MICRO 12 – Staphylococcus Flashcards
What is the main purpose of coagulase test
To differentiate Staphylococcus aureus from other staphylococci.
What are the common types of Staphylococcal Species and associated characteristics.
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
Where are Staphylococcus aureus commonly found.
Found in moist skin folds, mucosal surfaces, nasopharynx.
What are the common associated characteristics of Staphylococcus aureus.
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
How does Staphylococcus aureus infection occur.
Infection occurs when there is a break in the skin or there is entry through the mucous membranes allowing access to adjoining tissues
How does Staphylococcus aureus get into the body.
- Ingestion
- Inhalation
- Penetration - Break in skin
- Sexual
- Transplacental
Where does it attache to in the cells.
- Surface proteins
attachment to epithelial & endothelial proteins (e.g. laminin & fibronectin of the extracellular matrix) & foreign bodies (NB – Biofilm formation) - Capsule
inhibits chemotaxis, phagocytosis & facilitates adherence to foreign bodies, e.g. intravascular (IV) catheter - Fibrin/fibrinogen binding protein (clumping factor)
attachment to blood clots & traumatised tissue - Matrix binding proteins
Fibronectin, fibrinogen & collagen binding
Adhesin that promotes collagen attachment found in strains that cause osteomyelitis/septic arthritis
Does Staphylococcus aureus defeat the immune system? If yes how does it?
Yes.
By inhibition of phagocytosis with survival within phagocytes
Production of extracellular substances that promote invasion e.g
Invasins
Enzymes
What are the common Enzymes in the human body.
- Coagulase
- Protein A
- Alpha toxin (alpha-haemolysin)
- Leukocidin
- Staphylokinase
- Hyaluronidase
- Other extracellular enzymes
>Protease
>Catalase = lipase (staphylococci are catalase +ve & >streptococci are catalase neg)
>Deoxyribonuclease (DNase)
>Fatty acid modifying enzyme (FAME)
Mention any type of toxins possibly found in the human body.
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)
How does Staphylococcus aureus spread
Person-to-person
direct contact via skin carriage, especially hands
Environment
shed on to surfaces
Staphylococcal infections can be classified in various group. State this classification.
1.Skin & soft tissue e.g Necrotizing fasciitis – potentially fatal (deep muscle involvement)
Scalded skin syndrome (toxin)
Toxic shock syndrome (toxin)
- Systemic - invasive e.g Bloodstream infection (BSI)
Endocarditis
Bone/joint infections
Deep abscesses, e.g. brain, liver
- Systemic - invasive e.g Bloodstream infection (BSI)
- Systemic -toxin-mediated
What are the common types of systemic Staphylococcus aureus infections?
Bloodstream infection (BSI) Endocarditis Bone/joint infections Deep abscesses, e.g. brain, liver
What are the toxin mediated conditions?
- Food Poisoning/Gastroenteritis
- Scalded Skin Syndrome
- Staphylococcal Toxic Shock Syndrome (TSS)
How is TSS investigated.
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
How can one manage TSS?
Recognise it quickly
Rapid IV antimicrobials, source control / debride infected or necrotic wounds
Resuscitation & critical care input
What is MRSA
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
How does MRSA result?
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
What are the common community acquired MRSA and the associated features?
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
How can one manage patients with Staphylococcus aureus infections?
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
Explain antibiotic treatment of Staphylococcus aureus
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
What is S. Epidermidis Infections.
BSI often secondary to IV lines
Endocarditis
prosthetic valves
Prosthetic joint infections
Continuous ambulatory peritoneal dialysis peritonitis
Ventriculitis/ shunt-associated meningitis
How does one diagnose S. Epidermidis Infections.
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
Staphylococcus saprophyticus is the common cause of uncomplicated UTI (cystitis) in women during reproductive years. TRUE/FALSE
TRUE
What is the function of coagulase Enzyme?
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
Briefly describe the functions of Protein 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
What is the function of alpha toxin
Alpha toxin also (alpha-haemolysin)
Bind to platelets & monocytes causing small pores - osmotic lysis
What is the function of Leukocidin
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
What does Staphylokinase do?
Staphylokinase
Plasminogen activator that lyses fibrin
Dissolves fibrin clots & helps bacterial spread
What does Staphylokinase do?
Staphylokinase
Plasminogen activator that lyses fibrin
Dissolves fibrin clots & helps bacterial spread
What does hyaluronidase do?
Hyaluronidase
Helps spread by breaking down hyaluronic acid in connective tissues
Briefly describe Endocarditis
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
Grief a brief description of pneumonia
Haematogenous
septic emboli / R side endocarditis/ IV device
Risk factors;
>Viral respiratory infection (influenza or measles)
>Cystic fibrosis
>Ventilation
>Aspiration
Give an overview of Osteomyelitis
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
What characterizes Septic arthritis
Hot swollen joint
Knee, hip, elbow and shoulder are most common joints affected by metastatic spread, i.e. from BSI +/- endocarditis
Give an overview of food Poisoning
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
Scalded skin syndrome is a toxic mediated condition. Give a brief discussion
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
Describe Staphylococcal Toxic Shock Syndrome.
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)
