M6- Staphylococcus Flashcards

1
Q

Describe staphylococcus species.

A
  • Gram +ve
  • Non-motile
  • Irregular grape like clusters
  • aerobe + facultative anearobe
  • Catalase +ve (usually)
  • Oxidase -ve
  • Coagulase +ve or -ve
  • Tolerate 15% NaCl
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2
Q

what shape is coccus?

A

round

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3
Q

what is facultative anaerobe?

A

grow anaerobically

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4
Q

who carries S.epidermis?

A

Found in everyones skin and mucosal membranes and only cause problems in immunocompromised individuals (cannula, burns, catheter)

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5
Q

what is a nosocomial infection?

A

hospital acquired infection

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6
Q

who carries S.aureus?

A

3 different states:

  • permanent carrier
  • never carry it
  • transient carrier
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7
Q

Describe transmission of staphylococci.

A

-Contact:
direct- hand , skin, mucous
Indirect- instruments

-Air-borne- shedding of cocci from infected site into atmosphere

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8
Q

Describe entry (opportunistic).

A
  • Hair follicles and sebaceous glands
  • damaged/diseased skin
  • broken skin
  • catheters/implants
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9
Q

Describe pathogenicity of S. aureus.

A
•  Superficial lesions 
–  Boil to abscesses
•  Systemic
–  life-threatening
•  Toxinoses
–  Toxic Shock (only females)
–  Scalded Skin Syndrome
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10
Q

Name some virulence factors of staphylococcus aureus.

A
  • fibrinogen binding protein -adhesin
  • Leukocidin -kills leukocytes
  • TSST-1 -shock, rash, desquamation
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11
Q

what does fibronogeon promote?

A

clot formation

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12
Q

Evasion of host defences.

A
  • protein A
  • proteases
  • superantigens
  • lipases.
  • coagulase
  • capsule
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13
Q

what is toxinoses.

A

single component or toxin that causes damage to the host (true poison )

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14
Q

what are super antigens?

A
  • binds outside super variable cleft

- antigen is not processed by PMN, binds directly to MHCII complex i.e outside conventional binding groove

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15
Q

what do super antigens cause?

A

Massive release of cytokines and inappropriate immune response

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16
Q

what does protein A bind?

A

binds Fc portion of IgG antibodies

17
Q

when is protein A produced?

A

during exponential growth

18
Q

what do proteases do?

A

– Cleave antibodies, defensins, Platelet Microbiocidal
Proteins (PMPs)
– destruction of host tissue

19
Q

what do lipase,phospholipases, esterase do?

A

– combat surfactants produced to disrupt bacterial membrane
– post-exponentially expressed scavenging enzymes

20
Q

what is PVL?

A

panton - valentine leukocidin

  • severe skin infections (sepsis, necrotising fascitis)
  • linked to necrotising pneumonia (MRSA)
21
Q

Describe features of necrotising pneumonia.

A
-rapid progression : 
acute respiratory disease, deterioration in pulmonary function , multi-organ failure despite antibiotic therapy 
-young 
-community acquired 
-more than 75% mortality
22
Q

Describe coagulase.

A
  • Coagulase forms Staphylothrombin promotes conversion of fibrinogen to fibrin and clotting
  • Coagulase may also assist deposition of fibrin on surface and prevent phagocytes recognising them
23
Q

Describe capsule.

A

– 90% clinical isolates produce capsular polysaccharides

– 2 types Mucoid & Microcapsule

24
Q

What is the antibiotic treatment .

A

50-80% resistant (ß-lactamase +ve)
• Flucloxacillin (meticillin) β-lactamase resistant
• Penicillin
• Erythromycin

25
Q

summary slide.

A

• S. aureus & S. epidermidis
• S. aureus
– major pathogen, variety of diseases
• Wide number of virulence associated proteins – virulence factors
• Different strains carry different virulence factors.
• Virulence factors;
– enable colonisation/adhesion,
– evasion of host defenses, & damage to the host.
• Antibiotic treatment/therapy, MRSA & resistance.

26
Q

Describe how S.aureus can affect patients?

A
–  20%-(60%) colonisation (carriage)
–  anterior nares & perineum
–  nosocomial & community
–  nasal strain can protect
–  MRSA