Flashcards in 2: staph: bacteremia, sepsis, and MRSA Deck (75)
what type of colonies does staph form on blood agar?
coag (+): golden B-hemolytic colonies
coag (-): small, white nonhemolytic colonies
rate of S. aureus colonization higher among:
-patients undergoing hemodialysis
-individuals w/ skin damage
sites of S. aureus human colonization
-skin (especially when damaged)
how many people are colonized?
25-50% of healthy people may be transiently or persistently colonized
diseases w/ increased risk for S. aureus infection
-congenital or acquired qualitative or quantitative defects of PMNs (neutropenia, CGD, chediak-higashi)
does MRSA invade much?
not really (only 5-10% of time) - mostly affects skin and soft tissue
describe pathogenesis of staph
-pyogenic -> abscesses
-inflam response, initial infiltrate of PMNs, then macrophages and fibroblasts
-localized/contained (coagulase) OR spreads to adjacent tissues/bloodstream
what does ER give anyone with a skin infection?
Bactrim + Kephlex - don't try to distinguish b/w staph and strep, so they give two drugs to cover both
-Bactrim: shitty dude for MRSA
-Kephlex: for methicillin sensitive + strep
3 toxins of staph
2. pyrogenic toxin super Ag's
3. exfoliative toxin
what does the pyrogenic toxin super Ag's of staph mediate?
food-borne illness - toxin formed in food, sx present in absence of viable bacteria (enterotoxin)
staph TSS - toxin produced at site of colonization, causes clinical illness (TSST-1)
what does the exfoliative toxin of staph mediate?
staph scalded skin syndrome
why no staph vaccine?
anti-staph Ab's may be protective in vitro but have not shown protection in clinical trials
stops bacterial protein synthesis to stop toxin production
clinical manifestations of staph
-skin and soft tissue infection
-sepsis and TSS
-bone and joint infection
describe skin and soft tissue infections of staph
-folliculitis (superficial dermis)
-furuncules, carbuncles, abscesses (deep dermis)
-hidradenitis suppurativa (follicular infection of intertriginous areas)
-cellulitis, erysipelas, fasciitis (subQ tissues)
-pyomyositis (skeletal muscle)
describe CV infections of staph
-infective endocarditis (acute)
-cardiac device infection
-intravascular catheter infection
describe bone and joint infections of staph
-osteomyelitis - hematogenous, or secondary to a contiguous focus of infection
-prosthetic joint infection
-septic arthritis or bursitis
describe meningitis of staph
-most commonly occurs in the setting of head trauma or neurosurgery
describe bacteriuria of staph
-may be associated with indwelling urinary catheter
-probably a skin contaminant
-not typical urine infections symptoms
is necrotizing fasciitis more common with staph or strep?
what is the leading cause of both community acquired and healthcare acquired bacteremia?
three categories of staph bacteremia
-healthcare-associated hospital onset (nosocomial)
-healthcare-associated community onset (long term care facilities)
risk factors for staph bacteremia
-implanted prosthetic devices
-injection drug use
history associated with staph bacteremia
-recent skin or soft tissue infection
-presence of indwelling prosthetic devices
-injection drug use
-recent hospital exposure
symptoms of metastatic infection with staph bacteremia
-bone or joint pain (vertebral osteomyelitis, discitis, epidural abscess)
-protracted fever or sweats (endocarditis)
-abdominal pain (LUQ = splenic infarction/abscess)
-CVA tenderness (renal infarction, psoas abscess)
-headache (septic emboli)
what must you make sure to include in physical exam of a patient with staph bacteremia?
careful cardiac exam for:
-new murmurs or evidence of heart failure
-stigmata of endocarditis
what should you get as part of diagnostic eval for staph bacteremia?
-blood cultures (always 2 sets)
-echocardiography (TTE +/- TEE)
-other imaging based on symptoms
difference b/w strep and staph endocarditis ??
Strep viridans gets killed off pretty quickly by abx
staph blows through abx
treatment of staph aureus bacteremia in adults
-control source of infection
-empiric antibiotics pending sensitivity results (vancomycin)
-tailored therapy once sensitivities available
-MSSA: anti-staph PCN (nafcillin/oxacillin), cefazolin
-MRSA: vancomycin or daptomycin
-blood cultures 48-72h after start of therapy
duration of therapy in uncomplicated infection w/ no cardiac abnormalities
14d IV therapy
duration of therapy w/ deep focus of infection + more severe disease
sepsis vs. SIRS (definitions)
sepsis: clinical syndrome complicating severe infection, signs occur in tissues remote from site of infection
SIRS: clinical syndrome complicating a noninfectious insult (i.e. pancreatitis, pulmonary contusion)
diagnostic criteria for SIRS include:
-temp above 38C or less than 36C (100.4F or 96.8F)
-HR above 90 bpm
-RR above 20 breaths/min of PaCO2 less than 32 mmHg
-WBC above 12,000 or less than 4000
-SBP less than 90 mmHg
special management problems with central catheter related infections?
