Lecture 10- Staphylococcus aureus Flashcards

1
Q

How common is Staphylococcus aureus? How is it spread?

A

1/5 people carry (usually in nose), much more common then meningitis. Not evenly spread due to population density, and is higher in cities. Higher in North island and in summer

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2
Q

SA is..

A

a common cause of disease, hospital-acquired infection, death.
An array of virulence factors.
Exists everywhere

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3
Q

Cellulitis

A

common staph infection that affects deeper layers of the skin.

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4
Q

What do staph aureus look like under microscope?

A

grape-like clusters, purple because their thick peptidoglycan cell wall takes up the stain.

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5
Q

Where does staph come from?

A

Predominantly human pathogen.

  • human transmission to domestic animals can occur
    eg) Bonvine mastitis. (pain suffering, reduced milk/growth in cows, cost to industry)
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6
Q

What can cause colonisation / disease

A

bacterial, host and environmental factors, + exposure&raquo_space; colonisation (20-25%)&raquo_space; disease

NOTE: bacteria usually always needs to colonise first before it can cause disease, therefore not all hosts get disease

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7
Q

When did cow staph occur?

A

~200 years ago when dairy farming became popular, cows in dense large populations. From humans to cows.

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8
Q

Where do you find staph infection sites on the body

A

SA carriers usually always carry SA in the nose (can handle noses salty environment)
-also many other places in the body

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9
Q

When is SA colonisation most common

A

First year of life (infected by mum)

-declines with old age

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10
Q

Different types of SA carriers, which is seen in the nose

A

Persistent: always have staph. Increased disease risk

Intermittent:

non-: Beta-3 defensins that fight bacteria. No/low risk of SA

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11
Q

What can SA do…

A

Food posioning: common, not from direct infection but from toxins.

Skin infection: 3%

Asymptomatic: 60%

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12
Q

SA and hair follicles.

A

Bacteria can fall into hair follicle, interacts with epithelial cells

  • damaged cells release CKs, immune system is triggered.
  • also chemotaxis recruits more cells to area.
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13
Q

How are bacteria dissolved??

A

A phagosome with bacteria in it is formed when the neutrophil injests bacteria. Toxic granules form around the lysosome, converting it to a lysosome. Bacteria gets dissolved by produced H202

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14
Q

With such an active IS, how is it that SA is ever able to infect us?

A
  • use enzyme catalase changes H2O2> H20 and O2 so cant be killed in cell.
  • Can kill off WBC with haemolysinz
  • can use clumping factor to coat itself in fibrinogen and hide from the IS
  • Covered in Protein A, binds to Human Ig the wrong way and hide from the immune system
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15
Q

Treatment if s. aureus

A

1) stabilise the patient
2) drain pus
3) antibiotics

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16
Q

Main AB treatment of SA

A

Penicillin inhibits transpeptidase (enzyme that chops off an amino acid, causing a cross links within the SA cell wall), so that the cell wall opens and SA explodes

17
Q

What happened to the relationship of SA and penicillin over time

A

SA developed immunity against penicillin. Beta-lactamase that breaks the beta-lactam ring of penicillin.
-new drug made ‘methicillin’, the same year resistance ocurred, ‘MRSA’