Bacterial Pathogenicity Flashcards

1
Q

Define pathogen

A
  • Pathogen: microorganism that is able to produce disease
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2
Q

Define pathogenicity

A
  • Pathogenicity: ability of microorganism to cause disease
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3
Q

Define virulence

A
  • Virulence: degree of pathogenicity
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4
Q

Define opportunistic pathogen

A
  • Opportunistic pathogens: bacteria that do not need to cause disease to enable transmission
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5
Q

Define obligate pathogen

A
  • Obligate pathogens: require a host for survival and transmission. Usually cause disease
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6
Q

Define virulence factors

A
  • Virulence factors: mechanisms to avoid host defences and multiply
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7
Q

What are 3 categories of factors that enable disease in a host + examples within each category

A

Pathogen factors
* Virulence
* Enviro stability
* Route of entry
* Infective dose
* Tropism
* Susceptibility to host defence
Host factors
* Species
* Breed
* Age
* Sex
* Genetics
* Physiologic
* Immune status
Modifying factors
* Stress
* Enviro
* Poor nutrition
* Tissue damage
* Immunosuppression
* Metabolic dysfunction
* concurrent disease

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8
Q

List 5 types of host defences used

A
  • Peristalsis/ciliary movement will clear
  • Commensal microbiota
  • Glycoproteins
  • Mucus: lysozyme/peptides/Ig/complement
  • Tight junctions of epithelium
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9
Q

What are the 2 mechanisms of pathogenicity

A

invasiveness

toxogenesis

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10
Q

Define invasiveness

A

Invasiveness: ability two invade tissue
* Mechanisms for colonization: adhesins/invasins
* Ability to overcome host defence

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11
Q

Define toxogenesis

A

Toxogenesis: ability to make toxins

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12
Q

Define endotoxin

A
  • Endotoxin: bacterial cell-associated substance
    o Transported by blood/lymph
    o Cytotoxic to cells away from original point of invasion/growth
    o Mainly from gram (-)
    o From cell wall (lipid A/LPS) – released when cells die and wall breaks
    o Causes nonspecific signs related to inflam:
     Fever/WBC change/DIC/hypotension/shock/death
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13
Q

Define exotoxin

A
  • Exotoxin: make from bacterial cells and act at tissue sites away from bacteria
    o Mainly from gram (+)
    o Enzymes and proteins that are secreted - with specific target
    o Heat sensitive
    o High biological activity
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14
Q

Provide 2 examples of exotoxin related disease

A

Pyoderma in Dogs: Staphylococcus pseudointermedius exfoliating toxin
* Exotoxin: specific toxin targeting specific receptor

Enterotoxigenic enteritis: E. coli enterotoxins causing scours
* Toxin activated ion/water pump = osmotic diarrhea
* Colonize microvilli of small intestines
* Causes functional lesion – no structural lesions

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15
Q

What are superantigens

A
  • Pyrogenic exotoxins made by S. aureus and S. pyogenes = superantigens
    o Directly bind T cells/APC
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16
Q

What are the steps of pathogenesis

A

Establish Infection/Colonization

Evade Host Defences

17
Q

List the 4 portals of entry for bacteria

A

Portals of Entry: urogenital/GI/resp/conjunctiva

18
Q

What is the mechanism of colonization? Define the different parts.

A
  • Receptor; carbohydrate or peptide residue on eukaryotic cell
  • Bacterial ligand: adhesin (macromolecular component of bacterial cell surface)
    o Ex. fimbriae

adhere to eukaryotic cell/tissue (need receptor/ligand)

19
Q

What are 3 factors that adherance depends on?

A
  • Tissue tropism
  • Species specificity: infect certain species
    o Enteropathogenic E. Coli K88 in pigs only
  • Age specificity
20
Q

What is tissue tropism

A
  • Tissue tropism: preference for tissue
21
Q

What is the counter attack complex? Provide an example

A

Counter attack: understanding virulence mechanisms can help prevent disease
* Ex. Pigs have receptor for F4 E. coli K88 fimbrae > breed them to not have the receptor or use vaccine to make anti-F4 (fimbrae) Ig

22
Q

What virulence factor allows bacteria to enter

A
  • Invasins: factors that allow internalization of bacteria
23
Q

What is the type 3 secretion system? give an example

A
  • Type 3 secretion systems
    o Many gram (-) have: deliver effector proteins
    o Hijack host cell signalling
    o Secretion (into ECF) or translocation (directly into host)
    o Ex. Salmonella typhimurium: deliver effectors/invasins that change host actin = increases uptake in membrane vacuoles
     Effector protein SopB induces enterocytes = induce transformation into M cells = increase colonization and invasion
24
Q

What are spreading factors

A
  • Spreading factors: bacterial enzymes that impact physical properties of tissue matrices/intracellular spaces = increase pathogen spread
25
Q

List 4 types of spreading factors. What do they do? Which types of bacteria use them?

