow of urine- takes and removes bacteria with it

58
Q

How does neisseria gonorrhoea fight against urine?

A

bacteria has these long fimbriae
allows it to bind to epithelial cells- which are distance away

once it adheres, it contracts and brigns bacteria close to uroepithelial cells

59
Q

How are exotoxins described?

A

proteins released from bacteria

enterotoxins = affect enterocytes in gut lumen produced by E. coli and V. cholera

neurotoxins= affect neural cells= e.g. TETANUS, BOTULISM

leukocidins= against white cells= released by STAPH AUREUS

ciliostatic toxins= stops ciliated epithelial cells working= RELEASED BY BORDETELLA PERTUSSIS- CAUSE whooping cough

60
Q

What are the functions of toxins?

A
  • promote adhesion
  • promote survival or spread of bacteria like hyaluronidase and collagenase
  • damage or destroy cells and cell membranes by using phospholipases and pores
  • interfere with cell metabolism like cholera and diphtheria
  • affect nerves
61
Q

How many different types of toxins are there?

A

3

62
Q

How do type 1 toxins act?

A

act at cell membranes
not transported into cell
cleave and damage surface proteins
damage metabolism or the ability of the cells to respond to signals

63
Q

How do type 2 toxins act?

A

act on the cell membrane and damage it

exotoxins can create pores in the cell membrane damaging it

64
Q

How do type 3 toxins act?

A

intracellular
after translocation
disrupt cellular function

65
Q

What are the extraceullar functions of toxins?

A

damage the cellular matrix and connective tissue and destroys the tissue structure

once tissue structure is destroyed, the immune response cannot work= so cant recruit correct immune responses

66
Q

What are examples of type 1 toxins?

A

E.coli produces toxin
super-antigen
toxins produced by staph aureus
toxins produced by strep pyogenes

67
Q

Talk about toxins produced by E.coli

A
  • genes code for enterotoxin= short polypeptide (temperature stable Ecoli)
  • react with G protein on surface of enterocytes
  • massive increase in cGMP inside enterocyte
  • activate chloride channels and passive diffusion of water out of cell
  • watery diarrhoea
68
Q

What is a superantigen?

A

bacterial toxin
leads to T cell activation
but there isnt an acc antigen
(non antigen dependent clonal T cell activation)

69
Q

What is strep pyogenes associated with?

A

scarlet fever

sore throat

70
Q

What can some strains of strep pyogenes cause?

A

produce a series of toxins, and one of them is a super-antigen that leads to cytokine storms

-the cytokine storm causes desquamation of cells on the tongue forming a strawberry like appearance called strawberry tongue

−some of the other toxins in these genes cause an erythematous rash which is typical of someone who has scarlet fever

71
Q

What do type 2 toxins do?

A

damage membrane by forming pores

72
Q

What are type 2 toxins?

A

alpha toxin of staph aureus
streptococcus pyogenes
streptococcus pneumoniae
bacillus cereus causes food poisoning in uncooked rice produces cerolysin which forms pores

73
Q

What does the alpha toxin of staph aureus do?

A 
binds to cell membrane
oligomerizes 
forms a heptamer pore
this damages the membrane, and disrupts ion transport across the membrane
cause tissue damage and cell death
74
Q

What does streptococcus pyogenes produce to form a pore?

A

streptolysin

75
Q

What does streptococcus pneumoniae produce to form a pore?

A

pneumolysin

76
Q

What does bacillus cereus produce to form a pore?

A

cerolysin

77
Q

Which enzymes directly damage cell structure?

A

phospholipases and hemolysin molecules

78
Q

What is Clostriduim perfringens?

A 
dangerous
causes gangrene
gram +ve rod bacteria
- anaerobe
- forms spores
- found in soil and human gut
79
Q

What virulence factors does clostridium perfringens have?

A

alpha lecithinases
phospholipase C = damages lipid membrane

it kills WBCs, RBCs and if it escapes into blood stream it causes severe hemolysis and death

80
Q

What is the treatment for gangrene?

A

amputate

stop clostridium perfringens from spreading

81
Q

What is Necrotizing fasciitis caused by?

A

strep pyogenes- group A strep

82
Q

What is nectorizing fascitis?

