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ICM > 2: staph: bacteremia, sepsis, and MRSA > Flashcards

2: staph: bacteremia, sepsis, and MRSA Flashcards

1
Q

what type of colonies does staph form on blood agar?

A

coag (+): golden B-hemolytic colonies

coag (-): small, white nonhemolytic colonies

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2
Q

rate of S. aureus colonization higher among:

A
  • insulin-dependent diabetics
  • HIVers
  • patients undergoing hemodialysis
  • individuals w/ skin damage
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3
Q

sites of S. aureus human colonization

A
  • anterior nares
  • skin (especially when damaged)
  • vagina
  • axilla
  • perineum
  • oropharynx
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4
Q

how many people are colonized?

A

25-50% of healthy people may be transiently or persistently colonized

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5
Q

diseases w/ increased risk for S. aureus infection

A
  • diabetes
  • congenital or acquired qualitative or quantitative defects of PMNs (neutropenia, CGD, chediak-higashi)
  • skin abnormalities
  • prosthetic devices
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6
Q

does MRSA invade much?

A

not really (only 5-10% of time) - mostly affects skin and soft tissue

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7
Q

describe pathogenesis of staph

A
  • pyogenic -> abscesses
  • inflam response, initial infiltrate of PMNs, then macrophages and fibroblasts
  • localized/contained (coagulase) OR spreads to adjacent tissues/bloodstream
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8
Q

what does ER give anyone with a skin infection?

A

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
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9
Q

3 toxins of staph

A
  1. cytotoxins
  2. pyrogenic toxin super Ag’s
  3. exfoliative toxin
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10
Q

what does the pyrogenic toxin super Ag’s of staph mediate?

A

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)

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11
Q

what does the exfoliative toxin of staph mediate?

A

staph scalded skin syndrome

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12
Q

why no staph vaccine?

A

anti-staph Ab’s may be protective in vitro but have not shown protection in clinical trials

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13
Q

TSS treatment

A

Clindamycin

stops bacterial protein synthesis to stop toxin production

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14
Q

clinical manifestations of staph

A
  • skin and soft tissue infection
  • bacteremia
  • cardiovascular infection
  • sepsis and TSS
  • splenic abscess
  • bone and joint infection
  • pulmonary infection
  • meningitis
  • bacteriuria
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15
Q

describe skin and soft tissue infections of staph

A
  • impetigo (epidermis)
  • folliculitis (superficial dermis)
  • furuncules, carbuncles, abscesses (deep dermis)
  • hidradenitis suppurativa (follicular infection of intertriginous areas)
  • cellulitis, erysipelas, fasciitis (subQ tissues)
  • pyomyositis (skeletal muscle)
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16
Q

describe CV infections of staph

A
  • infective endocarditis (acute)
  • cardiac device infection
  • intravascular catheter infection
  • septic thrombophlebitis
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17
Q

describe bone and joint infections of staph

A
  • osteomyelitis - hematogenous, or secondary to a contiguous focus of infection
  • prosthetic joint infection
  • septic arthritis or bursitis
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18
Q

describe meningitis of staph

A

-most commonly occurs in the setting of head trauma or neurosurgery

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19
Q

describe bacteriuria of staph

A
  • may be associated with indwelling urinary catheter
  • probably a skin contaminant
  • not typical urine infections symptoms
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20
Q

is necrotizing fasciitis more common with staph or strep?

A

strep

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21
Q

what is the leading cause of both community acquired and healthcare acquired bacteremia?

A

staph aureus

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22
Q

three categories of staph bacteremia

A
  • healthcare-associated hospital onset (nosocomial)
  • community-acquired
  • healthcare-associated community onset (long term care facilities)
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23
Q

risk factors for staph bacteremia

A
  • intravascular catheters
  • MRSA colonization
  • implanted prosthetic devices
  • injection drug use
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24
Q

history associated with staph bacteremia

A
  • recent skin or soft tissue infection
  • presence of indwelling prosthetic devices
  • injection drug use
  • recent hospital exposure
  • intravascular catheter
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25
Q

symptoms of metastatic infection with staph bacteremia

A
  • 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)
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26
Q

what must you make sure to include in physical exam of a patient with staph bacteremia?

A

careful cardiac exam for:

  • new murmurs or evidence of heart failure
  • stigmata of endocarditis
  • neuro exam
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27
Q

what should you get as part of diagnostic eval for staph bacteremia?

A
  • blood cultures (always 2 sets)
  • echocardiography (TTE +/- TEE)
  • other imaging based on symptoms
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28
Q

difference b/w strep and staph endocarditis ??

A

Strep viridans gets killed off pretty quickly by abx

staph blows through abx

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29
Q

treatment of staph aureus bacteremia in adults

A
  • 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
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30
Q

duration of therapy in uncomplicated infection w/ no cardiac abnormalities

A

14d IV therapy

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31
Q

duration of therapy w/ deep focus of infection + more severe disease

A

varies

32
Q

sepsis vs. SIRS (definitions)

A

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)

33
Q

diagnostic criteria for SIRS include:

A
  • 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
34
Q

special management problems with central catheter related infections?

