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(2020-21 BY2MI1) Microbiology II > Staphylococci > Flashcards

Staphylococci Flashcards

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1
Q

Give a breif history of staphylococci

A
  • The first description was by Sir William Ogston (a Scottish surgeon) in 1881.
  • He noticed that some patients developed post surgical infections
  • When isolated visualised under a micropscope, the oirganisms looked like bunches of grapes
  • 3 years later these organisms were classified into two major groups: Golden colonies of S.aureus (2mm) ans White colonies of S.epidermidis (1mm) by Anton Julius Friedrich Rosenbach
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2
Q

What is the classification of Staphylococci?

What are their main characterisitics?

A

Kingdom: Bacteria; Family: Staphylococcaceae (Staphylé :Bunches of Grapes)

  • Gram-positive cocci: 0.5-1.0 µm diameter
  • Facultative anaerobes (grow in aerobic and anaerobic conditions); 18oC - 40oC
  • Catalase+ (Breaks down hydrogen peroxide into water and oxygen)
  • Approx 40 species; Tend to inhabit the skin and mucous membranes
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3
Q

What is the major differentiating feature between staphlococci?

A

The enzyme COAGULASE

  • It confers the ability to coagulate citrated plasmathrough the conversion of Fibrinogen to Fibrin. This is a defecnce mechanism which prevents antibiotic penetration and protects against host defences
  • Cogulase-positive staphylococci→Staphylococcus aureus
  • Cogulase-negative staphylococci→ 30+ species including:

Staphylococcus epidermidis + Staphylococcus saprophyticus

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4
Q

Describe the virulence factors and mechanisms of pathogenicity of 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 EXOELLULAR TOXINS
  • Ability to acquire RESISTANCE to antibiotics
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5
Q

What mechanisms do ‘true’ pathogens employ?

A
  • Attachment
  • Evade the hosts defences
  • Production of toxins that allow the organism to spread and cause disease
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6
Q

What helps S.aureus attach to healthy skin, damaged skin and deep wounds?

A

Cell surface proteins→Adhesins

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7
Q

What helps S.aureus evade the hosts defences?

A

Microcapsules→Surrounds the organisms cell wall

Protein A→ Binds antibodies the wrong way round (by the Fc portion) and acts as an ‘antibody sponge’

Invasins→ Hyaluronidase, Staphlysin, Leukocidin, Leukotoxin, Coagulase, Staphylokinase

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8
Q

What are the 3 main potent toxins produced by S.aureus?

A
  1. Enterotoxins→Cause vomiting (emesis)
  2. Toxic shock syndrome toxins→ Cause multifunction organ failure. They are superantigens with a very high affinity for MHC class II receptors of T cells. Upon binidng, this can lead to a cytokine storm due to the overactivation of T cells which can be fatal for the patient
  3. Exfoliating toxins→Causes skin blistering (scalded skin syndome)
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9
Q

Enterotoxins are heat stable. Are they also resistant to enzymes in the gut?

A

Yes

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10
Q

Which type of food products do stayphylococcus produce enterotoxins on?

A

Meat, carbohydrate and dairy products

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11
Q

What effect do enterotoxins have on the digestive tract?

How do they cause the feeling of nausea and vomiting?

A
  • They cause increased peristalsis
  • They cause local nerve receptor stimulation which stimulate the medullay center which causes feelings of nausea and vomiting.
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12
Q

Explain the adhesion and colonisation of a host by S.aureus

A

MSCRAMMS (Microbial Surface Components Recognising Adhesive Matrix Molecules)

  • (a) Expression of surface fibronectin and laminin bing proteins
  • fibronectin, laminin (and fibrinogen) form the extracellular surface matrix of healthy endothelial and epithelial surfaces
  • (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

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13
Q

Where is S.aureus likely to be found in the body?

A

At the back of your nose, in your armpit or groin region

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14
Q

How does S.aureus evade the hosts defences?

A
  • CAPSULAR POLYSACCHARIDE (Microcapsule) that surrounds it and prevents C3b from the complement system from attaching to its surface.
  • PROTEIN A (inhibits phagocytosis; immune ‘disguise’; antibody ‘sponge’. It attaches to the Fc portion of IgG (binds it the wrong way around→prevents antibody associated phagocytosis)
  • LEUCOCIDIN production (Panton Valentine Leucocidin -PVL toxin)

-pore-forming toxin; WBC destruction

Toxin carried by genes in bacteriophage which are injected into the staphylococcol chromosome

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15
Q

What percentage of S.aureus strains carry PVL?

A

1-2%

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16
Q

Hows does S.aureus invade the host?

