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Bacteriology > Pathogenic mechanisms of bacteria > Flashcards

Pathogenic mechanisms of bacteria Flashcards

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
Q

What does koch’s postulates show?

A

cause and effect relationship of disease

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26
Q

How are bacteria able to produce disease ?

A

virulence - capacity to cause disease

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27
Q

What factors in host-parasite interaction that determines whether bacterial agent cause disease?

A

virulence factors of bacteria, age, pili, IgA protease production, Iron capturing ability, production of coagulase, production of toxins, ability to survive inside phagocytic cells

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28
Q

What methods do pathogens use to cause disease?

A

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

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29
Q

Can bacteria penetrate the gut epithelial layer?

A

yes, ex. salmonella typhimurium (food poisoning)

30
Q

What are M cells?

A

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
Q

How do M cells play a role in the pathogenesis of Salmonella typhimurium?

A

S. typhimurium adheres and enters m cells which it kills (apoptosis). Having penetrated the epithelium it infects macrophages and gut epithelial cells

32
Q

How else can S. typhimurium enter the gut?

A

invade gut epithelial cells by adherence of their fimbriae to the luminal epithelial surface

33
Q

How do DCs play a role in S. typhimurium?

A

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
Q

What is the best mechanism of adherence?

A

attachment mediated by rod-shaped protein structure called pili or fimbriae

35
Q

What part of the pilus mediates adherence of bacteria?

A

the tip

36
Q

What are adhesins

A

cell surface proteins important for adherence; mediate tighter binding of bacteria to host cell

37
Q

What are invasins?

A

bacterial surface proteins that provoke phagocytic ingestion of bacteria by host cells –> cause changes in host cell cytoskeleton

38
Q

How do capsules help bacteria survive?

A

cover the surface of the bacteria and protects it from the host’s inflammatory response –> complement activation and phagocyte-mediated killing; avoid phagocytosis

39
Q

What are siderophores?

A

low molecular weight cmpds that chelate iron with very high affinity

40
Q

How do siderophores help bacteria survive?

A

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
Q

What are two results of a bacterial infection?

A

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
Q

What are different strategies evolved in bacteria?

A

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
Q

How do bacteria suppress antibodies?

A

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
Q

How do bacteria hide inside cells?

A

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
Q

What’s another immune evasion strategy for bacteria?

A

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
Q

What are characteristics of bacillus anthraces spores?

A

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
Q

What should you NOT do if you suspect anthrax in a dead animal?

A

don’t open the carcass –> exposed to oxygen –> form spores and can survive long time

48
Q

What are clinical signs of anthrax?

A

enlarged spleen, blood coming out of from all orifices –> blood smear –> gram stain –> gram +
*square cut ends

49
Q

What happens if you block spore formation?

A

little virulence is observed

50
Q

What happens to host if they ingest/inhale spores?

A

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
Q

Toxins produced by bacteria cause what?

A

tissue damage

52
Q

what is an exotoxin?

A

toxin excreted by microorganism, can cause damage to host by destroying cells or disrupting normal cell metabolism; highly potent

53
Q

Where are exotoxins released?

A

released and act on surface of host cells

Ex. botulinum toxin

54
Q

What is a toxide?

A

inactivated formalin toxin

55
Q

What is an endotoxin?

A

part of outer membrane of cell wall of gram -

56
Q

Are endotoxins secreted in soluble form?

A

NO, a structural component in bacteria which is released mainly when bacteria is lysed

57
Q

What do endotoxins trigger?

A

phagocytes to release cytokines that produce local or systemic inflammation (shock, fever, leukopenia)

58
Q

All gram - produce endotoxins?

A

True

59
Q

Define chemotaxis

A

chemical process by which phagocytes are led to the site of infection

60
Q

How do bacteria inhibit chemotaxis?

A

produce toxins which inhibit movement of phagocytes –> hinders them in their journey

61
Q

How do bacteria inhibit phagocytosis?

A

some bacteria evade by not presenting anything for the phagocyte to grip onto

62
Q

How do bacteria kill phagocytes?

A

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
Q

How do bacteria colonize a phagocyte?

A

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
Q

What are indirect mechs of tissue damage by pathogens?

A

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
Q

Characteristics of Botulism

A

makes 7 neurotoxins, toxins detected in feces, blood, and food source

66
Q

How are animals exposed to botulism?

A

ingestion of preformed toxins, but vegetative growth of bacteria in gut can occur

67
Q

Describe mech of botulism

A

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
Q

Clinical signs in botulism

A

blurred vision, swallowing difficulty; mortality depends on species and on toxin dose
*limberneck in birds, quadraplegia in mammals

69
Q

Describe tetanus

A

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
Q

clinical signs in tetanus

A

vascillating spasms occur, resp distress, victim remains conscious, resp arrest, death if toxin dose is high enough

71
Q

What are superantigens?

A

powerful immunostimulatory and disease-causing toxins

72
Q

What do superantigens do?

A

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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