Lecture 10 Staph Aureus II Flashcards

1
Q

What makes a successful pathogen?

A

It must be transmissible, durable, ubiquitous, resistant to antimicrobials, competitive and virulent

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2
Q

What are the virulence factors in S.Aureus?

A

Biofilm, capsule, surface adhesions, cell wall components, haemolysins and leucocidins, superantigens, Pathogenicity isalnds, resistant islands

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3
Q

How are biofilms a virulence factor in S.Aureus?

A

It allows colonization and persistence on prosthetic material
Includes compounds like Polysaccharide intracellular adhesion

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4
Q

What are the two phases of S.Aureus and how does it influence what virulence factors expressed?

A

In the exponential growth phase virulence factors that are key for binding such as adhesions are expressed while in the stationary phase other virulence factors such as toxins are expressed

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5
Q

Where are the S.Aureus reservoirs?

A

Carried by approx. 30% of people in anterior nares
may also be carried in the axillae, groin, throat and umbilical stump
Higher carriage rates in certain populations such as Intravenous drug users and haemodialysis patients

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6
Q

How is S.Aureus transmitted?

A

Through close contact with an infected individual or indirect contact through fomites

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7
Q

What is the importance of colonization in S.Aureus mediated disease?

A

It provides a reservoir from where bacteria can then be introduced if there is a breach of host barriers such as a skin breach, aspiration, insertion of indwelling object or surgery

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8
Q

What are the most common types of disease caused by S.Aureus?

A

Skin infections

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9
Q

What is the molecular test done to diagnose S.Aureus in modern microbiology labs?

A

16s rRNA gene sequencing as it is paradoxically cheaper and quicker

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10
Q

Why is the pattern of S.Aureus infections in NZ unusual?

A

It is the number one hospital associated pathogen globally
It is particulary unusual in NZ as it increases its infection rate year after year which is most likely due to environmental factors

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11
Q

What is the epidemiological triad?

A

A diagrammatic way of showing how there are three things that must work synergistically to cause disease, these are
The agent, host and environment

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12
Q

What are the differences between Staphylococcal infection in the north island compared to the south island?

A

The north island typically has three times the rate of disease this is due to population size and diversity as well as temperature, humidity allowing increased insect bites etc

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13
Q

Who are the type of people that typically get S.Aureus disease?

A

Severe disease is more likely to be older, male and maori
This makes sense as these are the type of people more likely to spend extended periods of time at hospital
Skin infections are more likely to be under 5s, male and maori

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14
Q

What are the three main messages of S.Aureus epidemiology in New Zealand?

A

Incidence of S.Aureus SSTI has risen significantly over the past decade
There is geographic variation in the incidence of S.Aureus SSTI
Marked ethnic disparity in disease

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15
Q

What is SCCmec?

A

Staphylococcal Cassete chromosome which contains mecA which codes for the abnormal transpeptidase not affected by beta-lactam antibiotics

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16
Q

How does SCCmec integrate into the S.Aureus genome?

A

Integrates between orfX found in all S.Aureus strains
Uses a recombinase produced by ccrAB
Some strains can take up SCCmec easier than others

17
Q

What is community acquired MRSA?

A

MRSA located from someone who has not been hospitalized, or within 48 hours of hospitilaztion
and has no invasive device at time of admission, or surgery, hospitalisation, dialysis or residence in LTCF 12 months prior to the culture date

18
Q

What is hospital acquired MRSA?

A

Hospital onset of infection determined as culutres taken 48 hours post admission to hospital

19
Q

What is SCCmec?

A

Staphylococcal Cassete chromosome which contains mecA which codes for the abnormal transpeptidase not affected by beta-lactam antibiotics

20
Q

How does SCCmec integrate into the S.Aureus genome?

A

Integrates between orfX found in all S.Aureus strains
Uses a recombinase produced by ccrAB
Some strains can take up SCCmec easier than others

21
Q

What is community acquired MRSA?

A

MRSA located from someone who has not been hospitalized, or within 48 hours of hospitilaztion
and has no invasive device at time of admission, or surgery, hospitalisation, dialysis or residence in LTCF 12 months prior to the culture date

22
Q

What is hospital acquired MRSA?

A

Hospital onset of infection determined as culutres taken 48 hours post admission to hospital

23
Q

What are the key differences between community and hospital acquired MRSA?

A

Hospital strains often have multiple antibiotics including resistance to non-beta lactams antibiotics while community strains are typically still susceptible to non-beta lactams
this is reflected by community strains having a small SCC compared to hospital strains
Panton-Valentine Leucocidin is common in community as it facilitates skin infections but less common in hospital infections
Hospital strains frequently have more invasive diseases while community strains tend to have skin infections

24
Q

Whats the difference between hospital and community acquired MRSA epidemiology?

A

Hospital acquired infections have remained relatively constant, largely due to a strict handwashing regime
Community acquire infections have continued to increase most likely related to the increase in skin infections