A

•Membrane damaging toxins

(eg. α-haemolysin, a pore forming toxin –type II toxin -attaches to the phospholipid membrane of cells and causes cell lysis)

•Coagulase – causes clotting; creates a protective layer around the bcterium

•Staphylokinase – fibrinolysis (breaks down fibrin clots): bacterial spread

  • Hyaluronidase – lyses hyaluronic acid in the ECM, allowing the bacterium to spread
  • DNAase – splits DNA: Use the by-products as nutrition
  • Fatty acid modifying enzyme (FAME)- converts (esterifies) bactericidal fatty acid in infected tissue to alcohols or cholesterol
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17
Q

Production of (exo)toxins: Enterotoxins (A-E, G-J)

A
  • 65% of strains produce this toxin
  • Enterotoxins are heat stable
  • Toxins ingested through contaminated foodstuffs (custards, pastries, milk)
  • Food poisoning (profuse vomiting) up to 6 hours following consumption
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18
Q

Poduction of (exo)toxins: Toxic shock syndrome toxin (TSST-1)

A
  • 5-25% strains produce this toxin
  • Toxins produced systemically
  • Associated with tampon use (early 80’s), not being changed often enough so S.aureus is able to colonise the tampon and get into the vaginal area
  • Fever, shock, skin rash
  • Multi-system involvement
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19
Q

Production of (exo)toxins: Exfoliative toxin: ETA / ETB

A
  • 5-10% of strains prtoduce this toxin
  • Toxins produced systemically (serine proteases that split the dermal junctions in your skin and causes blistering)
  • Associated with Scalded Skin Syndrome
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20
Q

Are S.aureus exotoxins(enterotoxins, TSST-1 and exfoliative toxins) classed as superantigens?

A

Yes

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21
Q

What are superantigens?

A

They bind non-spcifically to the major histocompatability complexes (MHC) of antigen presenting cells

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22
Q

Compare normal antigens to superantigens

A
  • Normal’ antigen - 1:10,000 T cells are activated
  • ‘Superantigen’ - 1:5 T cells are activated (20% of the T cell population); increased cytokine release TNF, interleukins; INF = toxic shock

Superantigens are the most powerful T cell mitogens ever discovered. They are type 1 becuase they act on the surface of the cell

23
Q

Antibiotic Resistance:

How did Methicillin Resistant Staphylococcus aureus (MRSA) evolve?

When was MRSA first described?

Where is it commonly found?

A
  • Methicillin; beta-lactam antibiotic produced in 1960 to withstand beta-lactamase producing staphylococci
  • MRSA: First described in 1961; recognised as a hospital pathogen in 1970s; rapid spread in hospitals 1980-2005
  • Found in hospitals (HA-MRSA), healthcare workers, patients and in the community (CA-MRSA)
  • Transmission: Patient to patient; environment to patient; HCW to patient
24
Q

What percentage of S.aureus is now MRSA?

A

50% of S. aureus are now MRSA

25
Q

How does S. aureus become MRSA?

A
  • The organism takes up the MecA gene (30-50kb) which is incorporated on staphylococcal cassette chromosome mec (SCCmec)
  • Encodes for additional penicillin binding proteins (PBP2a); they have a different structure to the conventional PBPs therefore confer a reduced affinity for beta-lactams
  • MRSA resistant to all beta-lactam antibiotics as cell wall remains intact in their presence
  • VANCOMYCIN: drug of choice for treatment

It is highly prominent and natually occuring

26
Q

Describe Vancomyosin’s mode of action

A
  • Vancomycin (glycopeptide antibiotic) interferes with cell wall synthesis by binding to D-ala-D-ala in the peptidoglycan, preventing addition of new wall subunits (no glycosidic bonds or peptide bonds can form)
  • Blocks transglycosidase and transpeptidase (PBP) enzymes that involved in gram positive cell wall manufacture. Vancomycin has a bacteriocidal effect on gram positive bacteria.
27
Q

What is a side effect of vancomyosin?

A

It can cause red man syndrome

This is an anaphylactoid reaction caused by the degranulation of mast cells and basophils, resulting in the release of histamine (independent of preformed IgE or complement). The extent of histamine release is related to the amount and rate of the vancomycin infusion

28
Q

True or false? Is S.aureus an α haemolytic bacterium?

A

FALSE

It is β haemolytic meaning that it results in the complete haemolysis of red blood cells in blood agar.

29
Q

What are MRSA with reduced susceptibility to vancomycin called?

A

Vancomycin Intermediate Staphylococcus aureus (VISA)

They are not fully sensitive or resistant to Vancomyosin

30
Q

Describe MRSA with reduced susceptibility to vancomycin?

When were they first reported?

What do they posses?

