Cross Staph Lecture Flashcards
differentiating lab properties of staphylococci?
nonmotile
no spores
catalase +
what does catalase do
degrade hydrogen peroxide from neuts
3 most important human staph pathogens
aureus
epidermidis
saprophyticus
how does staph aureus cause disease, generally?
producing toxins
inducing pyogenic inflammation
diseases caused by s aureus
abscess, septic arthritis, endocard, food poison, SSS, TSS; hosp-acq PNA ,septicemia, surgical wound infections; folliculitis, impetigo, bact conjunctivitis
what is predom organism of skin?
staph epi
diseases by staph epi?
endocarditis, prosthetic joint/ hardware infections
staph sapro causes what disease
UTI
what is carrier state
individual harbors pot’l pathogen and can infect others. Usually those who have recently recovered from a dis and still carry, OR those with asymp inf
What is colonization
acquisition of a NEW organism and may cause infection or may be elim by host defenses
what is colonization resistance
nonpathogenic resistant bacteria ocupy attachment sites on skin and mucosa, interfering with colonization by pathogenic bacteria
site of s aureus colonization
nose
s sapro site of colonization
skin around GU
what makes a s aureus plate yellow?
staphyloxanthin
Protein A
S. aureus. Binds Fc portion of IgG at complement binding site and prevents complement act; major comp of CW; **no C3b prod so phagocytosis of organisms is greatly reduced
P-V leukocidin
S. aureus. Pore-forming toxin kills cells, esp WBC, by damaging cell membranes; severe skin/soft tissue inf, also severe necrotizing PNA. Prod by MRSA, usually community-acq
Teichoic acids
S aureus. Mediates adherence to mucosal cells. Induces rel of IL-1, TNF from macs
peptidoglycan
S. aureus. Endotoxin-like prop. can act compelment, coag cascade, cytok
what strain of staph causes necrotizing PNA?
MRSA
main types of staph virulence factors?
surface proteins, enzymes, toxins
staphyloxanthin (carotenoid)
S. aureus. causes golden color. Inactivates microbicidal effect of superoxides and ROS in neuts
coagulase
S. aureus. Prothrombin –> thrombin, so fibrin clot forms. Walls off inf, delays migration of neuts to the site
hemolysins/alpha toxins
S aureus. hemolyze RBC and use the iron req for bact to grow. causes necrosis of skin and hemolysis
polysaccharide capsule
S. aureus. Stim macs to produce cytok, activates comp/coag
gamma-toxin/ leukotoxin
lyses phagocytes and RBC
pyogenic s aureus infections
endocarditis, septic arthritis, osteomyelitis, postsurg wound inf, PNA–>empyema/abscess, sepsis, mastitis, abscess both from local inoculation and result of bloodstream inf
MRSA is common cause of infection and outbreak where?
childcare centers, IV drug users, wrestling teams, prisons, etc
pathogenesis of SSS
S. aureus. Exfoliatin, Exfoliative toxins A and B. Acts as a protease that cleaves desmoglein in desmosomes, leading to sep’n of epidermis at granular cell level
SSS symptoms
newborns 3-7 days; febrile, irritable, diffuse blanching erythema with blisters. No muc memb
SSS lesions
serous fluid exudates, deH, elyte imbalance. Flaky desquam and sloughing as healing occurs. diffuse blanching erythema with blisters/bullae 1-2 days later in flexural areas, butt, hands, feet.
SSS recovery
no scarring
desquam
10 days
what mediates S aureus food poison
Enterotoxin A
What is enterotoxin A
S aureus food poisoning. superAg in GI tract, stim IL-1 and IL-2 from macs, Th cells. Heat resistent, acid resistant. Incubation period 1-8 hours
enterotoxin A symptoms
prominent vomiting, watery/non-bloody D+.
why vomiting in s aureus food poisoning
cytokines from enterotoxin A –>macs, Th cells stimulate enteric nervous system to vomit center in brain
cause of bullous impetigo
exfoliative toxin of s aureus.
bullous impetigo present
young children. Vesicles enlarge to flaccid bullae w clear yellow fluid which becomes darker. Thin brown crust when ruptured. TRUNK freq.
staph TSS pathogenesis
toxin-med/superAg. TSST at site enters blood–>toxemia. IL-1, 2, TNF. 5-25% s aureus carry TSST gene.
when can staph TSS happen
when people don’t have Ab to TSST
what clinical settings does staph TSS occur?
tampons, nasal packing in epistaxis, post-op inf
blood cultures in staph TSS
NEGATIVE
signs/symp of staph TSS
fever, hypoTN, dizzy, syncope, diffuse macular erythroderma that desquamates 1-2 wks post onset; V/D, severe myalgia w CPK ^, renal fail, hyperbilirubin, thrombocytopenia, AMS
Tx MSSA
b-lactamase, so naf/oxacillin, cephalosporins, vanc, augmentin if mild
MRSA tx
vanco, dapto, linezolid, ceftaroline, bactim/clinda (mild)
tx VISA/VRSA
dapto
linezolid
ceftaroline
resistance mech of MRSA?
changes in PBP in cell memb. MecA genes on bact chrom encode them
VRSA resistance mech?
genes encode enz that sub D-lactate for D-alanine
VISA resistance mech?
synthe of unusually thick CW
Tx staph TSS
supportive (10-20 L fluid/day, vasopressors like dopamine, NE); surgical; antibiotics (vanc/oxacillin + CLINDA)
why give clindamycin w vanc/oxacillin in staph TSS?
suppresses protein synth and therefore toxin syth. Linezolid can have same effect
prevent S aureus for surgeries
peri-op Cefazolin +/- vanc depending on rate of MRSA in that area
role of mupirocin?
S aureus prevention to reduce colonization intranasally. combine w Hibiclens for bathing +/- doxy, bactrim. 1 week
microbiologic props of S aureus
cat +
coag +
beta-hemolytic
ferments mannitol
microbiologic props of S epi
cat + coag - non-hemolytic urease + not mannitol ferm novobiocin sens
microbiologic props of s sapro
cat + coag - non-hemolytic urease + not mannitol ferm novobiocin RES
differences in novobiocin sesitivity
S epi sens
S sapro R
coagulase test for strep
+ for s aureus only
done with rabbit plasma
settings of S epi inf
foreign devices. probably inoculated at time of implant
pathogenesis of S epi
- bact adhere. Surf prots bind to fibrinogen, fibronectin, etc on foreign matl. Many have adhesins critical
- ECM, slime made to encase bact. barrier to antibiotic, interfere w defenses
what staph makes biofilm
S epi, aureus
S epi tx
VANCO. oxa/nafcillin if MSSE.
+ Rifampin, gent if prosth valve endocarditis
removedevice.
MRSE mech of resist
changes in PBP in cell memb. MecA genes on bact chrom encode them. just like MRSA
S sapro
2nd most common cause of comm-acq UTI in women
sex w/in 24 hrs
tx S sapro UTI
Bactrim, Cipro
Cipro
NOT for S aureus. Only S sapro