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CAM101 Microbiology > Staphlococcus > Flashcards

Staphlococcus Flashcards

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1
Q

Why do we study Staphlococcus aureus?

A
  1. Severity: it causes many life threatening diseases
  2. Many community acquired infections
  3. Frequency: most frequently acquired HCAI
  4. Cost: most costly HCAI
  5. Preventable
  6. Treatable
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2
Q

Impetigo

A

‘School sores’ occurring mostly in young children. It is superficial and usually caused by S. aureus but al Strep. Pyogenes

Stages:

  1. Erythematous macule
  2. Pustule forms
  3. Pustule pops, crust forms
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3
Q

Folliculitis, Faruncles, Carbuncles

A

Starts in hair follicle.
• Folliculitis: superficial, common
• Furuncle (boil): deep version
• Carbuncle: group of furuncles

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4
Q

Staphylococcal Scalded Skin Syndrome (SSSS)

A
  • Desquamation
  • Caused from exfoliative toxins
  • 0-5 years old
  • Looks bad
  • Good recovery
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5
Q

Toxic Shock Syndrome (TSS)

A
  1. Localised growth (e.g. wound, tampon)
  2. Toxic shock syndrome toxin (TSST) production
  3. Toxins move to blood
  4. Transported through body
  5. Desquamation, intravascular coagulation, multiple organ failure, death
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6
Q

Wound Infection

A
  • Following surgery or trauma
  • Often endogenous origin
  • Foreign body usually present (e.g. stitches, implant, splinter, dirt)
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7
Q

Cellulitis

A
  • 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
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8
Q

Bacteraemia, Septicaemia

A
  • Bacteraemia: bacteria in blood
  • Septicaemia: infection in blood
  • Often from infected wound
  • Growth at site
  • Movement into blood
  • Toxin produced
  • 80% mortality if untreated
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9
Q

Osteomyelitis

A

Bone infection

Due to:

  • Bacteraemia
  • Adjacent skin infection
  • Bone surgery
  • Bone trauma
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10
Q

Endocarditis

A
  • Infection of endocardium (inner lining of heart muscle and valves)
  • Due to bacteraemia
  • Fatal if untreated
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11
Q

Septic arthritis

A
  • Infection within joint
  • From joint wounds, surgery, injections, or bacteraemia
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12
Q

Pneumonia

A

• 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

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13
Q

Food poisoning

A
  • Severe vomiting, diarrhoea, abdominal pail
  • Self limiting
  • Highly handled meats, dairy and bakery products, salads
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14
Q

What are the stages of infection?

A
  1. Bacteria from food handler introduced into food
  2. Temperature abused storage
  3. Bacteria growth, release toxin
  4. After eating: toxin survives in GIT passage, bacteria do not.
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15
Q

How do you identify streptococci?

A
  • 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
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16
Q

What are the virulence factors of streptococcus aureus?

A
  • 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
17
Q

What are the S. aureus reservoirs?

A

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

18
Q

How is s. aureus transmitted?

A
  • Normally on skin or fomites
  • Survival for months on dry surfaces
19
Q

How are s. aureus infections prevented?

A

• 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
20
Q

Can we become immune to s. aureus?

A

No immunity
• Chronic colonization by one strain
• Repeated colonisation by the same strain
• Repeated infections by the same strain

21
Q

What are other staphyloccus species?

A
  • S. epidermidis
  • S. lugdunensis
  • S. haemolyticus
  • S. saprophyticus
22
Q

‘Coagulase-Negative Staphylococci’ (Aka CoNS)

A

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
23
Q

What are the virulent factors of Staphlococcus spp?

A
  • Relatively avirulent
  • Dessication tolerance
  • Slime layer: biofilm formation
  • Adherence to foreign bodies
  • Phagocytosis protection
  • Antibiotic protection

• Antibiotic resistance (like S. aureus)

24
Q

What is the transmission and reservoir of staphlococcus spp.

A
  • Most common NF on skin
  • Also much on mucosal surface
  • Skin-skin, skin-fomite spread
  • Self infections common
25
Q

How is staphlococcus spp. treated?

A

• Antibiotic resistance similar to S. aureus, so treated similarly

CAM101 Microbiology (5 decks)

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