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Medical Microbiology > 10. MRAS and VRE as hospital and community pathogens > Flashcards

10. MRAS and VRE as hospital and community pathogens Flashcards

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Biology 101 flashcards USMLE® Step 1 flashcards
1
Q

What is staphylococcus aureus?

A
  1. A very common pathogen
  2. Named for its gold colonies when cultured
  3. Grows in aerobic conditions
  4. It is very virulent
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2
Q

How is MRSA specifically tested for in the lab?

A
  1. Culturing in stress conditions
  2. This is salt agar at 30oC.
  3. This stress forces the expression of the MecA gene.
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3
Q

What environment is S. aureus found in?

A
  1. on mammals and there are specific strains for different mammals.
  2. It likes hot places like skin, nose and groin. Also mucous membranes
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4
Q

How is S. aureus spread?

A
  1. Direct contact
  2. Airborne
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5
Q

What are the risk groups for S. aureus infections?

A
  1. Diabetes mellitus patients
  2. Haemodialysis patients and other groups that have a lot of contact with healthcare settings.
  3. People who inject drugs.
  4. People living with HIV.
  5. People living in close quarters like prisons or homeless shelters
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6
Q

S. aureus pathogenesis: Cell Wall

A
  1. Polysaccharide capsule that inhibits phagocytosis
  2. Peptidoglycan and Teichoic acids activate the complement and cytokines like IL-1. This causes systemic immune activation
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7
Q

S. aureus pathogenesis: Enzymes

A
  1. Some are used for identification and diagnosis.
  2. ß-lactamases
  3. Coagulase to promote blood clotting
  4. Proteases
  5. Lipases
  6. DNases
  7. Phospholipase
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8
Q

S. aureus pathogenesis: Toxins

A
  1. Exotoxins like haemolysins that lyse WBC.
  2. Entertoxins that are heat stable so can cause food poisoning.
  3. Toxic shock syndrome toxin which is a superantigen causing hyper stimulation of T cells.
  4. Panton-Valentine Leukocidin (PVL) toxin is relevant transmission and disease presentation
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9
Q

What are the different clinical presentations of S. aureus infections?

A
  1. Soft tissue infections that normally come from an open wound and cause boils, abscesses and cellulitis.
  2. Bone and joint infections, which are from more invasive or long infections. A common cause of septic arthritis.
  3. Pneumonia but only in very sick patients
  4. Endocarditis - heart inflammation
  5. Bacteraemia
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10
Q

What are the 2 types of clinical S. aureus infections?

A
  1. Pyogenic infections
  2. Toxigenic infections
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11
Q

Pyogenic S. aureus infections

A
  1. Most common
  2. Start local and enter through breaks in the skin like surgical wound.
  3. Spread through the blood and invade the joints, kidneys and muscles. Also cause endocarditis.
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12
Q

Toxigenic S. aureus infections

A
  1. Commonly food poisoning with severe and rapid onset. Caused by a heat resistant toxin.
  2. Scalded skin syndrome
  3. Toxic shock syndrome which has severe manifestations like multi-organ failure and often end up need ITU care.
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13
Q

What is MRSA?

A

Methicillin-resistant Staphylococcus aureus

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14
Q

What is the cinical presentation of MRSA?

A

The same as S. aureus infections. the only difference is how you treat it

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15
Q

What is the mechanism of methicillin resistance in MRSA?

A
  1. Caused by the MecA gene.
  2. MecA produces an alternative PBP called PBP2a.
  3. This means penicillins cannot bind to it and it causes resistance.
  4. It is encoded on a mobile genetic element called SCCmec and can be acquired in horizontal gene transfer.
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16
Q

What is the origin of SCCmec genetic element?

A
  1. It has lots of different cross over points with S. Aureus.
  2. It may have originated in coagulase negative staphylococci and then transferred over. This could be a natural reservoir of resistance.
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17
Q

What was the pattern of emerging resistance to S. aureus and MRSA?

A
  1. S. aureus became resistant to penicillin quickly after it was introduced.
  2. Methicillin was introduced to treat these penicillin resistant infections in the 1960s.
  3. S. aureus very quickly also gained resistance to this as well.
  4. MRSA wasn’t a big problem until the late 90s.
  5. This was due to the emergence of MRSA-4, which carries other drug resistance mechanisms.
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18
Q

What is used to treat MRSA?

