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21 Cards in this Set

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General Staph facts:
S. aureus and S. epidermidis = major cause of hospital related bacteremias in US

Nosocomial infections often due to intravenous catheters or other prosthetic devices

Some staph have become multiply resistant - up to 60% res to methicillin - Vancomycin may be last resort yet vanco res is reported

Morbidity and mortality remains high AND economic costs of nosocomial infections is high
Staph characteristics:
G+ cocci, grape-like clusters

Facultative Anaerobes

Coagulase = some +, some -, enzyme, clots human or rabbit plasma by activating fibrinogen.
(+ = aureus, - = epidermidis, saprophyticus, hemolyticus, hominis)

Catalase: all +, converts H2O2 -> H2O and O2 (Strep is catalase -)
3 main staph species:

comparison:
colony, catalase, coagulase, mannitol ferm, DNase, hemolysis, novobiocin resistance, anaerobic growth, protein A, teichoic acid, phage receptor
ALL - Gram + clusters

S. aureus: yellow colonies, mannitol ferm +, DNase +, hemolysis +, novobiocin resistance -, anaerobic growth +, coagulase +
Protein A +, teichoic acid +, phage receptor + (USEFUL TO TYPE S. AUREUS INFECT!)

S. epidermidis: white colonies, coag -, mannitol ferm -, DNase -, hemolysis -, novobiocin resistance -, anaerobic growth +
Protein A -, teichoic acid + (different type), phage receptor -

S. saprophyticus: white colonies, coag -, mannitol ferm -, DNase -, hemolysis -, novobiocin resistance +, anaerobic growth SLOWLY
Protein A -, teichoic acid + (different type), phage receptor -
S. aureus:
where
nosocomial
tracing methods in outbreak
normal - found on skin, mucous memb and nares (30-40% colonization - higher in diabetics and drug addicts)

nosocomial infections more common in compromised pt's with foreign bodies (dialysis or IV catheters)

Trace by
1) serological
2) phage typing (sensitivity patterns to different bacterial phages)
3) DNA fingerprint
4) Ribotype (specific ribosomal RNA sequence)
5) Compare sequence of selected genes (ex protein A and coagulase)
S. aureus:
Pathogenesis of
1) toxin mediated disease
2) invasive disease
Toxin-mediated:

a) contamination with toxin (ex food or tampon)
Enterotoxins cause food borne diarrhea

b) colonization with toxin production in host
Colonization - specific receptor-ligand interaction (ex - S. aureus fibrinogen and fibrin receptors)
Toxin production -> toxic shock toxin (TSS) or efoliatins (scalded-skin syndrome)
S. aureus:
Pathogenesis of
2) invasive disease
Invasive disease:
=adehesins, toxins, evasive factor

S. aureus synth multiple surface adhesive molec. -> bind to host cell matrix esp fibrinogen, fibronectin, collagen, platelets of damaged skin (catheter and wound), disrupted airway epithelium, endothelial cells within bloodstream -> bact colonize, evade host -> synth toxins and enzymes -> spread to other infection sites (almost any organs accessible by blood)
S. aureus:
2) invasive disease
a) toxins and enzymes
b) blunting or evasion of host immune response
Toxins and enzymes:
1) alpha toxin (hemolysin) - lyse host cell memb
2) leukocidins - lysis of leukocytes
3) proteases - breakdown host proteins (@ least 3 kinds)
4) coagulase - clots human plasma
5) staphylokinase - blood clot lysis or fibrinolysis
6) hyaluronidase - dissolve hyaluronic acid - host cell matrix component
7) lipase - dissolve lipids and lipoproteins

evasion/blunting
1) Protein A - cell wall protein, B cell superantigen (leads to overproduction of specific IgM)has Fc receptor to bind host IgG -> "binding on the wrong end" -> less complement-med killing
2) Enterotoxins A-E, G, H, I: T-cell superantigens (reacts with cell outside of Ag recognition site), blunt a specific T cell response
3) capsule polysaccharides: antiphagocytic
4) Eap (Map): surface protein, impairs PMN recruitment
S. aureus:
consequences of infection
1) If host immune response contains inflamm and enzymatic actions via Ab, PMNs and macrophages -> infect remains localized (ex abscess)

2) Infection not contained -> invasion into blood -> blood-borne infection -> virtually any organ can be infected

(liver, spleen, lung, heart, kidney, skin, bone, meninges, brain)
S. aureus Clinical Syndromes:

