Pathogenesis Flashcards

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1
Q

Explain the components of exotoxins

A

They are often 2 subunit A-B exotoxins where the A is for the activity of the toxin. It’s the active subunit; the B subunit is for Binding to the host cell’s receptor so that the toxin can gain entry into the cell

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2
Q

How does the exotoxin for Corynebacterium diptheriae exert its effects?

A

It inhibits protein synthesis of the host cell by inactivating Elongation factor-2 which eventually leads to cell death

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3
Q

T or F

Exotoxins can only exert their effects on short distances

A

False
They can act locally as in C. Perfringes which cases gas gangrene or at a distance as with C. tetani that accesses the CNS via transport along axons via the bloodstream

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4
Q

Does V. cholera produce an exotoxin? If so, what is its mechanism of pathogenecity?

A

It does. It has a A-B subunit exotoxin that when inside host cell will prevent the inhibition of Gs which causes the perpetual stimulation of cAMP which stimulates the opening of the Cl channel. Cl- will continually flow out of the cell taking Na and water with it. This is mass dehydration

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5
Q

What organism is responsible for global paralysis after stepping on a rusty nail?

A

C. tetanus. It works via ann A-B exotoxin that will prevent the release of inhibitory NTs so that only excitatory NTs are employed. This cause is non-stop stimulation of all muscle in the body. Leads to spastic paralysis, fever, and sweating

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6
Q

What organism is responsible for botulism?

A

C. botulinum. It can be found in honey. It is anaerobic. It has a A-B exotoxin that when inside a host cell will prevent the release of stimulatory NTs (Ach) so there is flaccid paralysis. This is the opposite of tetani

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7
Q

If you get shady looking mail from someone you don’t know, what should you suspect? Does this bug have an exotoxin you should be worried about?

A

Suspect Anthrax from bacillus (rod) anthracis. its an aerobe that has 2 toxins made from 3 subunits - 2A and a B.
The B subunit is the “protective antigen” that is used in vaccines and each of the toxins.
One of the A’s is for edema, the other A is for “Lethal Factor”. Scary.

…so Edema-Protective and Lethal Factor-Protective

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8
Q

What is a toxoid?

A

It is a non-toxic but still antigenic compound that is partially denatured EXOtoxin (either by heat or acid) and is used for immunizations. Exotoxins are highly antigenic and heat labile

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9
Q

What is the difference btwn endotoxins and exotoxins?

A

Exotoxins are secreted into the extracellular spaces but endotoxins are actually on the bacterial wall. its an integral part of the bacteria. An ex of endotoxin is LPS which is an integral part of gram - bacteria and is liberated when the bacterium lyses and can cause septic shock.
An exotoxin is heat and acid labile, whereas endotoxins are relatively stable. Exotoxins don’t cause fever (except for the pyrogenic toxins), but endotoxins cause fever and septic shock

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10
Q

What kind of toxin is LPS and what part of it is toxic

A

It is an endotoxin of gram - bacteria.The toxic portion is Lipid A on the outer membrane

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11
Q

How do endotoxins cause septic shock?

A

When the endotoxin is released into the bloodstream, it is will bind to receptors on macrophages causing cytokine release (IL-1, TNF-a) and activates inflamm response and coag cascades which can lead to septic shock.

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12
Q

Can gram + bacteria cause septic shock even tho they dont have LPS?

A

Yes they can. It’s prob due to the peptidoglycan wall or the techoic acid which is less toxic than LPS and LPS is less toxic than exotoxin.

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13
Q

Adherence of bacteria to host cell

A

This is called localization and is the first step of entry, or secretion of proteins into host cell.
Its mediated by adhesin on bacteria and host cell receptors. Abs against adhesins can block this

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14
Q

How does the strain of E. coli that causes pyelonephritis bind to host cells?

A

This strain of E. coli has to have a P pilus. It has a lot of them and these pili bind to the P blood group antigen. Without this, it can climb its way to the kidney and will just simply cause a UTI

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15
Q

What is the type III secretion sys and what kind of bugs use it?

A

This sys is used by pathogenic gram - rods to detect euk cells and inject virulent proteins into them. They can infect, survive, and evade host’s immune sys with this sys
They can induce or prevent uptake (Salmonella and Yersinia, resp) and induce or prevent apoptosis (yersinia and chlamidya, resp)

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16
Q

What bacteria can induce its uptake inside a non phagocytic cell and how does it do this?

A

Salmonella. Does this by using the hosts cytoskeleton to create a ruffled border which takes in the bug.

17
Q

What are the 3 survival strategies inside a host cell?

A

Survive inside the phagolysosome (Coxiella)
Inhibition of phagolysosomal function (Chlamydia)
Escape back into the cytosol (Listeria, uses actin to create a comet tail which looks like a shooting star so it can move from cell to cell)

18
Q

How does staph aureas evade phagocytosis?

A

It has Protein A on its surface which binds the Fc region of IgG.

19
Q

How does a polysaccharide capsule help a bug evade the immune resp? Which demographic is this a problem for?

A

It induces a T-cell independent immune response, but its poor in kids under 2 y/o.
Ex are Neisseria menigitidis, strep pneumonia, haemophilus infuenza. Kids under 2 are at incr risk for getting meningitis from this bugs bc their immune sys can’t recognize the capsule.
There are Abs against capsules but they are specific for their own target capsule. Abs protect against sys infection, but not mucosal colonization

20
Q

How does Neisseria gonorrheae evade hosts immune response?

A

It will shift its expression of its surface Ags (lipooligosaccharide, pili, Opa proteins) to different antigenic forms so that they cant be recognized by Abs. It also cleaves IgA which is important for mucosal immunity

21
Q

What is IgA protease and which bugs produce it?

A

It is an enzyme that cleaves IgA which is important for mucosal immunity. N. gonarrheae and menigitidis, h. influenza, and strep pneumonia

22
Q

What are three examples of regulation of virulence factors?

A

Bordatella pertusis optimal at 37 degrees C versus 20
Yersinia has higher expression with low levels of Ca
C. diptheriae toxin has higher expression in absence of Fe 3+

23
Q

Where are the virulence genes on a pathogen located?

A

They are usu located on mobile DNA elements such as plasmids or bacteriophages.

Virulence genes are spread among diff bacteria via horizontal transfer and mechanisms of pathogenesis are conserved among bacteria.

24
Q

What is antitoxin?

A

It is the antisera produced in response to the toxoid and can be given as treatment.