Why do we study Staphlococcus aureus?
- Severity: it causes many life threatening diseases
- Many community acquired infections
- Frequency: most frequently acquired HCAI
- Cost: most costly HCAI
- Preventable
- Treatable
Impetigo
‘School sores’ occurring mostly in young children. It is superficial and usually caused by S. aureus but al Strep. Pyogenes
Stages:
- Erythematous macule
- Pustule forms
- Pustule pops, crust forms
Folliculitis, Faruncles, Carbuncles
Starts in hair follicle.
• Folliculitis: superficial, common
• Furuncle (boil): deep version
• Carbuncle: group of furuncles
Staphylococcal Scalded Skin Syndrome (SSSS)
- Desquamation
- Caused from exfoliative toxins
- 0-5 years old
- Looks bad
- Good recovery
Toxic Shock Syndrome (TSS)
- Localised growth (e.g. wound, tampon)
- Toxic shock syndrome toxin (TSST) production
- Toxins move to blood
- Transported through body
- Desquamation, intravascular coagulation, multiple organ failure, death
Wound Infection
- Following surgery or trauma
- Often endogenous origin
- Foreign body usually present (e.g. stitches, implant, splinter, dirt)
Cellulitis
- Subcutaneous and cutaneous skin infection
- Erythema, swelling, pain, sometimes supporative (pus formation)
- Can spread very fast, along tissue planes
- Maybe from minor injury
- Potentially very serious
Bacteraemia, Septicaemia
- Bacteraemia: bacteria in blood
- Septicaemia: infection in blood
- Often from infected wound
- Growth at site
- Movement into blood
- Toxin produced
- 80% mortality if untreated
Osteomyelitis
Bone infection
Due to:
- Bacteraemia
- Adjacent skin infection
- Bone surgery
- Bone trauma
Endocarditis
- Infection of endocardium (inner lining of heart muscle and valves)
- Due to bacteraemia
- Fatal if untreated
Septic arthritis
- Infection within joint
- From joint wounds, surgery, injections, or bacteraemia
Pneumonia
• Lung infection
• Inhaled or haematogenous (from blood)
• Abscesses, haemoptysis (coughing up blood)
• Variable in severity
• Necrotizing pneumonia
o Most severe type
o Massive haemoptysis
o High mortality
Food poisoning
- Severe vomiting, diarrhoea, abdominal pail
- Self limiting
- Highly handled meats, dairy and bakery products, salads
What are the stages of infection?
- Bacteria from food handler introduced into food
- Temperature abused storage
- Bacteria growth, release toxin
- After eating: toxin survives in GIT passage, bacteria do not.
How do you identify streptococci?
- Microscopy: gram positive cocci in bunches
- Colony morphology: large, white-yellow colonies
- NaCl tolerance: up to 10%
- Carbohydrate fermentation: acid from mannitol
- Produces catalase
- Produces coagulase: the only Staphylococcus spp.
- Presence of protein A: only S. aureus
- DNA method: species and strain identification
What are the virulence factors of streptococcus aureus?
- Tolerance to salt, dehydration: allows survival on skin
- Slime layer: attachment to tissues, foreign bodies
- Adhesion proteins: attachment to host tissues
- Capsule: inhibits phagocytosis by PMN leukocytes
- Protein A: inactivates IgG by binding Fc receptor
• Coagulase: converts soluble fibrinogen to insoluble fibrin
- Causes clots and tissue necrosis
- S. aures clumps providing protection from immune system
- Hyaluronidase: breakdown intracellular bridges in connective tissue
- Fibrinolysin: breakdown fibrin clots
- Lipase: breakdown fats, particularly sebum
- Nuclease: reduces pus viscosity, also breakdown of neutrophil extracellular traps (NET)
- Cytolytic toxins: damage host cell membranes
- Exfoliative toxins: breakdown intracellular bridges in epidermis
- Enterotoxins: cause food poisoning. Heat, acid stable.
- Toxic shock syndrome: penetrates vaginal mucosa, systemic dissemination, systemic inflammation
- Superantigens
- Special class of secreted toxins
- Huge non specific CD4 T cell activation
- Cytokine storm
- Massive systemic inflammation
- Specific immune response retarded
- Shock, organ failure, death
- TSST (TSS toxin) most important example
- Exterotoxins, exfoliative toxin A also, but less systemic effects
Antibiotic resistance
- Resisted all antibiotics
- Penicllin resistance usually assumed
- MRSA = methicillin resistant Staphylococcus aureus
- MSSA = methicillin sensitive Staphylococcus aureus
- o VRSA = vancomycin resistance Staphylococcus aureus
What are the S. aureus reservoirs?
Asymptomatic persistent carriage in 30% of healthy adults and 40-50% of health care workers and patients.
Locations
• Anterior nares, nasopharynx
• Perineum, axilla (less)
• Skin: frequent but in low numbers
Most infections are of endogenous origin
How is s. aureus transmitted?
- Normally on skin or fomites
- Survival for months on dry surfaces
How are s. aureus infections prevented?
• Active surveillance cultures
- Screen for colonized staff and patients
- Gloves, gowns: when working with colonised patients
- Hand hygiene
- Disinfection of fomites
- Eradication therapy if colonised
- Antibiotic stewardship
- Education and record keeping
Can we become immune to s. aureus?
No immunity
• Chronic colonization by one strain
• Repeated colonisation by the same strain
• Repeated infections by the same strain
What are other staphyloccus species?
- S. epidermidis
- S. lugdunensis
- S. haemolyticus
- S. saprophyticus
‘Coagulase-Negative Staphylococci’ (Aka CoNS)
Opportunistic infections
- Sterile sites
- Immunocompromised
- Often infections of surgical implants or catheters
- >50% of all catheters and shunt infections
- UTIs
- Bacteraemia
- Endocarditis around artificial valves
- Prosthetic joint infections
What are the virulent factors of Staphlococcus spp?
- Relatively avirulent
- Dessication tolerance
- Slime layer: biofilm formation
- Adherence to foreign bodies
- Phagocytosis protection
- Antibiotic protection
• Antibiotic resistance (like S. aureus)
What is the transmission and reservoir of staphlococcus spp.
- Most common NF on skin
- Also much on mucosal surface
- Skin-skin, skin-fomite spread
- Self infections common