A

beta hemolytic
strains carry a genes= form enzyme called cysteine proteases
once bacteria enter skin, they produce many enzymes and toxins
when the structural layers of the skin have been compromised, any inflammatory response will not get to where the bacteria is (as the structure of the tissue is disrupted)−the blood supply gets cut off•the bacteria spreads and spreads and eats away the whole structure of the tissue

83
Q

What are the virulence factors of strep pyogenes group A?

A
  • M proteins = adhesins
  • streptococcal pyogenes exotoxins- A,B,C= toxins
  • capsule (hyaluronic acid) = block opsonisation
    (bc our cells have hyaluronic acid so bacteria is not recognized as foreign)
  • streptolysin and leucocidins =make pores in cell memb and damage WBC
84
Q

What causes a pore in clostidirum perfringens?

A

perfringolysin

85
Q

What do type 3 toxins do?

A

go into cells

cause damage

86
Q

What is ADP ribosylation?

A

natural process
normally:after translation, enzymes modified to change its properties

ADP ribosylating enzymes= toxins
target proteins to stop cell metabolism and cause cell lysis

87
Q

Which conditions can cause ADP ribosylating enzymes?

A

cholera
pertusiis (whooping cough)
diphtheria

88
Q

What are Zn2+ dependent endopeptidases and where are they found?

A

neurotoxins

found in botulism and tetanus

89
Q

What do the toxins target?

A

G proteins
protein synthesis by changing rRNA
actin and microfibril

90
Q

What mechanism is inhibted in shigella?

A

protein synthesis

91
Q

What bacteria causes shigella?

A

bacteria- shigella dysenteriae

92
Q

What happens in shigella?

A

acute watery diarrhoea with blood and pus

means it invaded into local and submucosa

93
Q

Which toxin does shigella involve?

A

toxin which has N-glycosidase activity
cleaves that 28s ribosomal RNA and stops the cell from making proteins
this affects enterocytes

94
Q

What mechanism is inhibited in diptheria?

A

protein synthesis

95
Q

What bacteria is involved in diptheria?

A

C. diptheria

96
Q

What does C diptheria do?

A
  • ADP ribosylates things
  • targets elongation factor 2
  • undermines protein synthesis causing cell death
  • toxin release
97
Q

What does C diptheria cause?

A
  • upper respiratory tract infection
  • production of a pseudomembrane consisting of pus and bacteria and fibrous tissue
  • life threatening situation (through asphyxiation)
98
Q

What does cholera produce?

A

watery poo

white colour

99
Q

What does cholera toxin do?

A

cholera toxin binds receptor on cell surface
release active subunits that ADP ribosylate G proteins and activates adenylate cyclase
changes the activity of Cl-channels
activated of Cl-channels leads to hypersecretion of water leading to profuse watery diarrhoea

100
Q

What causes tetanus?

A

clostridium tetani

101
Q

What bacteria is clostridium tetani?

A 
gram positive
rod
lives in soil
forms spores
anaerobic
102
Q

What is tetanus?

A

metallopeptidase

targets protein in presynaptic vesicles of CNS

103
Q

What does the tetanus block and what does this cause?

A

synaptobrevin = component of the vesicles

prevents release of neurotransmitters from interneuron

cause overexcitation of motor neurone from sensory neurone

leads to spastic paralysis

104
Q

What causes Infantile botulism/floppy baby syndrome?

A

clostridium botulinum

gram positive anaerobe= forms spores

105
Q

What happens in infantile botulism?

A

this toxic targets the presynaptic vesicles in the neuromuscular junction

this blocks the release of Ach which is the neurotransmitter at the NMJ

without Ach, there is flaccid paralysis

106
Q

What is the difference between heat labile and heat stabile e. coli toxin causing diarrhoea?

A 
Heat stable
Activate guanylate cyclase
High cGMP
Activate protein kinase
Ion channel disruption
Chloride secretion
Water follows 
Watery diarrhoeha
Heat labile
Multimeric protein
Stim adenylate cyclase
More cAMP
More protein kinase
More chloride secretion
More watery diarrehoa

WEEK 11 SEM 4 (9 decks)

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