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ID2 > representative infections in health systems due to gram positive pathogens > Flashcards

representative infections in health systems due to gram positive pathogens Flashcards

1
Q

define bacteremia

A

viable bacteria in the blood

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2
Q

bacteria in the blood becomes a bloodstream infection when _____

A

immune response mechanisms fail or are overwhelmed

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3
Q

what is CRITICAL with bacteremia

A

determining the primary source of the infection— may be the cause or consequence of another infection

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4
Q

what is the common etiology of hospital-acquired bacteremia

A

respiratory tract and indwelling catheters (central venous catheters)

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5
Q

what is the common etiology of community-acquired bacteremia

A

untreated UTIs

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6
Q

what is the common etiology of post-operative bacteremia

A

soft tissue and intraabdominal infections

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7
Q

what gram positive pathogen most commonly causes bacteremia

A

staphylococcus aureus

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8
Q

why has gram positive bacteremia increased over past decades

A

aging population, device-related procedures

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9
Q

which is most commonly associated with community-acquired bacteremia: gram positive or gram negative? and which pathogen is most common?

A

gram negative– escherichia coli is most common

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10
Q

bacteremia pathophysiology: reproducing bacteria may lead to septicemia with failure of _____ (2 things)

A
  • cellular innate & adaptive immune responses responsible for initial microbe clearance
  • liver and spleen filtration of active bacteria in the circulating blood
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11
Q

what are some complications of bacteremia

A

endocarditis, osteomyelitis, pneumonia, cellulitis, meningitis, progression to sepsis, multiorgan dysfunction that can be fatal

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12
Q

what is the classical presentation of bacteremia

A

fever.
chills/rigors do not need to be present, but indicate bacteremia

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13
Q

when bacteremia leads to sepsis and septic shock, it commonly causes ____

A

hypotension, altered mental status, and decreased urine output due to hypovolemia from leaky capillaries. other organs can become affected as the infection disseminates

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14
Q

diagnosis of bacteremia

A

IDENTIFY THE SOURCE
Initial labs in all bacteremic patients should include blood cultures: ideally 2 sets assessing for aerobic and anaerobic organisms from each arm
WBC are often elevated (non specific)

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15
Q

general approach to treatment for bacteremia ?

A

URGENT– delay associated with increased morbidity and mortality
APPROPRIATE antibiotics– broad spectrum, bactericidal, high dose, empiric antibiotics

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16
Q

antibiotic selection for bacteremia is based on

A

community or hospital acquired
recent healthcare exposure or surgery?
local antibiotic resistance (antibiogram)
rapid diagnostic tools

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17
Q

what antibiotic route is preferred for bacteremia

A

IV preferred initially
Oral when afebrile for greater than 48 hours, clinically improved and stable unless complicated by another infections, highly bioavailable drugs

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18
Q

what is the duration of treatment for bacteremia

A

based on source and source control
gram positive bacteria may range up to 14 days
if complicating infections present may be 4-6 weeks or longer

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19
Q

when does the clock start for duration of therapy for bacteremia

A

from the first sterile blood culture and/or source control

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20
Q

how to evaluate therapeutic outcomes for bacteremia (clinical, microbiological)

A

clinical: resolved signs & symptoms, source control, drug specific toxicity, no complicating infections
microbiological: susceptibility data, sterilization of blood cultures

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21
Q

classifications of infective endocarditis

A

acute or subacute, native or prosthetic valve, community or healthcare acquired, by microbiological etiology

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22
Q

impact of infective endocarditis

A

high mortality, fatal without antimicrobial therapy, staph. aureus associated with healthcare and acute bacterial

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23
Q

risk factors for infective endocarditis

A

predisposing heart conditions, people who inject drugs

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24
Q

what predisposing heart conditions are high risk per AHA (name 4)

A
  1. an artificial (prosthetic) heart valve, including bioprosthetic and homograft valves
  2. previous bacterial endocarditis
  3. complex cyanotic congenital heart disease
  4. surgically constructed shunts or conduits
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25
Q

what is the pathogenesis of infective endocarditis

A
  1. pathogen accesses bloodstream (dental, IV, catheter, PWID)
  2. adheres to valve surface (abnormal blood flow predisposes)
  3. pathogen persists and proliferates– vegetation forms (fibrin, platelets, bacterial haven)
  4. pathogen disseminates (metastatic infections)
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26
Q

what are 3 complications of infective endocarditis

A

embolization, heart failure, peri annular extension

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27
Q

what can embolization result in

A

metastatic infections

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28
Q

what are the most common microbiological etiologies of IE

A

streptococci, staphylococci, enterococci

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29
Q

what are the etiologies of native valve IE?

