ICL 2.9: Staphylococci Flashcards
what’s the microbiology of staphylococci?
gram (+) coccus
nonmotile
non-spore forming
grape-like clusters
clinical specimens can be clusters, single, paired, or chained cocci
are staphylococci catalase positive or negative?
catalase positive
H2O2 –> H2O + O2
this is what differentiated staph from strep!! strep is catalase negative
are staphylococci anaerobes or aerobic?
facultative anaerobes
how strong/resistant are staphylococci?
hardy bacteria; not fastidious
can withstand heat, drying, high salt concentrations
this is due to their capsule
antibiotic resistance is a worsening problem….
what are the two general groups of staphylococci?
- coagulose-positive staphylococci
2. coagulase-negative staphylococci
what are coagulase postitive staphylococci?
coagulase does fibrinogen –> fibrin
so it allows bacterial aggregation/clumping or clot formation
β-hemolytic
ex. S. aureus
what are coagulase negative staphylococci?
part of the normal skin flora!
most have low virulence and are non-hemolytic
but slime layers allow for adherence to catheters, prosthetic valves and joints
ex. S. epidermidis, S. haemolyticus, S. hominis,
S. lugdunensis
which staph bacteria is coagulase positive?
s. aureus
which staph bacteria are coagulase negative?
S. epidermidis,
S. haemolyticus,
S. hominis,
S. lugdunensis
what color is staphylococcus aureus in cultures? why?
gold! aureus duh
comes from production of carotenoids
what type of hemolysis do stephylococcus aureus do?
B-hemolytic
what are the important cell wall components of staphylococcus aureus?
- polysaccharide capsule
- peptidoglycan
- teichoic acids
- protein A
what are the characteristics of the capsule of s. aureus?
polysaccharide capsule
11 capsule serotypes
inhibits phagocytosis by PMNs
what are the characteristics of the PG of s. aureus?
thick because gram (+) bactiera
immunostimulatory
methicillin resistance and penicillin resistance due to PBP2’ which blocks penicillin binding
what are the characteristics of the teichoic acids of s. aureus?
parts of the cell wall
bound to PG NAM or cytoplasmic membrane (lipoteichoic acids)
binds fibronectin for adhesion
what are the characteristics of the protein A of s. aureus?
binds Fc portion of IgG1, IgG2, IgG4
inhibits Ab-mediated clearance
what is the structure of the PG of s. aureus?
alternating NAG-NAM backbone = very stable
side chains (tetrapeptide) are linked to NAM and crosslinked by a pentaglycine bridge = staph specific*
PG is a target for B-lactam and glycopeptide antibiotics
PG is immunostimulatory!!!**
how is PG of s. aureus immunostimulatory?
- IL-1 production from monocytes
- attracts PMNs
- activates complement
- has some endotoxin-like activity
what are the important virulence enzymes of s. aureus?
- coagulase
2. catalase
what is the function of coagulase in s. aureus?
s. aureus is coagulase (+) and it’s a virulence enzyme for it
it stimulates the reaction fibrinogen –> fibrin which allows for clumping/aggregation of bacteria
activation of the clotting cascade occurs with sepsis
fibrin bound to S. aureus inhibits phagocytosis!!
there is either bacterial-associated (bound coagulase) or extracellular (free coagulase)
what is the function of catalase in s. aureus?
it’s a virulence enzyme
it catalyzes the reaction H2O2 –> H2O + O2
this is important because PMNs release H2O2 to kill pathogens but then catalase just breaks it down
**catalase production is also used to differentiate Staph (+) from Strep (-)
how can you differentiate staph from strep?
staph is catalase positive
strep is catalase -
so staph will form bubbles with the catalase test!
H2O2 –> H2O + O2
what are the s. aureus toxins?
- 5 cytolytic toxins
- 2 exfoliative toxins
- 8 enterotoxins
- toxic shock syndrome toxin-1
which s. aureus toxins are superantigens?
exfoliative toxin A
all 8 enterotoxins
toxic shock syndrome toxin-1
what are superantigens?
they bind MHC II on macrophage to force interaction with T cell TCR
macrophages release IL-1β (fever) + TNFα (hypotension, shock)
T cells release IL-2, IFNγ, TNFβ (hypotension, shock)
what do the different cytolytic toxins of s. aureus do?
α toxin = forms pores that allow loss of osmoregulation
β toxin = cleaves lipids in membranes of RBC, fibroblasts, leukocytes, macrophages
𝛿 toxin = has detergent-like qualities that disrupt membranes of many cells
γ and PV toxin = forms pores in leukocytes
what does exfoliative toxin A do?
it’s an s. aureus toxin that’s a superantigen*
causes staphylococcal scaled skin syndrome (SSSS) = exfoliative dermatitis (literally pealing baby skin)
exfoliative toxins are proteases that cleave desmoglein 1, which disrupts cell-to-cell adhesion in epidermis
Ab can neutralize toxin!
less than 5-10% of strains contain these toxins
what do enterotoxins A-I do?
