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21 Cards in this Set

  • Front
  • Back
Staphylococci Characteristics
gram positive, non-motile, non spore forming, 0.5-1um diameter

isolates grow in clusters

aerobes or facultative anaerobes

grow best on blood enriched media and are beta-hemolytic

grow at 18-40 C

CAN grow in 10% NaCl

ALL CATALASE +
*S. aureus is COAGULASE +, others negative
3 main pathogens of Staph
S. aureus = most virulent
*in nares, skin, vagina
*golden colonies

S. epidermidis = foreign body
*normal flora of skin and
mucus membranes

S. saprophyticus = UTI
*genitourinary skin
Staph Diseases
S. aureus
1. skin/soft tissue infection
*furuncle (boil) =
follicultilis or
sebaceous gland infection
very painful, drain,
antibiotics
*carbuncle = deep seated
infection of several hair
follicles, spread into
inelastic tissue of neck,
results in- fever,
bacteremia, leukocytosis,
severe pain
treat via systematic ab
2. bone/joint infection
3. bacteremia, endocarditis
4. toxin mediated disease,
food poisoning, toxic
shock
5. necrotizing pneumonia

S. epidermidis
1. opportunistic infections
of catheters, shunts,
prosthetic devices,
surgical wounds,
bactermia, and
endocarditis

S. saprophyticus
*community acquired UTI
Staph Cell Wall Virulence Determinants
1. capsule- inhibits phagocytosis, chemotaxis, proliferation of mononuclear cells

2. peptidoglycan- 50% of cell wall weight, endotoxin like activity, activates complement and attracts neutrophils

3. protein A- inhibits Ab mediated clearance by binding Fc terminal of most IgG (anti-inflammatory)
Staph Cell Enzymes as Virulence Determinants
1. catalase- neutralizes oxidative burst of phagocytes

2. coagulase- converts fibrinogen to fibrin by binding prothrombin
*promotes clots w/aids in a
place to hide from immune
response

3. fibrinolysin

4. hyaluronidase

5. lipases/nucleases
Toxins as Virulence Determinants
1. cytotoxins alpha, beta, gamma, and delta = toxic to leukocytes, RBCs, macrophages, platelets, and fibroblasts

2. ***exofoliative toxins- serine proteases act on stratum granulosum of epidermis

3. panton-valentine leukocidin - damages neutrophils via membrane pore formation
Toxins as Superantigens

(S. aureus and GAS have these)

*antigen binds to MHC II, activate T cell and bind to invariant region- stimulate massive cytokine production by CD4+ cells
1. enterotoxins B,C = release inflammatory mediators in gut = increased peristalsis and CNS effect contributes to puking
*food poisoning
*staph toxic shock syndrome

2. TSST-1, generalized inflammatory mediator
*staph toxic shock syndrome
Staphylococcal Scalded Skin Syndrome

(exfoliative toxin at work)
infants w/sudden onset of skin tenderness and eruptions

NIKOLSKY'S SIGN = gentle lateral pressure displaces normal skin into bullae

manage fluids/electrolytes

treat via systemic ab
Toxic Shock Syndrome
rapid, fever, hypotension, sunburn rash w/desquamates

1. menstrual TSS
*s. aureus producing TSST-1

2. nonmenstrual TSS
*wound associated (adult) or suppurative (child)
*s. aureus, TSST-1 and toxin B and C
*GAS - strep pyrogenic exotoxin
TSS treatment/prevention
staph =bactermia, rash is less than strep

vanco + clindamycin to inhibit

recurrences are seen w/menstrual cases- due to failure to produce ab to TSST-1
Staphylococcal Food Poisoning
vomiting onset 1-6 hrs
*custard, canned food,
potato salad, ice cream

pre-formed enterotoxin in food

no antibiotics- fluid as necessary
Bone/Joint Infections
S. aureus leading cause

empiric therapy must cover STAPH
Pelvic Syndrome
Bone/Joint Infection
Septic Thrombophlebitis
Septic emboli to lungs
Osteomyelitis
kids- long bones

nasal/skin colonizations = transient bacteremia w/minor trauma

acute onset of fever, pain, refusal to bear weight or other functional limitation

dx: x-ray, bone scan, blood and bone cultures

tx: empiric: IV than PO ab
*ESR and CRP used as guide
Cystic Fibrosis
most common CF infection : Pseudomonas aeruginosa
MRSA
pencillinase producing s. aureus has second alteration and becomes PBP2a-producing S. aureus
CA-MRSA
USA300 clone- 98% carry Panton-Valentine leukocidin
(direct toxin of neutrophils and epithelial cells)

skin decolonization by weekly bleach or chlorhexidane baths to rid in community or nares decolonization by mupirocin (bactroban) or retapamulin (altebax)
S. saprophyticus
CA-UTI in young women
*distant #2 behind E. coli

greater adhererance to urinary epithelium

no virulence factors shared with s. aureus- does express urease (degrades urea to NH4 for growth)
S. epidermidis
adheres to foreign bodies
*associated w/indwelling catheters, prosthetic devices

hard to eradicate

antibiotic resistance...treat with vanco
Infective Endocarditis

(path: deposition of platelets, thrombin...vegetations)
pre-existing valvular abnormality are targetted

freq of valves involved: MV > AV > MV + AV > TV >> PV
Endocarditis

(right sided w/ IVDU)

(need 3 independent blood samples which are negative after seven days of incubation)
causative mo:

GRAM +
1. S. aureus
*prosthetic valve - early
*acute - janeway lesion on skin and spots in eyes
2. Viridans streptococci
*subacute (glomerulonephritis)
3. S. epidermidis
*prosthetic valve - late
4. Enterococci
*surgery for endocarditis
5. other streptococci

Gram -

1. HACEK organisms

Fungi