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, [[Stain::Gram-positive]] [[Shape::coccus]]
* Catalase and coagulase positive
*Catalase-[[Catalase::positive]] and coagulase-[[Coagulase::positive]]
* Microscopy: groups or clusters ("cluster of grapes")
*Microscopy: groups or clusters ("cluster of grapes")
* 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====


⚫
*Surface proteins for fibrinogen and other substances (used for binding to host endothelial cells)
⚫
=== Virulence factors ===
⚫
*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
⚫
**Toxic shock syndrome toxin 1 (TSST-1) is implicated in [[TSS|Staphylococcal toxic shock syndrome]]
⚫
**Exotoxins B and C cause [[TSS|Staphylococcal toxic shock syndrome]] and also food poisoning


====Antibiotic Resistance====
⚫
* 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
⚫
** Toxic shock syndrome toxin 1 (TSST-1) is implicated in TSS
⚫
** Exotoxins B and C cause TSS and also food poisoning


*Mechanisms of resistance are myriad
⚫
== Clinical Presentation ==
*Common ones:
**''bla'' gene encodes penicillinase, conferring resistance to penicillin
**''mecA'' encodes PBP2a, conferring broad β-lactam resistance (MRSA)
**''vanA'' on a plasmid confers [[vancomycin]] resistance (VRSA)


⚫
==Clinical Manifestations==
=== 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
*Cellulitis, usually purulent


=== 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
* Essentially bullous impetigo
*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)
*Sunburn-like, bullous rash that can lead to skin loss (most common in kids with Staph infections of the nasopharynx or skin)


=== 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
* See [[Staphylococcus aureus endocarditis]]
*See [[Staphylococcus aureus endocarditis]]


===Other Infectious Syndromes===
=== Myriad other infections ===


* Osteomyelitis
*[[Osteomyelitis]]
* Native and prosthetic joint infections
*[[Septic arthritis|Native]] and [[prosthetic joint infection]]
* Pyomyositis
*[[Pyomyositis]]
* Deep organ abscesses
*Deep organ [[abscess]]
* Surgical site infections
*[[Surgical site infection]]
* Pneumonia, especially ventilator-associated or influenza-related
*[[Pneumonia]], especially ventilator-associated or influenza-related


=== Superantigen-related syndromes ===
===Superantigen-Related Syndromes===


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


=== ''Staphylococcus''-Associated Glomerulonephritis ===
⚫
== Management ==


* Occurs ''during'' acute infection
⚫
* Duration depends on clinical syndrome
* See also [[Staphylococcus-associated glomerulonephritis]]


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


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


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


* First-line: [[vancomycin]]
*First-line: [[cloxacillin]], then [[cefazolin]] or [[cephalexin]] (for oral)
* Others: [[linezolid]] (if lungs) and [[daptomycin]] (if blood), but also consider [[TMP-SMX]], [[ciprofloxacin]], [[doxycycline]], and [[clindamycin]]
*Others: [[clindamycin]], [[fluoroquinolones]], [[TMP-SMX]], [[doxyxycline]], [[erythromycin]]

⚫
===Methicillin-Resistant ''Staphylococcus aureus'' (MRSA)===

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


{{DISPLAYTITLE:''Staphylococcus aureus''}}
{{DISPLAYTITLE:''Staphylococcus aureus''}}

Latest revision as of 00:50, 22 February 2021

Background

Microbiology

  • Facultative anaerobic, Gram-positive coccus
  • Catalase-positive 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
  • Common ones:
    • bla gene encodes penicillinase, conferring resistance to penicillin
    • mecA encodes PBP2a, conferring broad β-lactam resistance (MRSA)
    • vanA on a plasmid confers vancomycin resistance (VRSA)

Clinical Manifestations

Colonization

Skin and Soft Tissue Infections

  • Boils and carbuncles
  • Cellulitis, usually purulent

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

Other Infectious Syndromes

Superantigen-Related Syndromes

Staphylococcus-Associated Glomerulonephritis

Management

  • Duration depends on clinical syndrome

Methicillin-Susceptible Staphylococcus aureus (MSSA)

Methicillin-Resistant Staphylococcus aureus (MRSA)

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