A

viridans streptococci, staphylococci aureus, enterococci

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30
Q

what are the etiologies of prosthetic valve IE?

A

coagulase negative staph, staph aureus

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31
Q

signs and symptoms of IE

A

fever, chills, weak, dyspnea, cough, dyspnea on exertion, night sweats, weight loss, malaise, fatigue

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32
Q

physical exam findings of IE

A

fever, heart murmur, heart failure signs, EKG changes, neurological deficits, embolic phenomena

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33
Q

what embolic phenomena are signs of IE

A

splenomegaly, roth spots, splinter hemorrhages, skin (osler’s nodes, janeway lesion)

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34
Q

labs & tests for IE?

A

normal/increased WBC
anemia, thrombocytopenia
increased ESR, CRP
proteinuria, hematuria, pyuria
valvular vegetation on echo
positive blood cultures
abnormal chest x-ray

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35
Q

approach to therapy for IE

A

bactericidal, high dose, IV, long duration (6 weeks or more)– starting at the time of source control and sterilized blood cultures

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36
Q

what is the rationale for the long treatment course of IE

A

organisms produce biofilm on valve structure; difficult to penetrate vegetation. non-reproductive bacterial growth phase. high risk of recurrence

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37
Q

IE evaluation of therapeutic outcomes

A

clinical: resolving signs & symptoms (including metastatic infections), source control, adherence, drug specific toxicity, heart function at treatment completion (EOT echo)
microbiological: susceptibility data, sterilized blood cultures

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38
Q

the microbiological etiology of meningitis varies by ___

A

age and other risk factors

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39
Q

etiology for meningitis in neonates

A

strep agalactiae, e. coli

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40
Q

etiology for meningitis in small children

A

strep. pneumoniae, neisseria meningitidis

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41
Q

etiology for meningitis in older children/young adults

A

neisseria meningitidis

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42
Q

etiology for meningitis in older adults

A

strep. pneumoniae

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43
Q

etiology for meningitis in immunocompromised, <3 months old, or >50 years old

A

listeria monocytogenes

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44
Q

etiology for nosocomial meningitis

A

aerobic GNRs

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45
Q

etiology for meningitis in adults

A

strep. pneumoniae, strep. agalactiae, neisseria meningitidis, listeria monocytogenes, haemophilus influenzae

46
Q

what are 3 sources of pathogen entry for meningitis

A
  1. nasopharyngeal colonization followed by inflammation
  2. direct inoculation
  3. para meningeal focus
47
Q

how does meningitis happen from nasopharyngeal colonization?

A

(i.e. upper respiratory infection)–> allows access to the bloodstream (bacteremia and hematogenous spread to the CNS)–> pathogen evades immune system–> bacteria secrete enzymes that degrade protective immunoglobulins in nasal secretions that otherwise inhibit colonization—> bacteria with polysaccharide capsules resist neutrophil phagocytosis complement opsonization

48
Q

how does meningitis happen by direct inoculation

A

CSF catheter, trauma

49
Q

how does meningitis happen by para meningeal focus

A

middle ear or paranasal sinus infection

50
Q

what are patient symptoms of meningitis

A

headache, fever, neck stiffness, confusion, photophobia, nausea, vomiting, seizures, rash

51
Q

physical exam findings of meningitis

A

nuchal rigidity, meningismus, altered mental status, neurologic deficits

52
Q

what are lab findings of meningitis

A

CSF analysis: increased WBC (neutrophils predominate), increased protein, decreased glucose
other: culture, PCR

53
Q

general approach to meningitis treatment

A

-typically start antimicrobial therapy empirically then based on patient specific CSF culture data (obtaining CSF fluid may be delayed for pt. safety)
-antibacterial and antiviral (acyclovir) often both initiated

54
Q

what is the empiric antibacterial backbone of meningitis treatment

A

3rd generation cephalosporin (ceftriaxone or cefotaxime) + IV Vancomycin

if risk for nosocomial GNR- ceftazidime or cefepime

55
Q

what antibiotic do you add for listeria monocytogenes risk?

A

IV ampicillin

56
Q

why do we do high doses for meningitis?

