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Intro Microbio > Pathogens > Flashcards

Pathogens Flashcards

1
Q

do all strains of a species have the same ability to cause disease?

A

no

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2
Q

pathogen usually identified by the set of ________ that it carries and expresses

A

virulence genes

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3
Q

virulence

A

ability to cause damage to the host

-depends on virulence factors

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4
Q

mutually exclusive

A

when two outcomes can’t happen or be true at the same time

ex) coin toss

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5
Q

invasivness definition and what different virulence factors does the pathogen use?

A

the ability of the microorganism to become established in the host
uses different virulences factors:
- adhesions capsules
-enzymes
-invasions
-type 3 secretion system and type 4 (T3SS and T$SS)

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6
Q

toxigenicity definition

A

the capacity of the microogrganism to produce substances known as toxins that damage specific tissues of the host

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7
Q

two basic features of virulence (that are NOT mutually exclusive)

A

toxigenity and invasivness

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8
Q

what are Adhesins?

A

prompt specific attachment to the host cell surfaces

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9
Q

what adhesions mediate close attachment?

A

fibril adhesins (glycolic/lipo proteins )

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10
Q

what adhesion mediate loose attachment?

A

Fimbriae/Pili

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11
Q

Capsule

A

produced by some bacterial pathogens

  • prevent the pathogen from being destroyed by the host immune cells (phagocytes)
  • also mediates attachment to the host cells
  • essential virulent factor for some bacterial species
  • NOT only a virulent factor( non-pathogenic bacteria produce it too sometimes)
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12
Q

which 2 exotoxin enzymes have an effect on the ECM? which 1 on the host cell membrane

A

Hyaluronidase
Collagenase
host cell membrane - lecithinase

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13
Q

Hyaluronidase

Hya-lur-on-i-dase

A

degrades hyaluronic acid, a sticky polysaccharide that holds host cells together. Staphylococci and streptococci and clostridia

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14
Q

Collagenase

A

degaraades collagen present in connective tissue. Clostridia

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15
Q

Lecithinase

A

degrades lecithin in cell membrane and casques the lysis of red blood cells and destroys tissue cells

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16
Q

Gas gangrene

A 
Clostridium perfringens (strict anaerobe) 
infection in deep wounds
  • uses lecithinase to lyse host cells, collagenase and hyaluronidase to destroy ECM
  • gross stitches picture on slide
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17
Q

Hyaluronidase producer (such as streptococcus progenies) attaches to _____.

A

epithelia

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18
Q

Hemolysins

A
  • cause lysis of RBC and other cell types
  • some are enzymes (lecithinase and phospholipase)
  • some are cytolysis (pore-forming).
  • produces by a great variety of bacteria
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19
Q

Leucocidin

A

causes lysis of leucocytes- WBC

- produced by staphylococci, streptococci and few other gram- neg

20
Q

Coagulase

A

produced by virulent staphylococci, causes insoluble fibrin to be deposited on bacterial cells and protects/blocks bacteria from the immune system
- invisible cloak

21
Q

Invasins

A

invasive surface proteins or injected proteins that allow microgansims (pathogens) to enter the cells (invade host)

22
Q

Which bacteria use invasin proteins

A

mycobacterium, salmonella, listeria, chlamydia

23
Q

Ways to modify the properties of the host cells

A
  • block phagosome maturation (block digestion)
  • increase size of the vacuole
  • acquire nutrients
  • block detection of intracellular infection and response (block host response)
24
Q

type 3 secretion systems (T3SS)

A
  • also called injectisome
    large number of gram neg use these systems
  • T3SS forms a channel through the bacterial cytoplasmic membrane, the periplasm, the outer membrane and the host cell membrane so that bacterial proteins can be injected into the host cell cytosol
25
Q

T4SS

A

similar to T3SS but absence of needle like structure

26
Q

timeline for pathogenicity

A

exposure–> adherence–> invasion through epithelium–> multiplication–> toxicity and invasiveness (further growth and into distant sites)–> tissue or systemic damage

27
Q

Toxigenicity

A

micro org to produce toxins that cause damage o specific tissues

28
Q

are extracellular enzymes toxins?