A

Vancomycin

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19
Q

What is the evolution of strains of MRSA?

A
  1. There are lots of different strains and they emerged in different places.
  2. It started with 1 sequence type that gained methicillin resistance.
  3. It then evolved over time depending on the location it spread to.
  4. This led to different strains being dominant in different locations.
  5. The different strains carry different genetic elements with different resistance mechanisms working with MecA.
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20
Q

What are the SCCmec subtypes?

A

They are different genetic elements with different resistance mechanisms and toxins. They all include MecA.

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21
Q

What are SCCmec subtypes 2 and 3?

A
  1. They are more common in hospitals
  2. They contain other resistance mechanisms to make it MDR.
  3. This MDR plasmid is big and comes with a fitness cost
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22
Q

What makes a S.aureus MRSA?

A

The presence of MecA

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23
Q

What are SCCmec subtypes 1,4 and 5?

A
  1. These remain susceptible to other antibiotic agents just not penicillins.
  2. Can contain PVL toxins
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24
Q

Community vs Hospital MRSA

A

Community:
1. SCCmec types 4 and 5
2. Increased virulence
3. often PVL+
4. Sensitive to fusidic acid, quinolones, tetracyclines and macrolides

Hospital:
1. SCCmex types 2 and 3
2. Carries a fitness cost.
3. Often PVL-
4. Often resistant to fusidic acid and tetracyclines
5. Maintains sensitivity to quinolones and macrolides

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25
Q

What is community onset MRSA?

A

MRSA when symptoms present in the community but the true origin is the hospital and it is likely to be a hospital strain.

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26
Q

What is community MRSA?

A

1, Originated in the community and no link to healthcare
2. Normally, a community strain.

27
Q

What are the risk factors for community MRSA?

A
  1. Young people usually living in close quarters like student, professional athletes and military service members.
  2. exposure to prisons and prisoners
  3. Activities with regular skin to skin contact
  4. Exposure to antibiotic
  5. IV drug abuse
  6. Recurrent skin infections
28
Q

Does community MRSA spread across regions?

A
  1. Some spread between the USA and Europe
  2. Most MRSA strains stay where they originated
29
Q

MRSA as a commensal

A
  1. Mostly young and healthy people so they are not effected by it
  2. We don’t really know how many people are colonised by MRSA but about 1-3% of the population.
  3. These strains are not transmitted in the community outside the risk groups.
30
Q

Why are most community strains of MRSA PVL+?

A
  1. This is because they have obvious symptoms that can be treated in the community.
  2. Forms boils which are painful and obvious.
  3. This is actually very common in MSSA as well.
31
Q

How is community MRSA and MSSA treated?

A
  1. Treat with antibiotics.
  2. Decolonisation of the person and environment.
  3. This is a long process and involves washing everything.
32
Q

How are PVL+ MSSA and MRSA infections treated?

A
  1. Incision and draining of abscesses.
  2. Intense regimen of personal hygiene, hand washing and sharing items.
  3. Antibiotics but there is an argument over which are best.
  4. Screening of close contacts
33
Q

When was MRSA first noticed?

A

1970s

34
Q

When did MRSA become endemic globally?

A

1990s

35
Q

What was the MRSA situation in the UK in the early 2000s?

A
  1. High deaths, the 2nd most in Europe.
  2. Mandatory reporting was introduced.
  3. MRSA bacteraemia had very high deaths
36
Q

Why does MRSA bacteraemia have high fatality?

A
  1. Severe infection
  2. Hard to treat.
  3. Patients are already very sick
37
Q

What was the UK response to bad MRSA situation?

A
  1. Set a very ambitious target.
  2. Introduced surveillance of everyone admitted to hospital which has only been reduced in the last few years.
  3. Infection control like isolation of patients, deep cleaning and changing staff habits.
38
Q

Why was isolation a problem for UK hospitals?

A
  1. They didn’t have enough side rooms due to old hospital design.
  2. This caused a change is how new hospitals were designed.
  3. More individuals rooms so most patients are already isolated
  4. This helps with all infection control.
39
Q

Why did the UK have increasing MRSA deaths despite strict measures?