A

to penetrate the blood brain barrier to access the CSF

57
Q

what is infective arthritis

A

inflammatory reaction within joint space associated with purulent effusion

58
Q

when is infective arthritis most common

A

young children, elderly, rheumatoid arthritis

59
Q

what is osteomyelitis

A

inflammation of bone, especially the marrow

60
Q

when is osteomyelitis most common

A

can affect any bone, persons of all age

61
Q

classifications of infectious arthritis

A
  1. duration of illness (acute <7 days, chronic >7 days)
  2. mechanism of infection
  3. microbiologic etiology (gonococcal, nongonococcal)
  4. number of joints affected (monoarticular, polyarticular)
  5. native or prosthetic joint
62
Q

classifications of osteomyelitis

A
  1. duration of illness (acute: recent onset symptoms for 1 week, chronic longer than 1-4 weeks/initial infection relapse)
  2. mechanism of infection
  3. presence or absence of peripheral vascular disease (PVD) and vascular insufficiency
  4. portion of bone affected
  5. patient’s physiologic status
  6. local environment
63
Q

hematogenous

A

infection that results from spread through the bloodstream

64
Q

direct inoculation

A

infection that results from a source outside the body

65
Q

contiguous spread

A

infection that results from progressive spread from an adjacent site (soft tissue infection to bone, or bone to joint)

66
Q

______ is a risk factor for osteomyelitis

A

peripheral vascular disease (PVD) that causes decreased vascular supply

67
Q

name the mechanisms of infection of infectious arthritis

A
  1. usually by hematogenous spread– highly vascular synovial tissue, no basement membrane, easy access for pathogens
  2. also by direct inoculation with a deep penetrating wound, intra-articular steroid injections, arthroscopy, prosthetic joint surgery
  3. may be acquired by contiguous mechanism– contiguous osteomyelitis expansion into joint (neonates)
68
Q

most infective arthritis infections are ____articular

A

monoarticular

69
Q

what is the most common site of infective arthritis

A

knee

70
Q

name the mechanisms of infection of osteomyelitis

A
  1. hematogenous: more common in tubular bones of children. vertebral (spine) osteomyelitis is more common in patients >50 yo. vascular structure of long bones predisposes to infection. sickle cell diseases, PWID
  2. direct inoculation from penetrating wound, open fractures, invasive orthopedic procedures (surgery)
  3. contiguous spread from injected tissue adjacent to bone (multiple bones may be affected if PVD involved)
71
Q

what are the most common bacterial pathogens of infectious arthritis in adults

A

mostly: staph aureus, strep
less often gram negative: E. coli (most common), pseudomonas aeruginosa (PWID), neisseria gonorrhoeae (adults in developing countries)

72
Q

what is the most common bacterial pathogen of infectious arthritis in children <3 years old

A

K. kingae

73
Q

what is the most common bacterial pathogen of infectious arthritis in children >4 years old

A

S. aureus

74
Q

most common etiologies of osteomyelitis

A

Hematogenous: S. aureus most common, PWID also pseudomonas aeruginosa, H. flu was common in children prior to vaccines, salmonella spp in sickle cell
Direct inoculation and contiguous spread: S. aureus most common. multiple organisms (polymicrobial): E. coli, pseudomonas aeruginosa, strep species, staph. epidermidis

75
Q

clinical presentation of infectious arthritis

A

painful swollen joint in absence of trauma, restriction of joint motion, warmth at joint, fever (children), tenderness/ redness/ effusion at the joint

76
Q

clinical presentation of osteomyelitis

A

pain, tenderness, swelling, restriction of motion in the area of the affected bone
fever, chills, malaise

77
Q

lab/diagnostic tests for infectious arthritis

A

-increased ESR, CRP
-increased serum WBC with left shift differential
(in acute infection ESR, CRP, WBC may be norm)
-positive blood culture
- needle aspiration of joint (synovial fluid): purulent fluid, gram stain results, synovial fluid culture, WBC 50-200, WBC differential with >90% PMLs, decreased glucose, increased lactic acid

78
Q

lab/diagnostic tests in osteomyelitis

A

-increased ESR, CRP
-WBC/differential: increased WBC with left shift in acute, may be normal in chronic
-blood cultures- positive in 50% with hematogenous
-X-ray bone changes 10-14 days after onset, 50% of bone matrix must be decalcified to detect
-MRI: most sensitive, common, positive within 1 day of onset
-bone aspirations or bone biopsy for bacterial etiology and to detect abscess
-culture of abscess: useful in acute disease

79
Q

general approach to treatment for infectious arthritis or osteomyelitis

A

early and appropriate empiric antibiotic therapy– typically initiate empiric therapy before pathogen identified

80
Q

pearls for empiric therapy for infectious arthritis

A

empiric selection based on gram stain of synovial fluid. combination therapy for prosthetic joint infection often includes rifampin

81
Q

general points for antibiotics for osteomyelitis or infectious arthritis

A

-start with high dose IV– oral therapy only after resolving signs/symptoms in select patients

