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Microbiology 11: Staphylococci -> Abscesses and Toxin-Mediated Diseases
Key Concepts:
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Considered pyogenic (pus) except toxic shock syndrome
Cause furuncles and abscess, food poisoning, toxin-induced diseases, osteomyelitis, kidney
abscess, endocarditis
S. aureus, S. epidermidis, S. saprophyticus (UTIs)
Virulence factors -> S. aureus produces peptidoglycan, teichoic acids, protein A, clumping factor
and other MSCRAMMs, coagulase, hemolysins, exotoxins, some β-lactamase and penicillinbinding protein 2a
Treat with antibiotics, draining, and supportive therapy
S. aureus (Gram + cocci) -> most common pyogenic bacteria, anterior nares, produce focal
abscess, secrete toxins (illness at distant site)
o Toxic shock syndrome (TSS) = from TSS toxin-1 (TSST1) and staph enterotoxin A-T
 Vaginal muscosal and respiratory infections
 Act systemically to interfere with normal immune system function
o Staphylococcal scalded skin syndrome (SSSS) = exfoliative toxin A-B
 In neonates w/ upper resp tract infection
o Staphylococcal food poisoning (SFP) = ingestion of enterotoxin A-E
o Clumping factor (bound coagulase) = binds fibrin, helps protect abscess from
phagocytes
 Distinguished from other species in genus by coagulase test (+)
o Grows in grape-like clusters (hardy), carotenoid pigmentation (golden), + mannitol
fermentation, - novobiocin resistance
S. epidermidis -> found on skin in most, infections in hospitals or with artificial device implants,
white colonies, - mannitol fermentation, - novobiocin resistance
S. saprophyticus -> causes only UTIs, white colonies, - mannitol ferm, + novobiocin resistance
S. lugdunensis -> aggressive endocarditis, white colonies, - mannitol fermentation, - novobiocin
resistance
ID strains with phage typing (pulsed field gel electrophoresis) = isolate DNA, treat with
restriction enzyme, resolve fragments
Cases:
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Abrasion of forearm -> abscess, tenderness over lower spine (osteomyelitis), high WBC, Gram +
cocci (S. aureus), resistant to penicillin but sensitive to nafcillin
o Features typical of S. aureus infection = initial lesion (boil) mild and localized,
osteomyelitis, could have led to endocarditis or kidney/brain abscess
Toxic shock syndrome -> vomiting, fever, diarrhea, sunburnlike rash, hypotension, high WBCs,
reduced platelets
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Prolonged hypotension -> gangrenous toes
Desquamation of skin (peeling) with resolution
S. aureus toxin-mediated disease = initial lesion subcutaneous abscess, minimal
inflammatory features
IV immunoglobulin treats streptococcal and staphylococcal TSS
Staphylococci
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Encounter
o Live on people and inanimate objects
 Grow at high salt and lipid []
 Make lipases and glycerol ester hydrolases (degrade skin lipids)
o Colonize anterior nares in 30% of healthly ppl
o MSCRAMMs (surface protein) binds to ECM proteins
 Fibronection-binding proteins (FnbpA/B) on surface of S. aureus
 Allow invasion of cells and attach to fibronectin on wounds
 CNAs for collagen binding
 Clumping factors A/B -> fibrinogen binding (endocarditis)
o Spread by contact or aerosols (after birth, 2° to influenza or croup, hospital workers,
diabetics, hemodialysis, IV drug abuse)
Entry
o Deep tissue if damaged skin/mucous membrane
o In large numbers can enter spontaneously (poor hygiene, prolonged moisture)
Spread and multiplication
o Depends on # of organisms, site, speed of body response, immune hx of host
Damage
o Local infection = abscess (pus)
 In skin = boils aka furuncles; multiple interconnected = carbuncles
 Acute inflammatory reaction (neutrophil) -> chemotactic factors made -> staph
lyse neutrophils (release lysosomal enzymes damaging surrounding) ->
MSCRAMMs and host response make thick-walled fibrin capsule
 Center necrotic, dead neutrophils/epithelial cells, dead & live bacteria,
edema fluid
