Gram positive cocci: Staphylococci Flashcards

1
Q

who first discovered Staphylococcus

A

Sir Alexander Ogston

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2
Q

who Differentiated between S.aureus and S. epidermidis

A

Anton Friedrich Julius Rosenbach

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3
Q

Nomenclature of staphylococcus

A

S.aureus was named after its golden colour.
S.epidermidis is named as it is found on the epidermis

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4
Q

how is staphylococci classified

A

Gram positive cocci(spherical): 0.5-1.0 µm in diameter
Facultative anaerobes.
Grow in 18oC - 40oC
Catalase positive
Major differentiating feature is coagulase

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5
Q

describe the classification of staphylococci

A

Kingdom: Bacteria, Family: Staphylococcoceae, Genus: Staphylococcus (Grape-like clusters), Species: 11 groups

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6
Q

how to test if bac is Coagulase positive or negative?

A
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7
Q

describe the Mechanisms of pathogenicity Staphylococcus aureus

A

Ability to COLONISE the host and invade tissues
Ability to EVADE host defences
Ability to damage host through production of invasins and exocellular toxins.
Ability to acquire RESISTANCE to antibiotics

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8
Q

true or false is Staphylococcus aureus known as a true pathogen

A

true

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9
Q

how is MRSA able to acquire RESISTANCE to antibiotics

A

Methicillin is a beta-lactam antibiotic used against beta-lactamase-producing staphylococci.
Only used for a year before MRSA was first described.
By 1970, it was recognised as a hospital pathogen.
Rapid spread through hospitals from 1980 to 2005.
50% of S.aureus are now MRSA

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10
Q

what does MRSA stand for

A

Methicillin-resistant staphylococcus aureus.

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11
Q

How does S.aureus become MRSA?

A

MecA (30-50kb) incorporated on SCCmec (staphylococcal cassette chromosome mec)

Encodes for additional penicillin binding protein (PBP2a); reduced affinity for beta-lactams

MRSA resistant to all beta-lactam antibiotics

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12
Q

what treatment is used for MRSA infection

A

vancomycin

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13
Q

How Vancomycin works

A

Interferes with cell wall synthesis by binding to D-ala-D-ala.
Blocks transglycosidase enzymes

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14
Q

describe the characteristics of MRSA with reduced susceptibility to Vancomycin (VISA)

A

VISA has the MecA gene AND a thick cell wall.
Acts as a sponge, making it difficult for Vancomycin to penetrate the cell wall.

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15
Q

what does VISA stand for

A

Vancomycin Intermediate Staphylococcus aureus (VISA)

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16
Q

describe the characteristics of Vancomycin resistant staphylococcus aureus (VRSA)

A

VRSA contains MecA gene AND vanA gene.
vanA gene alters the D-ala-D-ala subunit to D-ala-D-lac

17
Q

what are the Clinical manifestations

A

Localised CVC catheter infection
Deep seated CVC catheter infection

18
Q

name the Clinically important Staphylococci

A
  • Staphylococcus aureus (S.aureus)
  • Staphylococcus epidermidis (S.epidermidis)
  • Methicillin-resistant staphylococcus aureus (MRSA)
19
Q

name a specific clinical setting where S.aureus can be found

A

Over 60% of surgical infections are caused by S.aureus

20
Q

name a specific clinical setting where can S.epidermidis can be found

A

Over 60% of surgical infections are caused by S.aureus

21
Q

specific characteristic of mrsa

A

Causes same symptoms as S.aureus but more difficult to treat.

22
Q

Clinical significance of S.aureus and MRSA

A

S.aureus is a ‘true pathogen’ and can colonise anywhere on our skin.
S.aureus can colonise in the nose or on the skin of a healthy individual.
Particularly relevant to surgical site wounds.
Antibiotic resistant strains, like MRSA, make it difficult to treat the infection.

23
Q

describe what can be seen in a staphylococci infection of the skin

A

Impetigo Skin infection that starts with red blisters that burst to form yellow crusts.

Cellulitis Deep skin infection that causes the skin to be painful and hot

Skin abscesses A pocket of pus, deep within the skin.

Blepharitis Inflammation of the eyelids that causes scaly patches of skin near the eyelashes

24
Q

explain what Hospital infections are caused by Staphylococcus

A

Catheter-Related Urinary Tract Infection (CRUTI) Catheter introduces S.aureus or S.epidermidis directly to the bladder causing a UTI

Bacteraemia Bacteria in the blood. Can be fatal, as it triggers the bodies septic response

Endocarditis Inflammation of the inner values of the heart.

25
Q

explain how Staphylococcus aureus colonises the host

A

There are a group of proteins called Microbial Surface Components Recognising Adhesive Matrix Molecules (MSCRAMMS). Over 20 of these proteins have been discovered so far.
One of the MSCRAMMS is called Clumping factor (ClfA), which promotes adhesion to damaged tissue by binding to fibrinogen and expressing fibrin. It is sometimes also referred to as ‘bound coagulase’.
Another MSCRAMM is the Fibronectin binding protein (FnbpA), which binds to fibronectin. Fibronectin is present on the extracellular surface of healthy endothelial and epithelial surfaces.
Lastly, there are collagen (Cna) and elastin (EbpS) binding proteins, which help promote adhesion to severely damaged tissue.

26
Q

what is clumping factor A (ClfA)

A
27
Q

explain how Staphylococcus aureus evades the host

A
28
Q

explain neutrophil avoidance

A

Both bound coagulase and free coagulase when bound to fibrinogen in the plasma result in fibrin clots.

These clots allow for bacterial agglutination within the fibrin clots themselves.

This results in the neutrophils being unable to bind the bacterial cell surface.

As a result the phagocytosis is minimised.

29
Q

what is the function of Protein A

A
30
Q

explain how Staphylococcus aureus damages the host

A