A

o Hyaluronidase: attack intracellular matrix/connective tissue (form encapsulations in matrix)
 Made by streptococcus/staphylococcus/clostridia

o Collagenase: break collagen in muscles (facilitate gas gangrene)
 Made by clostridium histolyticum and perfringens

o Neuraminidase: degrade neuraminic acid (aka sialic acid)
 Form residue in intestinal mucus
 Made by vibrio cholerae and shigella dysenteriae

o Streptokinase/Staphylokinase: kinase enzymes convert plasminogen to plasmin (digest fibrin/prevent clotting)
 Made by streptococcus and staphylococcus

26
Q

What are the 3 main roles of complement

A

tag microbes for phagocytosis,

microbial lysis (MAC),

pro-inflam

27
Q

What are 3 mechanisms of complement evasion? How does it prevent complement

A

o Capsules: polysaccharide capsule = hide bacterial components
 Prevent complement formation

o LPS: main complement target for gram (-) = can change attachment of sialic acid resides to LPS 0 antigen
 Prevent MAC

o Destroy complement: extracellular enzyme (ex. Pseudomonas aeruginosa)

28
Q

What are 4 mechanisms of phagocytosis resistance

A

o Avoid contact with phagocytes
o Prevent engulfment
o Prevent lysozyme
o Kill/Damage phagocytes

29
Q

How do bacteria avoid phagocytes? Provide examples

A

 Stay in regions where phagocytes can’t go: lumen of GII/oral cavity/urinary/mammary/kidney tubule
 Hide antigenic surface
* Staphylococcus aureus: cell bound coagulase (clot fibrin on bacteria surface)
* Group A Streptococcus: hyaluronic capsule
 Inhibit phagocyte chemotaxis
* Mycobacterium tuberculosis

30
Q

How do bacteria prevent phagocytosis engulfment? Provide examples

A

 Antiphagocytic molecules on surface
* S. pneumoniae/Klebsiella pneumoniae: Polysaccharide capsule
* Group A streptococcus: M protein/fimbriae
* Pseudomonas aeruginosa: Surface slime polysaccharide
* E. coli: O antigen associated with LPS (capture heavy chain of Ig in a configuration where phagocytes can’t bind)
* S. aureus:Protein A (cell bound/soluble)

31
Q

3 mechanisms bacteria use to survive in phagocyte? Provide examples

A

 Inhibit phagosome-lysosome fusion
* Salmonella/Leigonella/Chlamydiae/Mycobacterium avium paratuberculosis

 Surrvivee in phagolysosome
* Bacillus anthracis/S. aureus/Coviella burnetii

 Escape phagosome
* Rickettsia (make phospholipase that lyse phagosome)

32
Q

Explain mechanisms bacteria use to kill phagocyte? Provide examples

A

 Kill before engulfment
 Hemolysin: extracellular enzymes made by gram (+)
* Pyogenic cocci (S. pyogenes/S. aureus)
 Streptolysin: secrete by pathogenic streptococcus
* Streptolysin 0 binds cholesterol in membranes = lysosomal granules in neutrophils explode + release contents into cytoplasm

 Kill after ingestion
* Mycobacteria/Brucella/Listeria

33
Q

List the mechanisms bacteria use to evade humoral immunity

A

o Attack: Aggressive/acute attack (no time for Ig prod.)/ proteinase (degrade Ig)

o Protect: Cell wall protection: capsule/peptidoglycan/LPS

o Hide: Intracellular hiding/antigenic mimicry (campy LPS/strep M protein)

o Superantigens: divert cell immune response + make non-neutralizing Ig

34
Q

List 2 mechanisms of host damage due to bacteria. What kind of damage do they do?

A

Direct bacterial (virulence factors): protease/hemolysin/toxin
* Cardiovascular disturbances
* Destroy blood vessel
* Diarrhea
* Disrupt NS and plasma membranes
* Inhibit protein synthesis
* shock

Induce host immunity: ROS/nitrogen species/inflammation/septic shock