A
  1. Mainly due to trying to change the habits and attitudes of the staff and patients.
  2. The new measures were not implemented or explained properly.
  3. They didn’t account for other staff like dinner staff, cleaners and porters.
40
Q

What did the UK government do to force compliance with measures and reduce MRSA infections?

A
  1. They introduced strict financial penalties for every case of MRSA.
  2. This came out of the budget so it was a big incentive to change behaviours.
  3. Tried to increase awareness of the problem.
  4. Monthly reporting.
  5. They made implementing measures easier for the busy staff by creating bundles. This inlcudes line care bundles and other things.
41
Q

What else contributed to the reduction in MRSA infections?

A

It is thought the main MRSA strain was on a natural decline anyway

42
Q

What has happened to the MRSA infection rates recently?

A
  1. They have remained low.
  2. Now mainly infects complex surgical and ITU patients.
43
Q

What is the genetic diversity of MRSA?

A

A lot less than MSSA.

44
Q

What is the future of MRSA prevention?

A
  1. Possibility of vaccination but no effective one has been found yet.
  2. Infection control through screening and decontamination.
  3. Decontamination includes strict washing with antibacterial body wash every day for 5 days inc hair and nose cream
45
Q

What is the future of MRSA treatment?

A
  1. New antibiotics.
  2. A new ß-lactam has been developed that remains active against MRSA and is as effective as vancomycin.
  3. Less toxic then Vancomycin, which is very damaging especially for the kidneys
46
Q

What are Enterococcus?

A
  1. Enteric bacteria so within the GI tract.
  2. Can live as commensals in the gut.
47
Q

What are the two most common infection-causing Enterococcus?

A
  1. Enterococcus faecalis
  2. Enterococcus Faecium
48
Q

Why are intrinsically enterococci not a problem?

A

They don’t really cause many infections

49
Q

How virulent are Enterococci?

A

Not very

50
Q

What clinical infections are caused by Enterococci?

A
  1. UTIs
  2. Abdominal wound infection especially from surgery like stoma or from wounds around the anus.
  3. Bacteraemia that needs hospital treatment.
  4. Endocarditis as enterococci like heart valves and has non-specific symptoms.
  5. Neonatal infections
51
Q

How are Enterococci infections treated?

A
  1. They are intrinsically resistant to many antibiotics.
  2. E. faecalis is usually sensitive to amoxicillin
  3. E. faecium is usually more resistance and not sensitive to amoxicillin
52
Q

What are most enterococci resistant to?

A
  1. Cephalosporins
  2. Ertapenem
  3. Clindamycin
  4. Aminoglycosides
53
Q

What are 20% of E.faecium resistant to?

A

Vancomycin

54
Q

What is the first line treatment for enterococci infections?

A

Vancomycin

55
Q

How do Enterococci gain resistance to vancomycin?

A

Through the Van group of genes usually VanA or VanB

56
Q

Where is the biggest problem of vancomycin resistant enterococci?

A

Eastern Europe

57
Q

What are the risk factors for vancomycin resistant enterococci?

A
  1. Mainly hospital patients and not common in the community.
  2. Immuno-compromised
  3. Previous treatment with certain broad spectrum antibiotics.
  4. prolonged hospital stays.
  5. Specialist hospital treatment like ITU or dialysis
58
Q

Why do vancomycin-resistant enterococci infections have poorer outcomes compared to susceptible enterococci infections?

A
  1. Antibiotic treatment is more difficult, longer, more invasive and done through IV.
  2. Treatment often leads to more complications.
  3. More likely in patients that have been in hospital for a long time.
59
Q

What measures are taken by hospitals to prevent vancomycin resistant enterococci infections?

A
  1. Similar to MRSA
  2. Isolation
  3. Line care
  4. Staff infection control measures
60
Q

What resistance can VanA cause?

A
  1. Vanconycin
  2. Teicoplanin
61
Q

What resistance can VanB cause?

A

Vancomycin

62
Q

Can vancomycin resistant enterococci become Vancomycin resistant?

A
  1. It can but not very often.
  2. Not clinically seen or important at the moment
63
Q

Is MRSA causing an increase in vancomycin-resistant enterococci infections?

A
  1. Vancomycin use has increased due to increased MRSA.
  2. This creates selection pressures for vancomycin-resistant enterococci.
  3. The remaining antibiotics are quite nasty and toxic like ceftaroline

Medical Microbiology (16 decks)

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