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Pathogenic mechanisms of bacteria Flashcards

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1
Q

What are a hosts 2 main defenses?

A

body surfaces and defenses of tissues and blood

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2
Q

What is the body’s first line of defense?

A

skin and mucosal surface- non-specific and specific induced defenses

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3
Q

What is the pH of the skin?

A

slightly acidic, pH of 5

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4
Q

Do most bacteria survive in acidic pH?

A

no

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5
Q

How does the dry, acidic low temperature of the skin function in defense?

A

limit bacterial growth

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6
Q

How does sloughing cells help to protect the skin?

A

remove and take bacteria off

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7
Q

How does resident micro flora help in defense?

A

competes for colonization

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8
Q

What type of immune tissue is present in the dermis layer of the skin?

A

SALT - skin associated lymphoid tissue

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9
Q

What is secreted in the mucous membrane as a defense mech?

A

mucus - secreted by the goblet cells

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10
Q

What is mucus’ function?

A

acts as a lubricant and as a physical barrier that traps bacteria before they reach the membrane

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11
Q

What does mucus contain?

A

secretory IgA - binds to bacteria

substances that either kill bacteria or inhibit their growth

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12
Q

What substances does mucus contain that kill/inhibit bacteria?

A

Lysozyme - degrades bacterial peptidoglycan
Lactoferrin - found in milk, tears and saliva –> protein that binds iron with a high affinity
Lacto peroxidase - antimicrobial agent in milk, saliva and tears –> toxic to many bacteria

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13
Q

What is GALT and MALT?
Where are they located?
What do they produce?

A

1) Gastrointestinal associated lymphoid tissue and Mucosa associated lymphoid tissue
2) line the edges of gut and mucosa
3) secretory Ab - prevent bacterial adherence to mucosal cells

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14
Q

What does tissue and blood produce as defense?

A

transferrin - limits iron availability
PMNs - phagocytosis
Monocytes - produce cytokines
Macrophages (tissue) - phagocytosis and Ag presentation
Complement - phagocytosis, opsonization, bactericidal

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15
Q

Describe ingestion of killing of microbe by a neutrophil

A

1) macrophage engulfs bacterium
2) form vacuole around it - phagosome
3) lysosome fuses with it - phagolysosome
4) enzymes are released and degrade bacteria
5) Fragments released

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16
Q

What does bacteria binding to macrophages initiate?

A

release of cytokines and chemokines –> attract and activate leukocytes

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17
Q

What abilities have bacteria developed to survive inside PMN’s?

A

1) escape phagosome before it fuses with lysosome
2) prevent phagosome-lysosome fusion
3) prevent acidification of vacuole or short-circuiting the process of fusion
4) reduce effectiveness of toxic cmpds released into phagolysosome

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18
Q

How do catalase and superoxide dismutase function?

A

detoxify reactive forms of oxygen

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19
Q

How do microorganisms avoid being killed by neutrophils?

A

1) resist ingestion
2) kills neutrophil
3) grows inside phagocyte
4) bacteria lives free in cytoplasm

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20
Q

Define pathogenesis

A

physiological process involved in generation of clinical signs of disease –> pathogen cause illness

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21
Q

Define pathogenicity

A

capacity of microbe to cause disease

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22
Q

Define virulence

A

ability of microbe to cause disease efficiently, degree of pathogenicity

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23
Q

Define virulence factor

A

component of pathogen that contributes to its disease producing potential

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24
Q

What are Koch’s postulates?

A

1) organism must always be found in infected humans/animals, NOT in healthy ones
2) must be isolated from infected inds and grown in pure culture
3) isolated in pure culture must initiate disease when re-inoculated into susceptible animals
4) re-isolated from experimentally infected animals