A = food poisoning, usually ham*
all are superantigens!!
also all are heat stable and acid-resistant
30-50% of S. aureus strains carry enterotoxins
what does TSST-1 do?
TSST-1 = toxic shock syndrome toxin-1 = toxin of s. aureus
it’s a superantigen –> stimulates cytokines leading to hypovolemia and shock
damages many cells, including endothelial cells, leading to vascular leakage
how is s. aureus spread?
- person-to-person
- fomites
30% chronically colonized, 50% intermittently colonized, 20% never colonized
s. aureus can survive on dry surfaces because of PG and capsule
what populations are more likely to be colonized with s. aureus?
- vaginal carriage of S. aureus occurs in 10% of women
- hospital personnel have high rates of colonization (50% - 90%)
- wounds or foreign body penetration (catheters, prosthetic valve/joints)
what is CA MRSA?
CA MRSA strain(s) carry the Panton-Valentine leukocidin (PVL) toxins*
association of PVL toxin in CA-MRSA with skin and soft tissue infections and severe necrotizing pneumonia with sepsis
what are the risk factors for CA-MRSA?
- skin trauma
- high BMI
- cosmetic body shaving
- prison residence
- physical contact with a person who has a draining lesion or is a carrier of MRSA
- sharing equipment that is not cleaned or laundered between users
- tattoo recipient
- military
what does the clinical disease of s. aureus depend on?
- adherence
- immune evasion
- penetration into tissue
- inoculum size
- host immune status
how does s. aureus adherence work?
s. aureus can adhere to:
1. mucosal cells/nasal epithelial cells
teichoic acids on bacterial cell wall bind fibronectin to allow adherence to mucosal cells
coagulase allows bacterial clumping/aggregation
- traumatized or broken skin
coagulase degrades fibrinogen –> fibrin (clot)
- endothelial surfaces
teichoic acids bind fibronectin
how does s. aureus perform immune evasion?
- Protein A binds antibodies to limit clearance
- Polysaccharide capsule inhibits PMN phagocytosis
- Catalase limits toxic effects of PMN H2O2
- Cytolytic toxins lyse a variety of immune cells
disease by S. aureus is a result of what combination of things?
- toxin action
- localized infection (pyogenic disease)
- systemic infection (disseminated infection; bacteremia)
what are the clinical diseases caused by s. aureus?
- SSSS
- staph food poisoning
- toxic shock syndrome
- cutaneous infections (pyogenic disease)
- bacteremia/endocarditis
- pneumonia
- osteomyelitis
- septic arthritis
what is SSSS?
SSSS = staph scalded skin syndrome
primarily in newborns
toxins act on the dermis –> staph secretes exfoliative toxins systemically
abrupt perioral erythema –> 2 days later whole body –> skin detaches easily –> may form bullae –> usually self-resolving in 7-10 days but may administer anti-Staph antibiotics or local wound care
antibodies neutralize toxins
what is staph food poisoning?
ingestion of preformed enterotoxin (usually enterotoxin A or B; superantigen); food appears normal
common with processed meats, especially ham*
there’s abrupt onset of nausea/vomiting, abdominal pain, diarrhea 2 - 6 h after ingestion; symptoms may last 24 h
usually occurs in community outbreaks but it’s self limiting!
Abs develop and are cross-protective
what is TSS?
TSS = toxic shock syndrome
associated with staph strains producing TSST-1 (superantigen)
abrupt onset of fever, hypotension, diffuse rash, vomiting, diarrhea, myalgia
rash progresses to desquamation of palms and soles** (unique)
CNS, GI, liver, blood, musculature, renal systems involved
2 scenarios:
1. non-menstrual = usually 48 hours after a surgical procedure; patient looks septic but wound looks good
- menstrual = young women age 15-25 using tampons during menses
how do you treat TSS?
remove source of the Staph (removes toxin production): abscesses, fluid collections, tampons
supportive measures, immunoglobulins, antibiotics
what are some of the cutaneous infections you can get from staph?
- impetigo
- folliculitis
- furuncles
- carbuncles
- hidradenitis suppurativa
- cellulitis
- lymphagitis
what is impetigo?
superficial infection of the skin, face, and limbs
young children
begins as a vesicular lesion (macule; flat and red) –> pustule (pus-filled) –> crusty erosion
80% of impetigo are Staph; 20% Group A Strep
what is osteomyelitis?
one of the possible disease outcomes of s. aureus
Hematogenous spread to bone or area adjacent to trauma
in children, affects long bones (rapid growth and highly vascularized)
in adults, affects vertebral column
Brodie abscess = foci of Staph
how do you diagnose s. aureus infections?
