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K Cards > MICRO 12 – Staphylococcus > Flashcards

MICRO 12 – Staphylococcus Flashcards

1
Q

What is the main purpose of coagulase test

A

To differentiate Staphylococcus aureus from other staphylococci.

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2
Q

What are the common types of Staphylococcal Species and associated characteristics.

A

1.S. aureus, causes common & or serious infections BUT also colonises mucosa & moist skin areas
2.’Coagulase-negative’ staphylococci predominate on the skin & are commensals, e.g.
S. epidermidis
S. saprophyticus
Generally cause less serious infections

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3
Q

Where are Staphylococcus aureus commonly found.

A

Found in moist skin folds, mucosal surfaces, nasopharynx.

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4
Q

What are the common associated characteristics of Staphylococcus aureus.

A

Increased in diabetes mellitus, intravenous drug users & where a foreign body is present

Lots of virulence factors
Even though it often just colonises healthy adults

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5
Q

How does Staphylococcus aureus infection occur.

A

Infection occurs when there is a break in the skin or there is entry through the mucous membranes allowing access to adjoining tissues

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6
Q

How does Staphylococcus aureus get into the body.

A
  1. Ingestion
  2. Inhalation
  3. Penetration - Break in skin
  4. Sexual
  5. Transplacental
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7
Q

Where does it attache to in the cells.

A
  1. Surface proteins
    attachment to epithelial & endothelial proteins (e.g. laminin & fibronectin of the extracellular matrix) & foreign bodies (NB – Biofilm formation)
  2. Capsule
    inhibits chemotaxis, phagocytosis & facilitates adherence to foreign bodies, e.g. intravascular (IV) catheter
  3. Fibrin/fibrinogen binding protein (clumping factor)
    attachment to blood clots & traumatised tissue
  4. Matrix binding proteins
    Fibronectin, fibrinogen & collagen binding
    Adhesin that promotes collagen attachment found in strains that cause osteomyelitis/septic arthritis
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8
Q

Does Staphylococcus aureus defeat the immune system? If yes how does it?

A

Yes.
By inhibition of phagocytosis with survival within phagocytes
Production of extracellular substances that promote invasion e.g
Invasins
Enzymes

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9
Q

What are the common Enzymes in the human body.

A
  1. Coagulase
  2. Protein A
  3. Alpha toxin (alpha-haemolysin)
  4. Leukocidin
  5. Staphylokinase
  6. Hyaluronidase
  7. Other extracellular enzymes
    >Protease
    >Catalase = lipase (staphylococci are catalase +ve & >streptococci are catalase neg)
    >Deoxyribonuclease (DNase)
    >Fatty acid modifying enzyme (FAME)
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10
Q

Mention any type of toxins possibly found in the human body.

A 
1. Super antigens
Toxic shock syndrome toxin (TSST-1). 
Enterotoxins 
6 antigenic types (A, B, C, D, E, G)
2. Exfoliative toxins
Scalded skin syndrome
3. Other toxins – cytotoxins
(alpha, beta, leukocidin etc)
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11
Q

How does Staphylococcus aureus spread

A

Person-to-person
direct contact via skin carriage, especially hands
Environment
shed on to surfaces

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12
Q

Staphylococcal infections can be classified in various group. State this classification.

A

1.Skin & soft tissue e.g Necrotizing fasciitis – potentially fatal (deep muscle involvement)
Scalded skin syndrome (toxin)
Toxic shock syndrome (toxin)

    1. Systemic - invasive e.g Bloodstream infection (BSI)
      Endocarditis
      Bone/joint infections
      Deep abscesses, e.g. brain, liver
    1. Systemic -toxin-mediated
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13
Q

What are the common types of systemic Staphylococcus aureus infections?

A 
Bloodstream infection (BSI)
Endocarditis
Bone/joint infections
Deep abscesses, e.g. brain, liver
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14
Q

What are the toxin mediated conditions?