82
Q

what is associated with failures and complications such as loss of limb or life

A

compromised immune systems/vascular supply and short courses

83
Q

how to achieve source control for infectious arthritis

A

joint drainage

84
Q

how to achieve source control for osteomyelitis

A

surgical debridement of bone

85
Q

duration of therapy for infectious arthritis

A

3-4 weeks in adults
10 days in children with normalized CRP

86
Q

duration of therapy for osteomyelitis

A

4-6 weeks in adults, 8 weeks for MRSA.
in acute hematogenous osteomyelitis in children 3 weeks minimum (some still do 4-6 weeks)

87
Q

ways to classify necrotizing fasciitis

A
  1. by anatomy
    -fournier’s gangrene: perineum
    -ludwig’s angina: submandibular space
    -cervical
  2. by depth of involvement
    -superficial fascia
    -subcutaneous/adipose tissue
    -fascia
  3. by microbial source (Type I-IV)
88
Q

what depths are NOT necrotizing fasciitis

A

dermis, muscle (myonecrosis)

89
Q

Type _ necrotizing fasciitis is the most common

A

I
accounts for 80% of all necrotizing soft tissue infections

90
Q

what happens in type I

A

anaerobes and facultative bacteria act synergistically to cause destruction of fat and fascia

91
Q

what happens in type II

A

streptococcal gangrene; flesh eating bacteria— rapidly extending necrosis (24-72 hr) of sc tissues/skin, gangrene, severe local pain, systemic toxicity

92
Q

type II is highly associated with ___

A

early onset shock, organ failure
increasing MRSA

93
Q

type III involves _____

A

skeletal muscle

94
Q

type III how common?

A

less than 5% of all NSTIs

95
Q

Type __ necrotizing fasciitis is the most rare

A

IV

96
Q

what is the etiology of type IV

A

fungal (candida)– traumatic wounds, burns, severe IC

97
Q

type I is ____microbial

A

poly

98
Q

what are the risk factors for type I

A

DM, PVD, PWID, HIV, ETOH abuse, obesity, kidney failure, abscess, insect bite, surgery, GI perforation, cirrhosis, immune compromise

99
Q

possible bacterial etiologies of Type I

A

anaerobes:
-bacteroides spp
- peptostreptococcus spp (aka finegoldia)
- fusobacterium spp
- clostridium spp

facultative bacteria:
- streptococcus spp.
-staphylococcus spp.
- enterococcus spp.
- enerobacterales (E. coli, Klebsiella spp)

aerobes:
-pseudomonas spp.
-acinetobacter spp.

100
Q

type II is ____microbial

A

mono

101
Q

what pathogens cause type II

A

Group A strep (GAS- strep pyogenes)
S. aureus (often MRSA)

102
Q

risk factors for type II

A

trauma, PWID, surgery, childbirth, burns, exposure

103
Q

type III is ___microbial

A

mono

104
Q

what pathogens cause type III

A

clostridium spp (C. perfringens)
vibrio vulnificus (salt water, seafood)
aeromonas spp (water, soil, wood)

105
Q

risk factors for type III

A

trauma, surgery, PWID

106
Q

clinical presentation of necrotizing fasciitis

A

difficult to differentiate early from cellulitis: hot, swollen, erythematous without margins, often shiny, exquisitely tender and painful

107
Q

where does necrotizing fasciitis occur

A

any area but typically abdomen, perineum, lower extremities

108
Q

what contrasts necrotizing fasciitis from cellulitis?

A
  1. severe pain, disproportional to clinical findings
  2. fails to respond to initial antibiotic therapy (regardless if IV or PO)
    -develop progressive redness and swelling despite antibiotics
    -followed by bullae with clear fluid
    -progresses rapidly
    -skin color change (maroon/violaceous)
    -after days evolves into frank cutaneous gangrene with myonecrosis
109
Q

necrotizing fasciitis requires _____ management

A

surgical!
IMMEDIATE/AGGRESSIVE debridement of all necrotic tissues is ESSENTIAL

110
Q

if surgical debridement of necrotic tissue >14 hours after diagnosis–> Increased _____

A

patient mortality

111
Q

non-surgical treatments of necrotizing fasciitis

A

antibiotics (broad empiric coverage, IV, ideally target suspected pathogens)
IV fluid replacement (maintain hydration bc wounds discharge large amounts of tissue fluid)
IVIG (may benefit streptococcal infections by neutralizing toxins, await pathogen ID)
hyperbaric oxygen potential benefit for clostridial myonecrosis

ID2 (13 decks)

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