- Pus contains few bacteria
- Culture from base of abscess
- Blood sample should be cultured, not stained
- rapid test = staphaurex
how does staphaurex work?
rapid test; latex agglutination for s. aureus infection
S. aureus bound coagulase binds fibrinogen that is bound to latex beads
S. aureus Protein A binds Fc region on rabbit IgG that is bound to latex beads
Latex beads and S. aureus clump together
how do you treat s. aureus infections?
remove foreign bodies or drain pus
duration of therapy depends on the type of infection
bone, foreign body, endocarditis require at least 4 weeks of antibiotics
how would you treat MSSA?
MSSA = methicillin sensitive s. aureus
good drug choices are β-lactams = nafcillin, oxacillin, cefazolin
how would you treat hospital acquired MRSA?
most frequently due to altered penicillin binding proteins (PBP2a)- mecA gene
Vancomycin best choice because it’s resistant to more drugs than CA-MRSA
how would you treat CA-MRSA?
clindamycin, doxycycline, trim-sulfa (Bactrim), linezolid, vancomycin good initial choices if CA-MRSA suspected
rifampin resistance occurs rapidly and combination therapy is useful
what causes VRSA?
VRSA = MRSA that is Vancomycin intermediate-sensitive or resistant
this is due to thickened PG or vanA gene from Enterococci (modified PG)
consider linezolid or Synercid or daptomycin
which staph bacteria are coagulase negative?
- s. epidermidis
- s. lugdunensis
- s. saphrophyticus
- s. hemolyticus
how do coagulase negative staphylococci work?
they typically produce polysaccharide slime layer that aids in attachment to surfaces (e.g. catheters, shunts, prosthetic joints)
what is the microbiology of s. epidermidis?
coagulase negative
catalase positive
γ hemolysis = white color on agar
what is s. epidermidis?
normal resident bacteria on skin, mucous membranes
antibiotic resistance encoded by plasmids; can easily transfer within or between genus/species
nearly all infections are hospital acquired
usually caused by infection after “hardware” is introduced into body or “line sepsis” specially artificial valves*
common cause of artificial valve endocarditis (40% S. epi)
requires aggressive treatment with Vancomycin + gent + rifampin and removal of the valve
what is s. lugdunensis associated with?
native valve endocarditis
what is the microbiology of s. lugdunensis?
β hemolytic on blood agar
coagulase negative
PYR) positive [rapid test] –> most staph are negative!!
requires aggressive treatment with vancomycin + gent + rifampin and removal of valve
what is s. saprophyticus associated with?
UTIs
infection occurs in healthy young women in an outpatient setting
what is the microbiology of s. saprophyticus?
catalase positive
coagulase negative
γ-hemolytic on blood agar
novobiocin resistant
what is s. hemolyticus associated with?
opportunistic infections
it’s a normal resident bacteria on skin, mucous membranes
infections similar to S. epidermidis
= line infections, endocarditis, septicemia, etc.
2nd most common cause of coag neg Staph infections
what is the microbiology of s. hemolyticus?
catalase positive
coagulase negative
non-hemolytic on blood agar
FLASHCARD: microbiology, pathology, epidemiology, clinical, diangnosis and treatment of staphylococcus aureus
MICROBIOLOGY: Gram + cocci; clusters; β-hemolytic; catalase positive; coagulase (clumping factor) positive; carbohydrate capsule inhibits phagocytosis
PATHOLOGY: PG immunostimulatory; teichoic acid binds fibronectin (adhesion); Protein A binds antibody; coagulase (clumping factor); catalase; hyaluronidase; fibrinolysin; nuclease; toxins (cytolytic, exfoliative, enterotoxins, TSS1; superantigens)
EPIDEMIOLOGY: colonized at birth; fomites; person-to-person; vaginal colonization; wounds
CLINICAL: Toxin-mediated (food poisoning, Scalded Skin Syndrome [SSSS], Toxic Shock Syndrome [TSS]); Cutaneous (impetigo, folliculitis, carbuncles, furuncles, sweat glands, wound infections); Bacteremia, endocarditis; Pneumonia;
DIAGNOSIS: Culture from abscess, blood, nasopharynx (SSSS), vagina (TSS); rapid disease (food poisoning); Staphaurex; PCR or PFGE
TREATMENT: Culture susceptibility; nafcillin, oxacillin, cefazolin; MRSA = vanc; CA-MRSA = clindamycin, doxy, bactrim, linezolid, vanc
FLASHCARD: s. epidermidis
Υ-hemolytic
resident on skin
hospital acquired infection; cath infections; artificial valve endocarditis >80% methicillin-res; >50% resistant to erythromycin, clindamycin, chloramphenicol, tetracyclines;
treat with vanc, rifamin, or cipro
FLASHCARD: s. lugdunensis
β hemolytic;
PYR test positive
native valve endocarditis
treat with vanc + gent + rifampin
FLASHCARD: s. saprophyticus
Υ-hemolytic
novobiocin resistant
UTIs
treat with fluoroquinolones or bactrim (trimethoprim-sulfamethoxazole)
FLASHCARD: s. hemolyticus
Υ-hemolytic; resident on skin
line infections, septicemia
less frequent UTI, wound infections, bone and joint infections