A
  1. Food Poisoning/Gastroenteritis
  2. Scalded Skin Syndrome
  3. Staphylococcal Toxic Shock Syndrome (TSS)
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15
Q

How is TSS investigated.

A 
Take a proper history
FBC, U+E, lactate
Wound swab culture if skin lesion
Blood cultures if febrile, systemically unwell, but rarely positive
Other cultures, abscess, cervix/vagina
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16
Q

How can one manage TSS?

A

Recognise it quickly
Rapid IV antimicrobials, source control / debride infected or necrotic wounds
Resuscitation & critical care input

17
Q

What is MRSA

A

Meticillin resistant S. aureus (MRSA) is S. aureus that has become resistant to the usual antimicrobial treatment
Meticillin was the laboratory form of what we now call flucloxacillin
All the usual features of S. aureus + resistance
MRSA can also be resistant to other antimicrobial classes

18
Q

How does MRSA result?

A

Results from production of an altered penicillin binding protein (PBP2a)
Encoded by mecA
Confers resistance to most beta-lactam antibiotics
mecA gene carried on a mobile genetic element known as staphylococcal cassette chromosome (SCCmec)
Originally predominantly healthcare-acquired

19
Q

What are the common community acquired MRSA and the associated features?

A

Skin infections & necrotizing pneumonia
Panton Valentine Leucocidin toxin (PVL) positive
Younger, healthier patients
Less antibiotic resistant, more virulent
Certain strains e.g. USA300; still more common in North America

20
Q

How can one manage patients with Staphylococcus aureus infections?

A

Clinical examination

Focus on possible source or evidence of metastatic (spread) infection if patient systemically unwell

Examine

Skin – IV line sites, surgical wound, look for soft tissue infection/abscess, scar to indicate joint or valve replacement or indwelling device

CVS – evidence of known or new murmur on ascultation

Musculoskeletal examination - osteomyelitis

Always consider possibility of deep-seated infection

21
Q

Explain antibiotic treatment of Staphylococcus aureus

A

Choice, route & duration of treatment depends on underlying infection site and complexity
No treatment for mild infections e.g. boil, folliculitis
Skin/soft tissue infections & RTI: Seven days
BSI: 14 days
Complicated infection (endocarditis, septic arthritis, osteomyelitis): At least four weeks, but may need longer

Flucloxacillin if susceptible (MSSA), 1st generation cephalopsorin (e.g. cefazolin) also an option

Vancomycin or Teicoplanin (glycopeptide) or alternatives (daptomycin, linezolid, tetracyclines) if MRSA

If BSI – Look for the source:

ECHO, radiology & repeat blood cultures after commencing antimicrobial treatment to confirm blood is now sterile

22
Q

What is S. Epidermidis Infections.

A

BSI often secondary to IV lines

Endocarditis

prosthetic valves

Prosthetic joint infections

Continuous ambulatory peritoneal dialysis peritonitis

Ventriculitis/ shunt-associated meningitis

23
Q

How does one diagnose S. Epidermidis Infections.

A

Often patient not systemically unwell

Blood cultures (at least two sets – Coagulase-negative staphylococci are very common skin contaminants of blood cultures)

Culture prosthetic material

Often the prosthesis must come out for effective treatment
Coagulase-negative staphylococci are often resistant to several different antibiotics, including (meticillin/flucloxacillin) resistant
Vancomycin is usual empiric treatment
Indication & duration of treatment depends on location of infection & if prosthetic material can be removed

24
Q

Staphylococcus saprophyticus is the common cause of uncomplicated UTI (cystitis) in women during reproductive years. TRUE/FALSE

A

TRUE

25
Q

What is the function of coagulase Enzyme?

