Staphylococcus aureus: Difference between revisions

From IDWiki
Staphylococcus aureus
(→)
(→)
 
(8 intermediate revisions by the same user not shown)
Line 1: Line 1:
== Background ==
==Background==
=== Microbiology ===
===Microbiology===
* Facultative anaerobic, [[Has Gram stain::Gram-positive]] coccus
* [[Has catalase test::Catalase-positive]] and [[Has coagulase test::coagulase-positive]]
* Microscopy: groups or clusters ("cluster of grapes")
* Colony morphology: large, round, golden yellow colonies, often hemolytic on blood agar


*Facultative anaerobic, [[Stain::Gram-positive]] [[Shape::coccus]]
=== Pathophysiology ===
*Catalase-[[Catalase::positive]] and coagulase-[[Coagulase::positive]]
==== Virulence factors ====
*Microscopy: groups or clusters ("cluster of grapes")
* Surface proteins for fibrinogen and other substances (used for binding to host endothelial cells)
*Colony morphology: large, round, golden yellow colonies, often hemolytic on blood agar
* 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


===Pathophysiology===
==== Antibiotic resistance ====
====Virulence Factors====
* Mechanisms of resistance are myriad
* Two common ones:
** ''bla'' gene encodes penicillinase, conferring resistance to penicillin
** ''mecA'' encodes PBP2a, conferring broad beta-lactam resistance


*Surface proteins for fibrinogen and other substances (used for binding to host endothelial cells)
== Clinical Presentation ==
*Membrane-damaging toxins (hemolysins), including Panton-Valentine leukocidin (PVL)
=== Colonization ===
*Exfoliative toxins (A and B) which disrupt the junction between epidermal cells, causing scalded skin syndrome
* About 20-30% of people carry it in their nares
*Superantigens that bind to MHC molecules and T-cell receptors, leading to release of huge amounts of cytokines
* See [[Staphylococcus aureus decolonization]]
**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====
=== Skin and soft tissue infections ===
* Boils and carbuncles


*Mechanisms of resistance are myriad
=== Scalded-skin syndrome ===
*Common ones:
* Aka Ritter disease
**''bla'' gene encodes penicillinase, conferring resistance to penicillin
* Caused by exfoliative toxin A or B
**''mecA'' encodes PBP2a, conferring broad β-lactam resistance (MRSA)
* Essentially bullous impetigo
**''vanA'' on a plasmid confers [[vancomycin]] resistance (VRSA)
* Sunburn-like, bullous rash that can lead to skin loss (most common in kids with Staph infections of the nasopharynx or skin)


==Clinical Manifestations==
=== Bacteremia ===
===Colonization===
* See [[Staphylococcus aureus bacteremia]]


*About 20-30% of people carry it in their nares
=== Infective endocarditis ===
*See [[Staphylococcus aureus decolonization]]
* Usually more acute presentation
* High mortality
* See [[Staphylococcus aureus endocarditis]]


=== Myriad other infections ===
===Skin and Soft Tissue Infections===
* Osteomyelitis
* Native and prosthetic joint infections
* Pyomyositis
* Deep organ abscesses
* Surgical site infections
* Pneumonia, especially ventilator-associated or influenza-related


*Boils and carbuncles
=== Superantigen-related syndromes ===
*Cellulitis, usually purulent
* 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


===Scalded-Skin Syndrome===
== Management ==
* Duration depends on clinical syndrome


*Aka Ritter disease
=== Methicillin-susceptible ''Staphylococcus aureus'' (MSSA) ===
*Caused by exfoliative toxin A or B
* First-line: [[cloxacillin]], then [[cefazolin]] or [[cephalexin]] (for oral)
*Essentially bullous impetigo
* Others: [[clindamycin]], [[fluoroquinolones]], [[TMP-SMX]], [[doxyxycline]], [[erythromycin]]
*Sunburn-like, bullous rash that can lead to skin loss (most common in kids with Staph infections of the nasopharynx or skin)


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

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

===Infective Endocarditis===

*Usually more acute presentation
*High mortality
*See [[Staphylococcus aureus endocarditis]]

===Other Infectious Syndromes===

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

===Superantigen-Related Syndromes===

*[[Food poisoning]]
*[[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 ===

* Occurs ''during'' acute infection
* See also [[Staphylococcus-associated glomerulonephritis]]

==Management==

*Duration depends on clinical syndrome

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

*First-line: [[cloxacillin]], then [[cefazolin]] or [[cephalexin]] (for oral)
*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)

Retrieved from "https://idwiki.org/index.php?title=Staphylococcus_aureus&oldid=7584"
Powered by MediaWiki
Powered by Semantic MediaWiki