causes 80% suppurative infections

2nd leading cause of nosocomial infections

community: 20-50%

healthcare workers: 90%

higher in hemodialysis patients

#1: anterior nares

others: skin, vagina, axilla, perineum, & oropharynx

common transmission of staphylococcus aureus

(epidemiology)

from hands of healthcare provider

patient to patient (hospital setting)

not seasonal (except warm seasons' prevalence for food poisoning)

community: major cause of soft tissue infection

1. structural

2. enzymes

3. toxins

1. capsule (inhibit chemotaxis/phagocytosis; adheres to foreign bodies)

2. peptidoglycan (inhibit phagocytosis; endotoxin-like)

3. teichoic acid (major component of cell wall; mediates attachment to mucosal surface; regulate cationic conc @ cell mem; bind Fn)

4. protein A (bind IgG-Fc frag; inhibit opsonization/complement activation)

bacteria makes genetic changes due to changes in growth density (different growth phases)

*S. Aureus is a classic example 

during initial part of infection, S. aureus growth density is low: bacteria doesn't need to produce toxins, it needs to produce cell surface proteins (ie. Protein A) to establish a colony

*agr locus of S. aureus regulates many of its cell surface proteins (RNA molecule rather than the usual protein gene-expression-regulator)

later on, once the infection is established and the organism needs more room, this feature of the bacteria allows it to produce the toxins against the host => degraded host cells serve as bacterial nutrients (tissue damage/disease)

1. coagulase (fibrinogen --> fibrin)

2. catalase (detoxify h202)

3. hyaluronidase (hydrolyze HAs (major component of host ECM)=spreading factor)

4. lipases (hydrolyze lipids in sebaceous areas of host)

5. nucleases (digest DNA/RNA=spreading factor)

Staphylococcus aureus virulence factor 

(toxins-4)

1. alpha/beta/delta/gamma & leukocidins

(toxic for: leukocytes, RBCs, platelets, macrophages, & fibroblasts)

2. ETA & ETB = serine proteases (digest anchors holding epidermis to dermis)

3. TSST-1 (superantigen; systemic effects)

4. enterotoxins (A-E) (superantigens; stim T cells/cytokine release/inflamm med by mast cells; incr intestinal peristalsis/fluid loss/vomiting)

activate T cell (binds TCR & MHC II on APC) => no antigen needed

*=> excessive T cell #s (up to 20% of total)

*high cytokine #s (IL-1/TNF/IL-2)

=> non-specific immune response (extremely dangerous)

catalase/superoxide dismutase mechanism

(S. aureus virulence factor)

SOD: 02+2H-->02+h202

catalase: h202-->h20+02

*s. aureus breaks down the h202 required by PMN myeloperoxidase to generate more toxic ROIs (to use against bacteria)

=> pts w/ chronic granulomatous disease vulnerable to s. aureus & NOT streptococcal infection because catalase-negative organisms are susceptible to the host immune system's use of h202 produced through the bacteria's metabolic processes

staph infections caused by MRSA (in the US):

1974

1995

2004

1974: 2%

1995: 22%

2004: 63%

1. invasive (cutaneous and non-cutaneous) 

-organism is located w/in the affected areas

2. toxigenic

-disease caused by bacterial toxins

Bacterial cause: (S. aureus: 80%; S. pyogenes OR mixed: 20%) invasive & cutaneous disease

limited to epidermis

acute & contagious

common in children (face & limb) AND during summer/tropical climates

progression:small macule (small discolored spot on skin) --> pustule on erythematous base --> pustule ruptures & is replaced by honey brown crusting

most common cause: S. aureus (invasive & cutaneous)

superficial & pyogenic infection of hair follicles

reduced risk: w/ good skin hygiene

most common cause: S. aureus (invasive & cutaneous)

boil: several hair follicles & adjacent tissues are affected

reduced risk: w/ good skin hygiene

most common cause: S. aureus (invasive & cutaneous)

folliculitis of eyelid

erythematous or pustular appearance

S. aureus disease: (invasive & cutaneous)

coalesced furuncles (more serious disease); extended to deeper subcutaneous tissue (multiple sinus tracts)

common locations: nape of neck, upper back, or buttocks

progression: tight/erythematic skin --> effaces & releases pus

associated symptoms: chills & fever

most commonly colonized by gram negative organisms

most common gram positive organism: staphylococcus aureus (invasive & cutaneous disease)

occurs after surgery/trauma

presentation: edema, erythema, pain, accumulation of purulent material

s. aureus intro into ductal system through cracked nipples (invasive & cutaneous disease)

presentation: tenderness, fever, fatigue, possibly aggressive, may require drainage

when s. aureus (invasive & non-cutaneous disease) is the cause

> 50% acquired after surgery OR from contaminated IV catheter

usually from innocuous-appearing skin infections

when s. aureus is the cause (invasive & non-cutaneous disease)

*does NOT require any pre-existing damage to heart tissues (as would endocarditis from other causes)

life threatening (50% mortality)

incr freq of embolization of friable vegetations (=> erythematous lesions in periphery)

prevalence: 2% of community pneumonia (*PV leukocidins important role here); 20% nosocomial-pneumonia (15-40% fatality <= those who develop are already ill)

cause: aspiration of oral secretions OR hematogenous spread

presentation: tissue destruction, massive hemoptysis, septic shock (all due to toxins)

remember: streptococcus pneumoniae is the most common cause of bacterial pneumonia

most common cause: s. aureus (invasive & non-cutaneous disease)

cause: hematogenous spread OR extension from subcutaneous infection

children: in metaphyseal areas of long bones (from low flow areas => time for bacteria to get out of the circulation)

adults: vertebra (rarely in long bones)

presentation: sudden onset of localized pain AND high fever

most common cause in most individuals:

s. aureus (however, N. gonorrhoeae (gram-negative coccus) is most common among the sexually active)

presentation: pain w/ mvmt, erythematous/swollen joints, pus in aspirated fluid

common location(s): knee (50% of cases), wrists, ankles, & hips

caused by: exfoliative toxins A & B (s. aureus-toxigenic disease) break desmoglein-1 (polypeptide) in desmosome (connect adjacent skin cells)