 Containment but protected from immune attack -> may be source of
toxins for TSST1 or enterotoxins
o Diffuse inflammation = cellulitis
o Neutrophils important to contain infection
 Chronic granulomatous disease = children defect in phagocyte fxn, frequent
infection with S. aureus, neutrophils unable to make H2O2 to kill
o Virulence factors prevent phagocyte ingestion
 Include soluble enzymes, toxins, cell-envelope constituents
o Defense against neutrophils ->
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Surrounded by capsule (common serotype 5 & 8) and slime layer
Peptidoglycan in cell wall (activates alternative complement path; interacts with
toll-like receptor-2 all for inflamm rxn)
 Teichoic acid (complement activation and adherence to mucosa)
 Protein A binds Fc terminus of IgG (incapacitates and reduces opsonization) and
free antibodies
 Secrete catalase converts H2O2 to H2O, coagulase converts fibrinogen to fibrin
 Pore-forming toxins damage phagocytes and other cells
 α, γ, δ = hemolysins
o β hemolysin = non-pore forming; sphingomyelinase
 γ-toxin and Panton-Valentine leukocidin = damage neutrophils
 Hyaluronidase = hydrolyzes CT matrix
 Virulence enhancers = lipases, proteases, DNases
o Substances difficult to treat with antibiotics = β-lactamase (penicillin resistance) and
penicillin-binding protein 2a (PBP2a) (methicillin resistant)
 SCC mec DNAs code for PBP2a
Usually disease limited by spontaneous drain through skin but if escape from abscess cleared by
blood and lymph (unless impaired host)
o In deep tissues, colonize previously damaged tissues
o Main sites of metastatic abscess = bones, joints, lungs, kidneys
Immunocompromised pts frequently have multiple staph metastases
Osteomyelitis = “boil of a bone”
Damage by Other Species of Staphylococci
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S. epidermidis (coag neg) rarely causes disease -> found in pts with implanted artificial devices
o Can cause septicemia and endocarditis
o Virulence factors = peptidoglycan and slime layer (stick to plastic devices)
S. saprophyticus (coag neg) only UTIs (cystitis in young women)
S. lugdunensis (coag neg) causes aggressive endocarditis
Staphylococcal Toxin Diseases
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Staphylococcal scalded skin syndrome (SSSS) = neonates, extensive sloughing of skin
o Exfoliative toxins A and B cause symptoms -> separate skin layers at desmosomes
Toxic Shock Syndrome (TSS) = fever, skin rash, hypotension, peeling of skin on recovery
o Originally from highly absorbent tampons (intro O2 into vagina for toxin production)
o O2 essential for toxin production
o Exotoxins = toxic shock syndrome toxin-1 (all menstrual cases) and staphylococcal
enterotoxins (B and C)
 Toxins = superantigens -> cross-link β-chain of T-cell antigen receptor with MHC
Class II on macrophage (mass release of cytokines)
 TNFα and TNFβ cause capillary leak (hypotension)
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 INFγ and Interleukin2 cause rash
Food Poisoning = staphylococcal enterotoxins serotypes A – E
o Intensive intestinal peristalsis
o Exotoxins are heat stable, resist proteases
Regulators include accessory gene regulator (Agr) and staphylococcal respiratory response
(Srr)
Diagnosis
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Localized abscess aspirated and gram stained
Also culture blood and use coagulase test
Treatment
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Drain abscess, antibiotic (semisynthetic penicillins for methicillin-sensitive S. aureus, MSSA)
Methicillin-resistant S. aureus (MRSA) treat with vancomycin and fluroroquinolones
Second-line agents = aminoglycosides, macrolides, trimethoprim.sulfamethoxazole, clindamycin,
tetracyclines
o Clindamycin (inhibits protein synthesis) prevents exotoxin synthesis prior to inhibiting
growth
Vancomycin-resistant S.aureus (VRSA) acquired from Enterococcus species in coinfection
o Can use linezolid, Synercid, and daptomycin
For TSS -> IV immunoglobulin (from human volunteers)