A

yes, anything that cause damage to the host cell

29
Q

toxins not always associated with high virulence. other factors that can damage host include

A

large number of pathogens

damage by hosts own immune system

30
Q

2 types of bacterial pathogens

A

infectious disease- result from pathogens own growth and multiplying
intoxications- result from pathogens toxins produced (food poisoning)

31
Q

2 types of toxins

A

exotoxins- excreted int the environment

endotoxins- part of the bacterial pathogen (internal)

32
Q

Exotoxins

A

soluble, secreted or release when the organism is lysed, usually proteins and heat liable (destroyed by heat)
- highly immunogenic (antibody response inactivates exotoxins)
-extremely potent
categorized by their target (neurotoxins, enterotoxins eat.)

33
Q

AB toxins- what are the 2 subunits

A 
A= enzymatic subunit 
B= binding/cell entry
34
Q

Subunit A’s job

A

modifies a target inside the host cell leading to damage to the host “ the actual toxic part”

35
Q

subunit B

A

binds to cell receptors providing tissue/cell type specificity “ the binding part” B for binding

36
Q

Clostridium botulinum

A

is an AB toxin/neuro toxin that blocks acetylcholine release in neuromuscular junction

  • leads to flaccid paralysis
  • effects human cattle horses and ducks
  • BOTOX
  • reduces wrinkle
37
Q 
AB toxin (Botulinum toxin)
normal state vs with botulism
A

normal- acetylcholine induces contraction of muscle fibers (think contracted is like wrinkles)
with botulism –> blocks release of Acetylcholine, inhibits contraction (flaccid)

38
Q

AB toxin: Tetanus toxin

A

found in soil
infects deep puncture wounds and produces toxin TeNT which causes spastic paralysis; bowed spine, locked jaw (weird picture on slide )

39
Q

Tetanus toxin normal vs with toxin

A

normal–> Glycine release from inhibitory interneurons stop acetylcholine release and allowing relaxation of muscles
with tetanus toxin–> prevents the release of glycine and therefore acetylcholine is released and muscles contract

40
Q

AB5 Toxin: Cholera toxin

A

B binds to intestinal cells
A activates adenylate cyclase, produces cAMP
- blocks Na+ uptake, neg ions travel in to balance and water moves with the ions

41
Q

explain how cholera toxin produces excess water in intestine

A

normally Na+ moves from intestine into blood stream
with toxin–> A subunit binds to adenylyl cyclase and this creates lots of cAMP which blocks Na+ uptake. because of surplus in + charge in intestine, CL- and HCO2- move out and with the ion movement water also moves out

42
Q

Endotoxins

A

Are apart of the toxin, as opposed to exotoxin which gets released from within the pathogen
lipid A of LPS (example)
- released during lysis
-heat stable, cannot be activated
- weakly immunogenic- (no antibodies are produced)
-BUT very effective activator of the immune system - produce general systemic effects- fever– septic shock

43
Q

key points of endotoxins

A

Main point is that they are HEAT STABLE and very effective activators of immune systems- fever and general systemic effects, BUT weakly immunogenic (no antibodies produced)
- can’t make vaccines bc can’t inactivated with heat (they are heat stable)

44
Q

Vaccines against toxins

A

exotoxins are highly antigenic meaning that they stimulate the host defese to produce antibodies that can neutralize them
so vaccines can imitate these BUT endotoxins cannot be inactivated by heat and so no vaccine!
-toxins are first inactivated by heat or formaldehyde–> toxoids (no longer toxic but still antigenic)

45
Q

toxoids

A

no longer toxic but still antigenic, can be used in a vaccine

46
Q

Acetylcholin causes

A

contracted muscles and winkles

so with botulism–> inhibits the release of acteltycholine–> flaccid
with tetanus–> prevents the release of glycine, which allows more acetylcholing–> stiff

47
Q

Diphtheria

A

AB, inhibits protein synthesis

Intro Microbio (18 decks)

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