Staphylococcus Flashcards
Staphylococcus aureus - species
- Genus Staphylococcus
- Gram + clusters
- aerobic
- coagulase +
- growth on mannitol salt agar
- fibronectin-binding proteins (FnBPs) on peptidoglycan cell wall
-Protein A
Staphylococcus aureus - Protein A
The peptidoglycan of the cell wall is overlaid with surface proteins. These include fibronectin-binding proteins (FnBPs) and one called protein A which binds to the Fc portion of IgG molecules and is able to stimulate cytokines, and B cells.
Staphylococcus aureus Exotoxins
•Alpha-toxin
- Protein secreted by almost all S. aureus strains but not by CoNS.
- Pore-forming by direct insertion into the lipid bilayer to form transmembrane pores.
- Action is similar to streptolysin O, complement, and the effector proteins of cytotoxic T lymphocytes.
- Another pore-forming toxin is a leukocidin (PV leukocidin) which lyses neutrophils. It is typically present in a minority of clinical isolates (<10%).
- Exfoliatin
-Causes intercellular splitting of the epidermis between the strratum spinosum and stratum granulosum by disruption of intercellular junctions.
Staphylococcus aureus Staphylococcal Superantigen Toxins (StaphSAgs)
•systemic
Staphylococcal Enterotoxins
- Stimulate gastrointestinal symptoms (primarily vomiting) in humans and animals
- Once formed, these toxins are stable, retaining activity even after boiling or exposure to gastric and jejunal enzymes.
- In addition to superantigen-mediated actions, act directly on neural receptors in the upper gastrointestinal tract, leading to stimulation of the vomiting center in the brain.
•Toxic Shock Syndrome Toxin (TSST)
- Major cause of staphylococcal toxic shock syndrome •
- In addition to superantigen action has direct toxic effects on endothelial cells leading to capillary leakage, hypotension, and shock.
Staphylococcus aureus Epidemiology
- The most common human habitat is the anterior nares.
- 30% carry the organism and rates among hospital personnel and patients may be much higher.
- Most S. aureus infections are auto-infections due to strains a carrier has shed from their anterior nares.
- Hospital outbreaks are caused by a virulent strain originally carried by the patient or a healthcare worker.
Staphylococcus aureus and Food Poisoning
- Food becomes contaminated with an enterotoxin-producing strain of S. aureus (StaphSAg mediated) by a preparer who is a nasal carrier or has a staphylococcal lesion.
- If food is inadequately refrigerated the staphylococcal multiply and produce enterotoxin in the food.
- Because of the heat resistance of the toxin, its toxicity persists even if the food is cooked before eating.
Staphylococcus aureus Primary Infection
- S. aureus is generally of low infectivity unless trauma, foreign matter, or other local conditions provide access for initiation of infection.
- The initial stages are mediated by the FnBPs, which bind to the glycoprotein fibronectin on epithelial cell surfaces.
- Protein A may aid in the initial stages by binding IgG
- This allows S. aureus to persist and to produce alpha-toxin and other cytolysins which injure the cell.
- The inflammatory cells, fibrin, and other tissue components form a wall which becomes the characteristic boil.
- In the skin, spontaneous resolution of the boil by granulation and fibrosis is the rule.
- In the lung, kidney, bone, and other organs the process may continue including spread to the bloodstream and distant organs.
The initial stages are mediated by the [], which bind to the glycoprotein fibronectin on epithelial cell surfaces. [] may aid in the initial stages by binding IgG.
The initial stages are mediated by the FnBPs, which bind to the glycoprotein fibronectin on epithelial cell surfaces. Protein A may aid in the initial stages by binding IgG
Initial attachment to fibronectin is mediated by fibronectin-binding proteins (FnBP), and the major injury is caused by the pore-forming [].
Initial attachment to fibronectin is mediated by fibronectin-binding proteins (FnBP), and the major injury is caused by the pore-forming α-toxin.
What if the strain of S. aureus also produces exfoliatin?
- If the strain of S. aureus causing any of the effects described above also produces one or more of the exotoxins those actions will be added to those of the primary infection. The primary infection serves as a site for absorption of the toxin and need not be extensive or even clinically noticeable for the toxin action to take place.
- Exfoliatin toxin-producing strains cause blister-like separation of the epidermis.
What if the strain of S. aureus also produces Toxic Shock Syndrome Toxin?
- If the strain of S. aureus causing any of the effects described above also produces one or more of the exotoxins those actions will be added to those of the primary infection. The primary infection serves as a site for absorption of the toxin and need not be extensive or even clinically noticeable for the toxin action to take place.
- In staphylococcal toxic shock syndrome (TSS) the StaphSAg is produced during the course of infection at any of multiple sites. Menstruation-associated TSS requires a combination of improbable events.
- Less than 5% of women carry S. aureus in their vaginal flora, and only some of these (~10%) produce TSST-1.
- Menstruation and high-absorbency tampon usage provide growth conditions that enhance the production of TSST-1.
- Toxin absorbed from the vagina can then circulate to produce superantigen-mediated TSS.
-SS. ayreus itself usuallly not in blood
- fever, diarrhea, shock, renal failure
- Some cases of TSS (non menstrual) are associated with StaphSAgs other than TSST-1.
S. aureus Clinical Manifestations in Primary Infection - Furuncle or Boil
- Furuncle or Boil
- A superficial skin infection that develops in a hair follicle, sebaceous gland, or sweat gland.
- Infection can spread from a furuncle with the development of one or more abscesses in adjacent subcutaneous tissues.
- May result in bloodstream invasion
S. aureus Clinical Manifestations in Primary Infection - Impetigo
- Most often a secondary invader in group A streptococcal pustular impetigo
- Can produce the skin pustules of impetigo on its own. Strains that produce exfoliatin cause bullous impetigo, characterized by blisters
S. aureus Clinical Manifestations in Primary Infection - Deep Lesions
- S. aureus can cause a wide variety of infections of deep tissues, by bacteremic spread from a skin lesion that may be unnoticed. These include infections of bones, joints, deep organs, and soft tissues including surgical wounds.
- Most of cases of acute osteomyelitis are caused by S. aureus.
S. aureus Treatment
- S. aureus can cause a wide variety of infections of deep tissues, by bacteremic spread from a skin lesion that may be unnoticed. These include infections of bones, joints, deep organs, and soft tissues including surgical wounds. • Most of cases of acute osteomyelitis are caused by S. aureus.
- Penicillin G is still effective for susceptible strains but no longer used due to the high frequency of penicillinase-mediated resistance
- Penicillinase-resistant penicillins (methicillin, dicloxacillin) and first generation cephalosporins are commonly used.
- For methicillin-resistant (MRSA) strains vancomycin and daptomycin are used for deep seated infections.
-Clindamycin and doxycycline are alternatives for superficial infections.
