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What are the general features of staphylococci? (shape, gram, aeration, biochemical, etc)
- gram positive
- fastidious (require AA and other growth factors)
- facultative anaerobe
- produce catalase (distinguishes them from streptococci)
- MOST secrete coagulase (causes plasma to clot) - S. epidermidis and S. saprophyticus do not
What is generally required for a S. aureus infection?
- significant host compromise such as...
- break in the skin
- insertion of foreign subject (surgical infection, central venous catheters)
- compromised immunity
What are the virulence factors for S. aureus? (no detail, just list)
- Cell wall virulence factors: protein A, Fibronectin-binding protein
- Cytolytic exotoxins
- Superantigen exotoxins: enterotoxins, toxic shock syndrome toxin, exfoliatin
Describe the cell wall virulence factors of S. aureus in detail (type, function)
- Protein A: major cell-wall component which binds to the Fc of IgG, exerting an anti-opsonin effect
- Fibronectin-binding protein (Fbp): promotes binding to mucosal cells and tissue matrices
Describe the cytolytic exotoxins of S. aureus in detail (type, function)
- hemolysins: α,β,γ, and δ toxins
- attack mammalian cell membranes (including RBC) resulting in osmotic lysis (frequently β hemolytic)
Describe the Superantigenic exotoxins of S. aureus in detail (type, function)
- Bind to TCR-MHC class II antigen complex and stimulate enhanced response, releasing a large amount of T cell cytokines and causing toxic shock syndrome
- Enterotoxins (A,B,C,D,E, and G): secreted into contaminated food
- B is most commonly associated with food poisoning
- cause inflammation of the intestinal tract lining (gastroenteritis)
- cooking may destroy the bacteria, but the endotoxin is resistant to heat and freezing
- Toxic shock syndrome toxin (TSST-1): classic cause of TSS
- AKA staphylococcal enterotoxin F (SEF)
- Exfoliatin (ET): causes scalded skin syndrome in children
What are the two effects of a superantigen on the host?
- Systemic toxicity: excess IFN-γ -> excessive activation of macrophages -> systemic release of inflammatory cytokines -> shock
- Suppression of adaptive immunity: non-specific activation of T-cells are "held hostage" and unable to target antigens with high specificity
What are the common localized skin infections caused by S. aureus with description?
- small, superficial abscesses involving hair follicles (folliculitis), sweat, or sebaceous glands
- sty: infection of an eyelash follicle
- furnucles: subcutaneous abscesses that form around foreign bodies like splinters
- carbuncles: larger, deeper infections that can lead to bacteremia and require antibiotics
- impetigo: localized, superficial, crusty skin lesion generally seen in children (more commonly caused by (Streptococcus pyogenes)
What are the potential infections that can result from S. aureus w/ examples if necessary, but no description?
- Localized skin infections (sty, furuncles, carbuncles, impetigo)
- Deep, localized infections (bone marrow infection)
- Acute endocarditis
- Septicemia (septic arthritis)
- Nosocomial infections
- Toxinoses (toxic shock syndrome, staphylococcal gastroenteritis, scalded skin syndrome)
What are the common Toxinoses caused by S. aureus with description?
- Toxic shock syndrome: results in high fever, desquamation, rash, vomiting, diarrhea, and hypotension
- Staphylococcal gastroenteritis: results in nausea, vomiting, diarrhea following <6hr incubation period
- triggered by actions of enterotoxin, not infection
- Scalded skin syndrome: superficial bullae (large blisters)
- caused by exfoliative toxin attacking intercellular adhesive of stratum granulosum
What can result from bacteremia with S. aureus?
- internal abcesses
- skin lesion
- infections in lung, kidney, heart, skeletal muscle, or meninges
What are the characteristics of S. aureus used for laboratory identification?
- microscopic and colony morphology (round and clustered)
- catalase positivity
- gram positivity
- coagulase and mannitol positivity distinguish S. aureus from other staphylococci
- colonies tend to be yellow and hemolytic (compared to grey and non-hemolytic of coagulase-negative staphylococci)
What antibiotics are used to treat S. aureus?
- Nearly all S. aureus is resistant to penicillin G
- this was replaced by methicillin and oxacillin
- MRSA has resulted from methicillin use
- Vancomycin was used on these strains, and resistance is now being seen
How is antibiotic resistance conferred to MRSA?
- chromosomal acquisition of the gene for a modified penicillin-binding protein PBP-2a which has a low affinity for currently available β lactam antibiotics
- *β lactam antibiotics work by having a higher affinity for the cross-linking transpeptidases than peptidoglycan
How does CA-MRSA differ from MRSA?
- MRSA implies hospital-aquired
- CA-MRSA tends to be less virulent than MRSA
- CA-MRSA is sensitive to many antibiotics which are useless against MRSA
What prevention methods are used to prevent S. aureus infections?
- No effective vaccine
- Barrier precautions, disinfection of hands and fomites are necessary for control of nosocomial infections
How can S. epidermidis and S. saprophyticus be distinguished from S. aureus?
They are coagulase negative
Give important information about S. epidermidis
- Present in large numbers as part of normal skin flora
- Common cause of infection of implants (heart valves, catheters)
- Acquired drug resistance is more frequent than S. aureus
- In general still vancomycin sensitive
Give important information about S. saprophyticus
- Part of normal vaginal flora
- Frequent cause of cystitis in women
- Sensitive to most antibiotics, even Penecillin G
- Natural resistance to novobiocin (distinguishes it from other coagulase-negative staphylococci)