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What are the general features of staphylococci? (shape, gram, aeration, biochemical, etc)
- Round
- 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
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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
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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
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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
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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)
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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
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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
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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)
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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)
- Pneumonia
- Nosocomial infections
- Toxinoses (toxic shock syndrome, staphylococcal gastroenteritis, scalded skin syndrome)
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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
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What can result from bacteremia with S. aureus?
- internal abcesses
- skin lesion
- infections in lung, kidney, heart, skeletal muscle, or meninges
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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)
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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
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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
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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
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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
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How can S. epidermidis and S. saprophyticus be distinguished from S. aureus?
They are coagulase negative
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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
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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)
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