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MICROBIOLOGY II > Lecture 1 - Staphylococcus > Flashcards

Lecture 1 - Staphylococcus Flashcards

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1
Q

Which surgeon noticed some post surgical infections. In absecesses recover adn visualise organisms to look like bunches of grapes

A

William Ogston 1881

First description of staph

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2
Q

3 years after Ogston what did anton rosenbach do

A

Classify organisms from absseces into two groups - golden colonies on agar and smaller white colonies

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3
Q

Can s.epidermidis cause disease

A

No it is non pathogenic

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4
Q

What is the size of the staphylococci

A

0.5-1 um

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5
Q

Is staphylococcus catalase + or negative

A

Catalase positive

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6
Q

Are staphylococcus aerobic or anaerobic

A

FACULTATIVE ANAEROBE

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7
Q

What can differentiate s aureus from other staph

A

Coagulase positive

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8
Q

What does s aureus do with coagulase

A

Coagulate CITRATED PLASMA

CONVERT FIBRINOGEN TO FIBRIN - SURROUND ORGANISM WITH HUGE FIBRIN CLOT FOR PROTECTION FROM ANTIBIOTICS ETC

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9
Q

Name the three main virulence factors that staph areus has (basic)

A

1- adhesins - cell bound proteins (ATTACHMENT)
2- Protein A and microcapsule (EVASION)
3- Toxins and Invasins (DAMAGE HOST)

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10
Q

Name the three toxins produced and what effect they have

A
  • TSST
  • EFT
    -SE A-G
    Enterotoxins so cause vomiting.

Cause toxic shock( multifunction organ failure), exfoliation (skin blistering) and emesis (vomiting)

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11
Q

What antibody binds to protein A

A

IgG

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12
Q

Describe in detail how staph aureus colonise host

A

MSCRAMMS - microbial surface components recognising adhesive matrix molecules

A) expression of surface fibronectin and laminin binding proteins -
Fibronectin, laminin (and fibrinogen) form extracellular surface matrix of HEALTHY endothelial and epithelial surfaces (hence carriers of s.aureus if can bind to healthy tissue)

B) Expression of fibrin/fibrinogen binding proteins (clumping factor) - promotes adhesion to DAMAGED tissue and BLOOD CLOTS.

C) Expression of collagen binding protein - promotes adhesion to SEVERELY DAMAGED tissue. Collagen deeper in tissue.

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13
Q

In detail how does staph aureus evade host defences

A

CASPSULAR POLYSACCHARIDE - aka microcapsule.

Protein A - prevent c3b of complement attaching to surface of bacteria so prevent complement associated oxidation phagocytosis. It binds IgG WRONG WAY ROUND via Fc receptor instead of FAB

Leucocidin - pore forming toxin. protein toxin burst open wbc . Genes carried by bacteriophage injected into staph chromosome. PVL (Panton Valentine - Leucocidin) can burst open cell

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14
Q

What % carry lethal form of leucocidin

A

1-2%

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15
Q

How does staph aureus invade tissue

A
  • membrane damaging toxins (alpha - haemolysin - type II toxin attack membrane )
  • coagulase - clotting protective layer
  • staphylokinase - fibrinolysis; bacterial spread (break down clot so can spread through tissue)
  • hyaluronidase -lyses hyaluronic acid (as ECM make up of HA - can spread through ECM now)
  • DNAase - split for nutrition
  • Fatty Acid Modifying enzyme (FAME) - converts bacterial FA in infected tissue to alcohols e.g. Cholesterol
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16
Q

What are the enterotoxins produced by 60-70% of s aureus

A

A-E, G-J
Toxins INGESTED through contaminated food stuffs (custards, pastries, milk )
- food poisoning (profuse vomiting)

-HEAT STABILE at 100 deg for several minutes. S aureus may die but toxin live

17
Q

What does the toxin TSST-1 do that some s aureus produce

A

Toxic shock syndrome toxin (TSST-1)
- toxins produced systemically
Associated with tampon use early 80s
Fever, shock, skin rash , multi system involvement

Carry sa in genital tract so don’t change tampons get this

18
Q

What does exfoliative toxin do that some s aureus produce

A

Exfoliative A and B (ETA and ETB)
Toxins produce systemically (serine proteases split dermal junctions in skin and cause severe blistering. May start as little pimple lead to big blistering. )
- hence SCALDED SKIN SYNDROME

19
Q

The s aureus exotoxins (enterotoxins A-E, G-J, TSST-1 and exfoliative toxins) are all superantigens. What does this mean

A

They all bind non specifically to MHC class II of antigen presenting cells

  • AVOID DIGESTION PROCESS
  • As it is non specific massive amount of t cells so increased cytokine release TNF, interleukins, get INF = toxic shock.

