Staphylococcus aureus: Difference between revisions

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Staphylococcus aureus
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== Microbiology ==
== Background ==
=== Microbiology ===

* Facultative anaerobic, [[Has Gram stain::Gram-positive]] coccus
* Facultative anaerobic, [[Has Gram stain::Gram-positive]] coccus
* Catalase and coagulase positive
* Catalase and coagulase positive
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* Colony morphology: large, round, golden yellow colonies, often hemolytic on blood agar
* Colony morphology: large, round, golden yellow colonies, often hemolytic on blood agar


== Pathophysiology ==
=== Pathophysiology ===
==== Virulence factors ====

=== Virulence factors ===

* Surface proteins for fibrinogen and other substances (used for binding to host endothelial cells)
* Surface proteins for fibrinogen and other substances (used for binding to host endothelial cells)
* Membrane-damaging toxins (hemolysins), including Panton-Valentine leukocidin (PVL)
* Membrane-damaging toxins (hemolysins), including Panton-Valentine leukocidin (PVL)
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** Exotoxins B and C cause [[TSS|Staphylococcal toxic shock syndrome]] and also food poisoning
** Exotoxins B and C cause [[TSS|Staphylococcal toxic shock syndrome]] and also food poisoning


=== Antibiotic resistance ===
==== Antibiotic resistance ====

* Mechanisms of resistance are myriad
* Mechanisms of resistance are myriad
* Two common ones:
* Two common ones:
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== Clinical Presentation ==
== Clinical Presentation ==

=== Colonization ===
=== Colonization ===

* About 20-30% of people carry it in their nares
* About 20-30% of people carry it in their nares
* See [[Staphylococcus aureus decolonization]]
* See [[Staphylococcus aureus decolonization]]


=== Skin and soft tissue infections ===
=== Skin and soft tissue infections ===

* Boils and carbuncles
* Boils and carbuncles


=== Scalded-skin syndrome ===
=== Scalded-skin syndrome ===

* Aka Ritter disease
* Aka Ritter disease
* Caused by exfoliative toxin A or B
* Caused by exfoliative toxin A or B
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=== Bacteremia ===
=== Bacteremia ===

* See [[Staphylococcus aureus bacteremia]]
* See [[Staphylococcus aureus bacteremia]]


=== Infective endocarditis ===
=== Infective endocarditis ===

* Usually more acute presentation
* Usually more acute presentation
* High mortality
* High mortality
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=== Myriad other infections ===
=== Myriad other infections ===

* Osteomyelitis
* Osteomyelitis
* Native and prosthetic joint infections
* Native and prosthetic joint infections
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=== Superantigen-related syndromes ===
=== Superantigen-related syndromes ===

* Food poisoning
* Food poisoning
* [[Staphylococcal toxic shock syndrome]]
* [[Staphylococcal toxic shock syndrome]]
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== Management ==
== Management ==

* Duration depends on clinical syndrome
* Duration depends on clinical syndrome


=== Methicillin-susceptible ''Staphylococcus aureus'' (MSSA) ===
=== Methicillin-susceptible ''Staphylococcus aureus'' (MSSA) ===

* First-line: [[cloxacillin]], then [[cefazolin]] or [[cephalexin]] (for oral)
* First-line: [[cloxacillin]], then [[cefazolin]] or [[cephalexin]] (for oral)
* Others: [[clindamycin]], [[fluoroquinolones]], [[TMP-SMX]], [[doxyxycline]], [[erythromycin]]
* Others: [[clindamycin]], [[fluoroquinolones]], [[TMP-SMX]], [[doxyxycline]], [[erythromycin]]


=== Methicillin-resistant ''Staphylococcus aureus'' (MRSA) ===
=== Methicillin-resistant ''Staphylococcus aureus'' (MRSA) ===

* First-line: [[vancomycin]]
* First-line: [[vancomycin]]
* Others: [[linezolid]] (if lungs) and [[daptomycin]] (if blood), but also consider [[TMP-SMX]], [[ciprofloxacin]], [[doxycycline]], and [[clindamycin]]
* Others: [[linezolid]] (if lungs) and [[daptomycin]] (if blood), but also consider [[TMP-SMX]], [[ciprofloxacin]], [[doxycycline]], and [[clindamycin]]

Revision as of 13:21, 10 November 2019

Background

Microbiology

  • Facultative anaerobic, Gram-positive coccus
  • Catalase and coagulase positive
  • Microscopy: groups or clusters ("cluster of grapes")
  • Colony morphology: large, round, golden yellow colonies, often hemolytic on blood agar

Pathophysiology

Virulence factors

  • Surface proteins for fibrinogen and other substances (used for binding to host endothelial cells)
  • Membrane-damaging toxins (hemolysins), including Panton-Valentine leukocidin (PVL)
  • Exfoliative toxins (A and B) which disrupt the junction between epidermal cells, causing scalded skin syndrome
  • Superantigens that bind to MHC molecules and T-cell receptors, leading to release of huge amounts of cytokines

Antibiotic resistance

  • Mechanisms of resistance are myriad
  • Two common ones:
    • bla gene encodes penicillinase, conferring resistance to penicillin
    • mecA encodes PBP2a, conferring broad beta-lactam resistance

Clinical Presentation

Colonization

Skin and soft tissue infections

  • Boils and carbuncles

Scalded-skin syndrome

  • Aka Ritter disease
  • Caused by exfoliative toxin A or B
  • Essentially bullous impetigo
  • Sunburn-like, bullous rash that can lead to skin loss (most common in kids with Staph infections of the nasopharynx or skin)

Bacteremia

Infective endocarditis

Myriad other infections

  • Osteomyelitis
  • Native and prosthetic joint infections
  • Pyomyositis
  • Deep organ abscesses
  • Surgical site infections
  • Pneumonia, especially ventilator-associated or influenza-related

Superantigen-related syndromes

  • Food poisoning
  • Staphylococcal toxic shock syndrome
    • Tampon-associated
    • Post-surgical (ENT): more of historic with changes in packing
    • Surgical site infections, even without obvious signs of localized infection

Management

  • Duration depends on clinical syndrome

Methicillin-susceptible Staphylococcus aureus (MSSA)

Methicillin-resistant Staphylococcus aureus (MRSA)