A

Extracellular protein which binds to prothrombin
Protease activity of thrombin is activated -fibrinogen to fibrin - causes blood to coagulate
Clots protect the bacteria from phagocytosis & other host defences
Slide coagulase test to differentiate S. aureus from coagulase-negative staphylococci

26
Q

Briefly describe the functions of Protein A

A

Cell wall surface protein
Binds IgG molecules in inverted orientation (by their Fc region) 🡪 prevent phagocytosis
Spa gene & commonly used for S. aureus genotyping

27
Q

What is the function of alpha toxin

A

Alpha toxin also (alpha-haemolysin)

Bind to platelets & monocytes causing small pores - osmotic lysis

28
Q

What is the function of Leukocidin

A

Leukocidin
Acts on polymorphonuclear leukocytes
Expressed by 2% of S. aureus isolates, but much higher rates of expression (90%) seen in isolates causing severe skin/soft tissue infections. ?important factor in necrotising skin infections

29
Q

What does Staphylokinase do?

A

Staphylokinase
Plasminogen activator that lyses fibrin
Dissolves fibrin clots & helps bacterial spread

30
Q

What does Staphylokinase do?

A

Staphylokinase
Plasminogen activator that lyses fibrin
Dissolves fibrin clots & helps bacterial spread

31
Q

What does hyaluronidase do?

A

Hyaluronidase

Helps spread by breaking down hyaluronic acid in connective tissues

32
Q

Briefly describe Endocarditis

A 
Usually secondary to BSI
High fever + rapidly progressive disease
Investigate for primary focus 
e.g. IV line site
Prolonged IV antibiotics
May need surgical replacement of valve
33
Q

Grief a brief description of pneumonia

A

Haematogenous
septic emboli / R side endocarditis/ IV device
Risk factors;
>Viral respiratory infection (influenza or measles)
>Cystic fibrosis
>Ventilation
>Aspiration

34
Q

Give an overview of Osteomyelitis

A

Haematogenous: BSI seeds to bone OR local invasion: trauma, diabetic foot ulcer
Can n occur in setting of implant/metalwork
Vertebrae the most common site for haematogenous spread
Long bone metaphyses in children
Microbiological diagnosis: bone biopsy or direct needle aspiration
Radiological diagnosis: MRI, bone scan
Radiological diagnosis: MRI, bone scan

35
Q

What characterizes Septic arthritis

A

Hot swollen joint

Knee, hip, elbow and shoulder are most common joints affected by metastatic spread, i.e. from BSI +/- endocarditis

36
Q

Give an overview of food Poisoning

A

Enterotoxins - 8 types

Stable to temp of 100oC, acid resistant, salt tolerant

Food contaminated with S. aureus enterotoxins

Hands of food handlers (+ no hand hygiene!)

Rapid onset of symptoms (1-6 hours later)

Usually lasts 1 day
Antibiotics not used; treatment is supportive, i.e. rehydration

37
Q

Scalded skin syndrome is a toxic mediated condition. Give a brief discussion

A

Spectrum of superficial blistering skin disorders
>Localized blisters
>Generalized exfoliation of entire body surface
Exfoliative toxins
-Split intracellular bridges in
skin layer
Most common in children < 6 yrs
-Mainly in neonates,
-Immunosuppressed adults
-Adults with renal failure
Contagious
Skin extremely painful
Mucous membranes usually spared
Large patches of necrotic epidermis slide off the underlying layers at the slightest pressure (Nikolsky’s sign)
Prognosis in children good unless associated with sepsis/underlying medical condition
Complications usually due to sepsis /super infection/dehydration
Management – rehydration, wound care & antibiotics

38
Q

Describe Staphylococcal Toxic Shock Syndrome.

A

TSS toxin-1 acts as a super antigen - massive cytokine release
Historically associated with high absorbency tampons
Rapid, dramatic & fulminant onset
Pyrexia, hypotension
Rash with subsequent desquamation, especially on palms and soles
Other organ involvement, e.g. renal failure, CNS (disorientation without focal neurological signs, muscular (severe myalgia, increase in CPK)

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