A
  • First strains reported in Japan (1996)
  • VISA possess the mecA gene AND their cell wall is thicker than usual, acting as a sponge, trapping vancomycin in the established peptidoglycan

Intermediate sensitivity to vancomyosin (higher concentrations and MIC necessary for treatment)

31
Q

How does VISA’s morphology differ from MRSA?

A

VISA has a much thicker cell wall

32
Q

Could MRSA become fully resistant to vancomycin?

A

Yes!

First fully resistant strain VRSA isolated in USA (2002)

•They posses the mecA gene AND the vanA gene which encodes for an altered (resistant) cell wall (pentapetide) structure ending in D-ala-_D-lac_

structure change: D-ala-D-ala →D-ala-D-lac

•VanA genes are plasmid-based; potential for HGT between MRSA (conjugation)

VanA comes from vancomyosin resistant enterococus (carried in the gut)►It encodes a ligase enzyme that has a very high affinity for D-lactate

33
Q

Draw a digram to explain vancomyosin resistance (MRSA vs VRSA)

A
34
Q

Describe the clinical manifestation range of S. aureus (+MRSA) infection

A

•Mild - severe suppurative (pus forming) infections

(A) superficial (skin)

(B) deep (organs, tissue, bone)

(C) systemic including toxaemia

35
Q

What is the carriage rate of S.aureus in healthy individuals?

A

40%

36
Q

What is the carriage rate of MRSA?

A

1-2%

37
Q

Name some Superficial, deep and systemic sites of S. aureus infection

A
38
Q

Name some predisposing factors for S.aureus infection

A
  • Carriage of the S. aureus
  • Diabetic patients
  • Immunosuppressed patients
  • Drug users
  • Hospital stay
  • Intravascular catheters
39
Q

Clinical manifestations of S. aureus infection: Name some superficial manifestations

A
  • Superficial staphylococcal boils
  • Surgical wound infection demonstrating inflammation and pus
  • Uninfected site following CVC insertion
  • Localised CVC infection: inflammation, exudate, erythema
40
Q

Clinical manifestations of S. aureus infection: Name some deep-seated staphylococcal infections

A
  • Skin and tissue destruction in a diabetic leg ulcer
  • Discharging staphylococcal sinus in a cancer patient
41
Q

Clinical manifestations of S. aureus infection: Name a systematic infection

A

Staphylococcal Skin Infection: Scalded Skin Syndrome (SSS)

(Superantigenic) Toxin-Associated

  • Generally follows a loclised focus of infection eg. skin
  • S.aureus infection and toxin production (superantigen)
  • Splitting of skin, erythema, blisters
  • Affects neonates and young children (reduced immunity)
  • Mortality rate ~4%
42
Q

What are nosocomial infections?

A

Hospital acqiured infections

43
Q

Which type of agar is allows you to identify S.aureus?

A

Mannitol-salt agar

  • The salt will only allow staphylococcus species to grow
  • If the bacteria can ferment mannitol then it is aureus → the agar will have a yellow colour.
  • Otherwise the agar will turn pink for other staphyloccus species e.g. epidermidis
44
Q

TRUE or FALSE: S.aueus is the most common cause of septic arthitis and Osteomyelitis in adults?

A

TRUE

In addition S.aureus can cause many skin infections, acute endocarditis (inflammation of the heart)

45
Q

True or false:

Staphlococcus epidermidis can produce a biofilm layer

A

TRUE

46
Q

True or false?

A biofilm layer is extracellular material that is reguarly organised to protect the bacterium

A

FALSE

A biofilm layer is extracellular material that is irreguarly organised to protect the bacterium.

This makes it more resistant to being washed off

47
Q

Which staphyloccus species is the most common cause of endocaditis after artificial heart valve surgery?

A

S.epidermidis

48
Q

Where is S.epidermidis commonly found?

When can it become dangerous?

A

On the skin

It can become dangerous if the skin is penetrated by un-sterile tools

49
Q

Which type of infections is S.saprophyticus commonly asociated with?

A

Urinary tract infections (UTI) in females

50
Q

What is the main difference between S.saphrophyticus and S.epidermidis?

A

S.saphrophyticus is novobiocin resistant

51
Q

Produce of a table of 3 stapylococcus species and the enzymes that they produce

A
52
Q

What is the function of the urease enzyme?

A
  • It breaks urea down into ammonia and carbon dioxide.
  • The ammonia raises the pH around the bacteria, allowing it to survice longer and be able to colonise. This is why the urease enzyme is considered as a virulence factor.
  • This species of bacteria prefer alkaline envirnoments.
53
Q

Describe the management of staphyloccal gastroenteritis (food poisoning)

A
  • Antiemetics are administered→ drugs that are effective against vomiting and nausea
  • Fluid replacement (IV or through the mouth) is provided

(2020-21 BY2MI1) Microbiology II (16 decks)

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