A

if you have a central line + a fever: blood cultures + Abs
no source for fever: switch line over wire (half assed)

not high yield

35
Q

steps of sepsis severity (4)

A
  1. SIRS
  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)
36
Q

definition of septic shock

A

sepsis-induced hypotension persisting despire adequate fluid resuscitation (=vasodilatory shock)

37
Q

problem with nafcillin

A
  • have to infuse every 4 hours

- causes phlebitis (irritation of veins)

38
Q

risk factors for sepsis:

A
  • ICU patient with nosocomial infection
  • bacteremia
  • age above 65 y/o
  • immunosuppression
  • diabetes
  • cancer
  • community acquired pneumonia
  • genetic factors contributing to susceptibility to infection
39
Q

where is daptomycin great? where is it not great?

A

bloodstream infection, but doesn’t get into lungs super well

40
Q

what is the increasing incidence of sepsis since the 1970s thought to be due to?

A
  • advancing age
  • immunosuppression
  • multi-drug resistant infections
41
Q

population with the highest incidence of sepsis

A

African American male
over 65 y/o
in winter (increased prevalence of resp infections)

42
Q

top three pathogens (by frequency) causing sepsis

A
  1. G(+) bacteria
  2. G(-) bacteria
  3. fungal pathogens
43
Q

only things that reliably kill off enterococcus

A

linazolid
penicillin (if sensitive)
vancomycin

44
Q

what should clinical evaluation of a septic patient include?

A
  • 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)
45
Q

early management of sepsis

A
  • control of airway (supplemental O2, intubation, ventilation)
  • establish venous access (central venous catheter)
  • maintain perfusion (IV fluids, vasopressors/inotropic agents)
46
Q

how to control the septic focus

A
  • early antibiotics (empiric therapy initially, then tailored to culture results)
  • possible debridement/surgical intervention
47
Q

what are some vasoactive agents used in septic shock?

A
  • dobutamine
  • dopamine
  • epi
  • norepi
  • phenylephrine
  • amrinone
48
Q

which vasoactive agent has largest effect on heart rate?

A

epi

49
Q

which vasoactive agents have largest effects on contractility?

A

dobutamine
epi
amrinone

50
Q

which vasoactive agents have largest effects on arterial constriction? which have opposite effects (dilation)

A

norepi
phenylephrine

dilators:
dobutamine
amrinone

51
Q

source control methods: sinusitis

A

surgical decompression of sinuses

52
Q

source control methods: pneumonia

A

-

53
Q

source control methods: empyema thoracis

A

-

54
Q

source control methods: mediastinitis

A
  • drainage
  • debridement
  • diversion
55
Q

source control methods: peritonitis

A
  • resection, repair, or diversion of ongoing sources of contamination
  • drainage of abscesses
  • debridement of necrotic tissues
56
Q

source control methods: cholangitis

A

-bile duct decompression

57
Q

source control methods: pancreatic infection

A

-drainage or debridement

58
Q

source control methods: UTI

A
  • drainage of abscesses
  • relief of obstruction
  • removal or changing of infected catheters
59
Q

source control methods: catheter-related bacteremia

A

-removal of catheter

60
Q

source control methods: endocarditis

A

-valve replacement

61
Q

source control methods: septic arthritis

A

-joint drainage and debridement

62
Q

source control methods: soft tissue infection

A

-debridement of necrotic tissue and drainage of discrete abscesses

63
Q

source control methods: prosthetic device infeciton

A

-device removal

64
Q

mortality rates with sepsis:

  • general
  • SIRS only
  • sepsis only
  • severe sepsis only
  • septic shock only
A

10-50% - increases with severity of sepsis

  • SIRS: 7%
  • sepsis: 16%
  • severe sepsis: 20%
  • septic shock: 46%
65
Q

what mediates methicillin resistance?

A

PBP2a - PBP encoded by mecA gene

66
Q

where is mecA located?

A

on a mobile genetic element (staph chromosome cassette SCCmec)

67
Q

what is the leading cause of surgical site infections?

A

HA-MRSA

68
Q

diagnosis of HA-MRSA electrophoresis?

A

USA100 or USA200 pulse-field pattern

69
Q

difference in type of infection associated with HA-MRSA vs. CA-MRSA

A

HA: severe, invasive disease

CA: skin and soft tissue infections in healthy young persons, community outbreaks

70
Q

diagnosis of CA-MRSA electrophoresis?

A

USA300 or USA400 pulse-field pattern

71
Q

risk factors for MRSA

A
  • recent hospitalization
  • residence in long-term care facility
  • recent antibiotic therapy***
  • HIV
  • MSM
  • injection drug use
  • hemodialysis
  • incarceration
  • military
  • sharing needles, razors, or other sharps
  • sharing sports equipment
  • diabetes
  • prolonged hospital stay
72
Q

what was the likely mechanism that brought about MRSA?

A

antibiotic selective pressure

-abx use (especially cephalosporin and fluoroquinoline) correlated with risk for MRSA colonization and infection

73
Q

key components of the infection control program at the Billings Clinic to prevent/cut down prevalence of MRSA?

A
  • hand hygiene
  • decontamination of environment and equipment
  • contact precautions for infected and colonized patients
  • active surveillance cultures (ASCs)
74
Q

describe the active surveillance

A

nares culture on admission, discharge, transfer, or death

75
Q

what is the next threat on the horizon?

A

VRSA

ICM (26 decks)

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