Toxin Mediated:
Food Poisoning
Food Poisoning = common cause of diarrheal outbreaks
-from heat stabile (resist boiling) enterotoxins A-E, G, H, I
(F is TSST-1)
- not all strains produce all enterotoxins, many are superantigens -> stimulate lots of IL-1, IL-2 and TNF
-Clinical syndromes = nausea, vomiting, non-bloody diarrhea (all from superAg effect)
S. aureus Clinical Syndromes:

Toxin Mediated:
Toxic Shock Syndrome
TSS:
-caused by TSST-1 (enterotoxin F) commonly assoc with tampons and pt's with wound infections or nasal packing
- TSST-1 = a superAg (stim IL1 , 2 and TNF
-Clinical Syndrome = fever, rash -> desquamation of palms and soles -> may develop hypotensive shock (5-12% pts)
S. aureus Clinical Syndromes:

Toxin Mediated:
Staphylococcal Scalded Skin Syndrome
SSSS:
- caused by EXFOLIATINS A and B = EtaA and EtaB
- Eta genes encoded in Plasmids!
- EtaA and B secreted by specific S. aureus phage group II
- unknown whether it's a superAg
- Exfoliation site may not be same as site of toxin production
- Usually occurs in INFANTS
- Clinical Syndrome - Erythematous (red, swollen) skin -> exfoliation
- Histology: superficial dermis detaches from underlying epidermis in response to toxin

** By the time these syndromes develop, Antibiotics are often not useful! (because they are mediated by superAg effect of toxins)
S. aureus Clinical Syndromes:

Invasive diseases:
Superficial
General - characterized by suppuration and abscess formation

Superficial:
- impetigo (red, vascular skin lesions)
-Folliculitis (hair follicle infection - hydradenitis suppurtive = follic. of armpit)
- Furuncles (skin boils)
- Carbuncles (larger boils)
- Cellulitis (spreading superficial infection)
- Lymphangitis
- Wound Infections (postsurgical)
- Catheter site infections (nosocomial)
- Paronychia (nail bed infect)
- Postpartum breast infect/Mastitis
S. aureus Clinical Syndromes:

Invasive diseases:
Deep seated
-Pneumonia (nosocomial or post-op)
- endocarditis (drug addict, congenital, or prosthetic heart valve problems)
- osteomyelitis (traumatic or hematogenous)
- arthritis (hematogenous, esp in children)
- abscess (liver, spleen, kidney, brain)
- meningitis (hematogenous or traumatic)
- sepsis (originate from localized lesions ex wound, catheter site or drug abuse)
S. aureus:

Treatment:
- Abscesses must be drained surgically

- S. aureus synthesizes penicillinase and are resistant to regular penicillin, but not synthetic -> therefore use Semisynthetic penicillin (doxacillin - oral, oxacillin - intravenous)

-Synthetic penicillin resistant S. aureus -> use vancomycin as last resort, some methicillin resistant strains are already resistant to vanco, so use it discriminately!

-Some S. aureus tolerant, are inhibited but not killed (high MBC/MIC ratio) -> consider combo with rifampin or gentamicin
S. aureus:

Prevention:
- Hospital personnel hand washing and isolation technique
- Judicious use of antibiotics to minimize resistance development
- Intranasal mupirocin to prevent nasal colonization
S. epidermidis:

Location
Susceptible population
- normal skin flora
- opportunistic
- especially colonizes foreign bodies (IV cath, dialysis cath, pacemakers, prosthetic heart valve and joints, sythetic vascular grafts)

- neonates, renal failure or immunocompromised patients
S. epidermidis:

Pathogenesis:
colonize prosthetic valves -> proliferate and invade blood stream (slower than S. aureus) -> surface carb mediates attach to synthetic surfaces -> form biofilms (surface carbs mediate intercell adherence and carb matrix)
*Mechanism of invasion poorly understood
S. epidermidis:

Clinical Syndromes:
- less toxic than S. aureus, may be indolent/slow
- infected prosthetic devices -> low grade fever, pain, discomfort
- bacteremia (pts don't look as toxic as with S. aureus)
- If culture shows + S. epidermidis but patient is fine, it may be a contaminated culture, and uninfected patient
S. epidermidis:

Treatment:
Remove prosthetic devices (if you can)

Resistant to semisynthetic penicillin, so treat with Vancomycin

Consider combining with rifampin or gentamicin if toxic
S. saprophyticus:

Location
Causes what?
skin commensal

common cause of UTI (secondary to E. coli among young women)
S. saprophyticus:

Clinical syndrome
Treatment
UTI with polyuria and dysuria

Treat with
- Bactrim (trimethoprim sulfamethoxazol
- Quinolone (norfloxacin)
*Drug penetration to bladder usually v. good