if you have a central line + a fever: blood cultures + Abs
no source for fever: switch line over wire (half assed)
not high yield
steps of sepsis severity (4)
2. Sepsis (2 SIRS + confirmed or suspected infection)
3. Severe Sepsis (Sepsis + signs of end organ damage + hypotension SBP less than 90 + lactate above 4 mmol)
4. Septic Shock (Severe sepsis w/ persistent: hypotension, signs of end organ damage, lactate above 4 mmol)
definition of septic shock
sepsis-induced hypotension persisting despire adequate fluid resuscitation (=vasodilatory shock)
problem with nafcillin
-have to infuse every 4 hours
-causes phlebitis (irritation of veins)
risk factors for sepsis:
-ICU patient with nosocomial infection
-age above 65 y/o
-community acquired pneumonia
-genetic factors contributing to susceptibility to infection
where is daptomycin great? where is it not great?
bloodstream infection, but doesn't get into lungs super well
what is the increasing incidence of sepsis since the 1970s thought to be due to?
-multi-drug resistant infections
population with the highest incidence of sepsis
African American male
over 65 y/o
in winter (increased prevalence of resp infections)
top three pathogens (by frequency) causing sepsis
1. G(+) bacteria
2. G(-) bacteria
3. fungal pathogens
only things that reliably kill off enterococcus
penicillin (if sensitive)
what should clinical evaluation of a septic patient include?
-determine source of infection (history and physical)
-assess respiratory status (O2 sats, respiratory effort)
-assess perfusion (BP, capillary refill, pulses)
-assess end-organ effects (lactate level, renal and hepatic fxn, mental status)
early management of sepsis
-control of airway (supplemental O2, intubation, ventilation)
-establish venous access (central venous catheter)
-maintain perfusion (IV fluids, vasopressors/inotropic agents)
how to control the septic focus
-early antibiotics (empiric therapy initially, then tailored to culture results)
-possible debridement/surgical intervention
what are some vasoactive agents used in septic shock?
which vasoactive agent has largest effect on heart rate?
which vasoactive agents have largest effects on contractility?
which vasoactive agents have largest effects on arterial constriction? which have opposite effects (dilation)
source control methods: sinusitis
surgical decompression of sinuses
source control methods: pneumonia
source control methods: empyema thoracis
source control methods: mediastinitis
source control methods: peritonitis
-resection, repair, or diversion of ongoing sources of contamination
-drainage of abscesses
-debridement of necrotic tissues
source control methods: cholangitis
-bile duct decompression
source control methods: pancreatic infection
-drainage or debridement
source control methods: UTI
-drainage of abscesses
-relief of obstruction
-removal or changing of infected catheters
source control methods: catheter-related bacteremia
-removal of catheter
source control methods: endocarditis
source control methods: septic arthritis
-joint drainage and debridement
source control methods: soft tissue infection
-debridement of necrotic tissue and drainage of discrete abscesses
source control methods: prosthetic device infeciton
mortality rates with sepsis:
-severe sepsis only
-septic shock only
10-50% - increases with severity of sepsis
-severe sepsis: 20%
-septic shock: 46%
what mediates methicillin resistance?
PBP2a - PBP encoded by mecA gene
where is mecA located?
on a mobile genetic element (staph chromosome cassette SCCmec)
what is the leading cause of surgical site infections?
diagnosis of HA-MRSA electrophoresis?
USA100 or USA200 pulse-field pattern
difference in type of infection associated with HA-MRSA vs. CA-MRSA
HA: severe, invasive disease
CA: skin and soft tissue infections in healthy young persons, community outbreaks
diagnosis of CA-MRSA electrophoresis?
USA300 or USA400 pulse-field pattern
risk factors for MRSA
-residence in long-term care facility
-recent antibiotic therapy***
-injection drug use
-sharing needles, razors, or other sharps
-sharing sports equipment
-prolonged hospital stay
what was the likely mechanism that brought about MRSA?
antibiotic selective pressure
-abx use (especially cephalosporin and fluoroquinoline) correlated with risk for MRSA colonization and infection
key components of the infection control program at the Billings Clinic to prevent/cut down prevalence of MRSA?
-decontamination of environment and equipment
-contact precautions for infected and colonized patients
-active surveillance cultures (ASCs)
describe the active surveillance
nares culture on admission, discharge, transfer, or death