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25
What does koch's postulates show?
cause and effect relationship of disease
26
How are bacteria able to produce disease ?
virulence - capacity to cause disease
27
What factors in host-parasite interaction that determines whether bacterial agent cause disease?
virulence factors of bacteria, age, pili, IgA protease production, Iron capturing ability, production of coagulase, production of toxins, ability to survive inside phagocytic cells
28
What methods do pathogens use to cause disease?
1) Adhesion - bacteria must first bind to host cell surface 2) colonization - some produce special proteins that help them to colonize parts 3) invasion - some produce proteins that either disrupt host cell membranes or stimulate endocytosis into host cells 4) immune response inhibitors - have virulence factors that inhibit hosts immune system defenses ) toxins - proteins made by bacteria that poison host cells and cause tissue damage
29
Can bacteria penetrate the gut epithelial layer?
yes, ex. salmonella typhimurium (food poisoning)
30
What are M cells?
epithelial cells found on the intestinal mucosa. they transport organisms and particles from gut lumen to immune cells across epithelial barrier --> stimulate mucosal immunity
31
How do M cells play a role in the pathogenesis of Salmonella typhimurium?
S. typhimurium adheres and enters m cells which it kills (apoptosis). Having penetrated the epithelium it infects macrophages and gut epithelial cells
32
How else can S. typhimurium enter the gut?
invade gut epithelial cells by adherence of their fimbriae to the luminal epithelial surface
33
How do DCs play a role in S. typhimurium?
DCs protrude dendrites btw epithelial cells. DCs open tight jns, send dendrites outside the epithelium which breach the epithelial layer and can be infected by salmonella
34
What is the best mechanism of adherence?
attachment mediated by rod-shaped protein structure called pili or fimbriae
35
What part of the pilus mediates adherence of bacteria?
the tip
36
What are adhesins
cell surface proteins important for adherence; mediate tighter binding of bacteria to host cell
37
What are invasins?
bacterial surface proteins that provoke phagocytic ingestion of bacteria by host cells --> cause changes in host cell cytoskeleton
38
How do capsules help bacteria survive?
cover the surface of the bacteria and protects it from the host's inflammatory response --> complement activation and phagocyte-mediated killing; avoid phagocytosis
39
What are siderophores?
low molecular weight cmpds that chelate iron with very high affinity
40
How do siderophores help bacteria survive?
they are excreted into the medium by bacteria --> iron-siderophore complex is taken up by receptors on bacterial surface *iron is essential for bacterial growth
41
What are two results of a bacterial infection?
1) immune system recognizes and destroys all of the organism present in given infection--> organism has failed to establish itself in body --> can't manifest in disease 2) immune system fails --> bacteria evolved a strategy for evading or suppressing the hosts immune response
42
What are different strategies evolved in bacteria?
1) against acquired immunity 2) against phagocytes (avoid fusion) 3) suppression of Abs - hiding inside cells 4) anti-oxidant enzymes 5) form spores 6) develop special adherence mechs 7) production of toxins and cause tissue damage
43
How do bacteria suppress antibodies?
bacteria target those cells of the immune system that specifically react against them - B cells -prevents body from mounting an immune response Ex. Mycobacterium tuberculosis - reduced IL-2 response
44
How do bacteria hide inside cells?
hide inside cells of immune cells - they don't present antigens that will evoke a response --> they multiply inside and then further invade the body Ex. brucella- macrophages
45
What's another immune evasion strategy for bacteria?
they avoid the immune system by existing within infected cells in cytoplasm Ex. Shigella and Listeria escape the vacuole to access cytoplasm Shigella - M cells --> epithelial cells --> spread Listeria - take over cell machinery --> propel out of the cell into another
46
What are characteristics of bacillus anthraces spores?
soil-borne and persist for a long time and at animal burial sites of anthrax-killed animals for many decades. spores known to reinfect animals over 70 yrs after burial sites were disturbed
47
What should you NOT do if you suspect anthrax in a dead animal?
don't open the carcass --> exposed to oxygen --> form spores and can survive long time
48
What are clinical signs of anthrax?
enlarged spleen, blood coming out of from all orifices --> blood smear --> gram stain --> gram + *square cut ends
49
What happens if you block spore formation?
little virulence is observed
50
What happens to host if they ingest/inhale spores?
spores germinate into vegetative bacilli --> org flourishes on mucosa --> septicemia --> rapid disease (resp distress, drooling, stupor, convulsions and collapse) --> death by asphyxiation and organ collapse
51
Toxins produced by bacteria cause what?
tissue damage
52
what is an exotoxin?
toxin excreted by microorganism, can cause damage to host by destroying cells or disrupting normal cell metabolism; highly potent
53
Where are exotoxins released?
released and act on surface of host cells | Ex. botulinum toxin
54
What is a toxide?
inactivated formalin toxin
55
What is an endotoxin?
part of outer membrane of cell wall of gram -
56
Are endotoxins secreted in soluble form?
NO, a structural component in bacteria which is released mainly when bacteria is lysed
57
What do endotoxins trigger?
phagocytes to release cytokines that produce local or systemic inflammation (shock, fever, leukopenia)
58
All gram - produce endotoxins?
True
59
Define chemotaxis
chemical process by which phagocytes are led to the site of infection
60
How do bacteria inhibit chemotaxis?
produce toxins which inhibit movement of phagocytes --> hinders them in their journey
61
How do bacteria inhibit phagocytosis?
some bacteria evade by not presenting anything for the phagocyte to grip onto
62
How do bacteria kill phagocytes?
some bacteria release toxins that are lethal to phagocytes so instead of bacteria being destroyed, the phagocytes are destroyed ex. mycobacterium tuberculosis, streptococcus pyogenes, staphylococci and bacillus anthraces
63
How do bacteria colonize a phagocyte?
bacteria allow themselves to be phagocytized but resist being killed within. many use macrophages as sites of sanctuary where they can multiply w/o interference from other cells of immune system
64
What are indirect mechs of tissue damage by pathogens?
1) immune complexes - immune response to pathogen can generate Ag:Ab complex --> activate macrophages 2) Anti-host Ab - Ab cross reacting to host tissues 3) cell-mediated immunity - T cells killing infected cells
65
Characteristics of Botulism
makes 7 neurotoxins, toxins detected in feces, blood, and food source
66
How are animals exposed to botulism?
ingestion of preformed toxins, but vegetative growth of bacteria in gut can occur
67
Describe mech of botulism
ingestion of toxin --> toxins move to blood --> invasion of peripheral nerves --> blocks release of Ach resulting in flaccid paralysis --> animals remain aware and can feel pain *no primary lesion
68
Clinical signs in botulism
blurred vision, swallowing difficulty; mortality depends on species and on toxin dose *limberneck in birds, quadraplegia in mammals
69
Describe tetanus
spores enter deep tissues with low oxygen tension; spores germinate and toxins are produced --> blocks NT release *toxins spread along: peripheral nerves (ascending) and hematogenous thru lymph (descending)
70
clinical signs in tetanus
vascillating spasms occur, resp distress, victim remains conscious, resp arrest, death if toxin dose is high enough
71
What are superantigens?
powerful immunostimulatory and disease-causing toxins
72
What do superantigens do?
overstimulate T cells by binding to MHC mol and TCR --> overproduction of cytokines (TNF-a) --> shock and MOF

Bacteriology (2 decks)

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