*stratum granulosum is susceptible be/c it lacks the Dsg-3 (polypeptide) that usually compensates for ETA/ETB hydrolysis of Dsg-1 in other strata

presentation/progression: abrupt onset of perioral erythema (covers entire body in 2 d) --> large bullae/cutaneous blisters (like burns) --> desquamation (in 5-7 d) --> blisters (2 wks) & positive nikolsky's sign

*blisters do NOT contain organism

localized SSSS

infection, NOT toxigenic => bacteria will be present w/in blister fluid

presentation: erythema does not extend beyond blister borders

cause: enterotoxin or enterotoxin-like TSST-1

*in menstruation-associated TSS cases: >90% caused by TSST-1

mechanism: TSST-1 strains multiply in hyper-absorbant tampons 

presentation: abrupt (fever, hT, whole-body-erythematous rash); multiple organs involved; entire skin desquamates (2-3 wks); markedly red tongue

fatality: previously high, currently 5%

most common cause of food borne illness: staphylococcus aureus (50% strains produce 8 distinct enterotoxins)

*heat stable (produced by bact in food @ RT, stable in re-heating)

superantigen mechanism? (not well understood)

presentation: severe vomiting (w/in 3-4 hrs)

*toxin w/in vomitus (bacteria absent)

therapy: fluid replacement NOT antibiotic (be/c this in an intoxication NOT an infection)

most common cause: Clostridium difficile 

2nd: staphylococcus aureus (produce ETA & leukotoxin E/D)

presentation: watery diarrhea, abdominal cramps, fever, inflammation of intestinal mucous membrane (bacteria present in stool)

increased risk: w/ use of broad spectrum antibiotics

s. aureus ID

abscess (scrape the base)

fewer organisms in pus

gram stains: gram positive cocci

s. aureus ID

bacteremia 

good: culturing blood

bad: staining blood (so few organisms)

s. aureus ID

ssss

good: look at nasopharyngeal sample

bad: looking at blister fluid (usually not here!)

s. aureus id

bullous impetigo

s. aureus id

tss

check vaginal samples, bacteria will be there

bacteria will NOT be in blood :(

s aureus id

food poisoning

:) bacteria in food/toxin in vomitus

:( bacteria NOT in feces/vomitus

s aureus id

blood agar

s aureus id

tellurite-glycine agar

positive: s aureus changes color --> black

glycine inhibits growth of species OTHER than staph

differential due to tellurite reduction to tellurium

staphylococcus epidermidis 

"CNS" or "CONS"

staphylococcus epidermidis virulence factors

 (3)

1. NO protein A, alpha-toxin, or coagulase (s epidermidis is often drug resistant)

2. teichoic acid (glycerol teichoic acid & glucosyl residues)

3. slime (facilitate adherence to catheters; forms protective biofilm; interferes w/ PMN phagocytosis)

What organism is this?

gram positive coccus

coagulase positive

catalase positive

grape-like clusters

tellurite-glycine/mannitol-salt agar positive

blood agar: golden-yellow colonies exhibiting hemolysis

1. major cause of infections associated w/ intravascular devices (ie. prosthetic heart valves, shunts, etc.); also in prosthetic joints, large wounds, and catheter induced UTIs

2. high incidence in hospital setting (contaminates pt care equipment/environmental surf w/ biofilm)

due to s. epidermidis (high mortality rate ~60%)

location of vegetations: prosthesis-tissue junction @ sewing ring (bacteria cannot grow on inert material of the prostheses)

complications: sepsis, embolization, congestive heart failure, cardiac rupture, etc.

gram positive coccus

catalase positive

coagulase negative

blood agar: white non-hemolytic colonies

mannitol-salt/tellurite-glycine agar negative

not known

can colonize periurethral skin & mucosa

cystitis (inflammed bladder)

pyelonephritis

*commonly present w/ dysuria and/or pyuria

bacterial UTI in sexually active women (7-20%)

*E. coli the most common cause

side note: commonly drug resistant

NOVOBIOCIN-RESISTANT

gram positive coccus

blood agar: white colonies

catalase positive

coagulase negative

mannitol-salt agar test negative (cannot ferment mannitol)

other staphylococci (2)

and their associated diseases

staphylococcus haemolyticus

staphylococcus capitis

endocarditis, UTIs, wound infections, opportunistic infections

osteomyelitis

acute form most commonly caused by staphylococcus aureus

septic arthritis

most common cause, generally: staphylococcus aureus

most common cause, among sexually active: neisseria gonorrhoeae

catalase positive: staphylococcus species

catalase negative: streptococcus & enterococcus species

mannitol salt agar

growth selective for staphylococcus <= high salt

test differential for S. aureus <= mannitol fermentation indicated by color change (positive result = orange/yellow)

tellurite-glycine agar

growth selective for staphylococcus <= normal flora growth inhibited by glycine

test differential for S. aureus <= tellurite reduction to tellurium (indicated by color change: positive result = black)

coagulase test (ONLY staphylococcus aureus is coagulase+)

positive result: w/ incubation in plasma, S. aureus => coagulation