TYPE I TOXINS

20
Q

What is the difference in ratios of t cell activation for normal antigen and super antigen

A

Normal - 1:10,000 T cells activated

Superantigen - 1:5 T cells activated

21
Q

Briefly describe mrsa history

A

Methicillin a beta Lactam antibiotic introduced in 1960 to withstand beta lactamase producing staph

  • MRSA: first described in 1961 ; recognised as a hospital pathogen in 70’s - rapid spread through hospitals 1980-2005
  • if found in hospitals it is HA-MRSA if found in community, healthcare workers, and patients then (CA-MRSA)
  • transmission patient to patient, environment to patient and HCW. To patient
22
Q

What percentage of s areus are now mrsa

A

50%

23
Q

How does s aureus become mrsa

A

MecA gene incorporated on SCCmec gene (staphylococcal cassette chromosome mec)
Encodes for additional pencilling binding proteins (PBP2a) ; reduced affinity for beta lactams
MRSA resistant to all beta lactam antibiotics

24
Q

What is drug of choice for mrsa

A

Vancomycin - drug of choice - glycopeptide bind to D-ala D-ala. work at membrane level. Blocks action of transglycosidase and PBP enzymes (transpeptidase)
Prevent new wall subunits being added

25
Q

What is visa

A

MRSA with reduced suscpetilbity to vancomycin
Vancomycin intermediate Staph aureus (VISA)
First strains reported in Japan 1996

26
Q

What does visa posses to make it slightly resistant to vanco

A

Possses Meca gene AND cell wallthicker than usual acting as a sponge to trap Vancomyocin in established peptidoglycan

27
Q

How can we attempt to resolve visa

A

Give even more vancomycin but this drug has side effects

28
Q

What is the type of mrsa to be fully resistant to vancomycin

A

VRSA - USA 2002

29
Q

WHAT DOES VRSA HAVE

A

Posses mecA gene aAND VANA gene encode for altered resistant cell wall structure from D-ala D-ala to D-ala D-lac
Van A genes are plasmid based; proteintial for HGT between MRSA (conjugation.)

Believed to have received VanA from vancomycin resistant enterococcus which is in our gut

30
Q

What is carriage rate of s aureus and MRSA

A

40% carriage rate of s aureus in healthy individuals

1-2% carriage rate MRSA

31
Q

What are 3 types of MRSA infection

A

Mild superficial (skin)
Deep (organs, tissue, bone)
Systemic (including toxaemia)

Purulent infections

32
Q

Name some sites of infections and the disease you get there

A 
Heart - endocarditis 
Bones - osteomyelitis 
Vagina/cervix - cystitis, TSS 
Skin - impetigo 
Eye - Stye 
Lungs - pneumonia 
Gut - emisis
33
Q

What are predisposing factors for s aureus infection

A 
Carriage of organism
Diabetic patients 
Immunsupporessed patiets 
Drug users
Hospital stay
Intrvascular catheters
34
Q

What are the clinical manifestations of s aureus infection (syperificial)

A

Staphylococcal boils

Surgical wound infection show inflammation and pus

35
Q

What is seen in an superficial infection associated with central venous catheters (CVC)

A

Localised CVC infection. Inflammation, exudate, erythema

36
Q

Where can deep seated staphylocall infections occur (two examples)

A

Skin and tissue destruction of diabetic leg ulcer

Discharging staphylococcal sinus in cancer patient

37
Q

Describe a systemic skin infection (Scalded skin syndrome SSS) - toxin associated

A
  • follows localised focus of infection e.g, skin
  • s aureus infection and toxin production (superantigen)
    Splitting of skin, erythema and blisters
    -affects neonates and young children (reduced immunity)
  • mortality rate approx 4%

MICROBIOLOGY II (9 decks)

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