representative infections in health systems due to gram positive pathogens Flashcards
define bacteremia
viable bacteria in the blood
bacteria in the blood becomes a bloodstream infection when _____
immune response mechanisms fail or are overwhelmed
what is CRITICAL with bacteremia
determining the primary source of the infection— may be the cause or consequence of another infection
what is the common etiology of hospital-acquired bacteremia
respiratory tract and indwelling catheters (central venous catheters)
what is the common etiology of community-acquired bacteremia
untreated UTIs
what is the common etiology of post-operative bacteremia
soft tissue and intraabdominal infections
what gram positive pathogen most commonly causes bacteremia
staphylococcus aureus
why has gram positive bacteremia increased over past decades
aging population, device-related procedures
which is most commonly associated with community-acquired bacteremia: gram positive or gram negative? and which pathogen is most common?
gram negative– escherichia coli is most common
bacteremia pathophysiology: reproducing bacteria may lead to septicemia with failure of _____ (2 things)
- cellular innate & adaptive immune responses responsible for initial microbe clearance
- liver and spleen filtration of active bacteria in the circulating blood
what are some complications of bacteremia
endocarditis, osteomyelitis, pneumonia, cellulitis, meningitis, progression to sepsis, multiorgan dysfunction that can be fatal
what is the classical presentation of bacteremia
fever.
chills/rigors do not need to be present, but indicate bacteremia
when bacteremia leads to sepsis and septic shock, it commonly causes ____
hypotension, altered mental status, and decreased urine output due to hypovolemia from leaky capillaries. other organs can become affected as the infection disseminates
diagnosis of bacteremia
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)
general approach to treatment for bacteremia ?
URGENT– delay associated with increased morbidity and mortality
APPROPRIATE antibiotics– broad spectrum, bactericidal, high dose, empiric antibiotics
antibiotic selection for bacteremia is based on
community or hospital acquired
recent healthcare exposure or surgery?
local antibiotic resistance (antibiogram)
rapid diagnostic tools
what antibiotic route is preferred for bacteremia
IV preferred initially
Oral when afebrile for greater than 48 hours, clinically improved and stable unless complicated by another infections, highly bioavailable drugs
what is the duration of treatment for bacteremia
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
when does the clock start for duration of therapy for bacteremia
from the first sterile blood culture and/or source control
how to evaluate therapeutic outcomes for bacteremia (clinical, microbiological)
clinical: resolved signs & symptoms, source control, drug specific toxicity, no complicating infections
microbiological: susceptibility data, sterilization of blood cultures
classifications of infective endocarditis
acute or subacute, native or prosthetic valve, community or healthcare acquired, by microbiological etiology
impact of infective endocarditis
high mortality, fatal without antimicrobial therapy, staph. aureus associated with healthcare and acute bacterial
risk factors for infective endocarditis
predisposing heart conditions, people who inject drugs
what predisposing heart conditions are high risk per AHA (name 4)
- an artificial (prosthetic) heart valve, including bioprosthetic and homograft valves
- previous bacterial endocarditis
- complex cyanotic congenital heart disease
- surgically constructed shunts or conduits
what is the pathogenesis of infective endocarditis
- pathogen accesses bloodstream (dental, IV, catheter, PWID)
- adheres to valve surface (abnormal blood flow predisposes)
- pathogen persists and proliferates– vegetation forms (fibrin, platelets, bacterial haven)
- pathogen disseminates (metastatic infections)
what are 3 complications of infective endocarditis
embolization, heart failure, peri annular extension
what can embolization result in
metastatic infections
what are the most common microbiological etiologies of IE
streptococci, staphylococci, enterococci
what are the etiologies of native valve IE?
viridans streptococci, staphylococci aureus, enterococci
what are the etiologies of prosthetic valve IE?
coagulase negative staph, staph aureus
signs and symptoms of IE
fever, chills, weak, dyspnea, cough, dyspnea on exertion, night sweats, weight loss, malaise, fatigue
physical exam findings of IE
fever, heart murmur, heart failure signs, EKG changes, neurological deficits, embolic phenomena
what embolic phenomena are signs of IE
splenomegaly, roth spots, splinter hemorrhages, skin (osler’s nodes, janeway lesion)
labs & tests for IE?
normal/increased WBC
anemia, thrombocytopenia
increased ESR, CRP
proteinuria, hematuria, pyuria
valvular vegetation on echo
positive blood cultures
abnormal chest x-ray
approach to therapy for IE
bactericidal, high dose, IV, long duration (6 weeks or more)– starting at the time of source control and sterilized blood cultures
what is the rationale for the long treatment course of IE
organisms produce biofilm on valve structure; difficult to penetrate vegetation. non-reproductive bacterial growth phase. high risk of recurrence
IE evaluation of therapeutic outcomes
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
the microbiological etiology of meningitis varies by ___
age and other risk factors
etiology for meningitis in neonates
strep agalactiae, e. coli
etiology for meningitis in small children
strep. pneumoniae, neisseria meningitidis
etiology for meningitis in older children/young adults
neisseria meningitidis
etiology for meningitis in older adults
strep. pneumoniae
etiology for meningitis in immunocompromised, <3 months old, or >50 years old
listeria monocytogenes
etiology for nosocomial meningitis
aerobic GNRs
etiology for meningitis in adults
strep. pneumoniae, strep. agalactiae, neisseria meningitidis, listeria monocytogenes, haemophilus influenzae
what are 3 sources of pathogen entry for meningitis
- nasopharyngeal colonization followed by inflammation
- direct inoculation
- para meningeal focus
how does meningitis happen from nasopharyngeal colonization?
(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
how does meningitis happen by direct inoculation
CSF catheter, trauma
how does meningitis happen by para meningeal focus
middle ear or paranasal sinus infection
what are patient symptoms of meningitis
headache, fever, neck stiffness, confusion, photophobia, nausea, vomiting, seizures, rash
physical exam findings of meningitis
nuchal rigidity, meningismus, altered mental status, neurologic deficits
what are lab findings of meningitis
CSF analysis: increased WBC (neutrophils predominate), increased protein, decreased glucose
other: culture, PCR
general approach to meningitis treatment
-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
what is the empiric antibacterial backbone of meningitis treatment
3rd generation cephalosporin (ceftriaxone or cefotaxime) + IV Vancomycin
if risk for nosocomial GNR- ceftazidime or cefepime
what antibiotic do you add for listeria monocytogenes risk?
IV ampicillin
why do we do high doses for meningitis?
to penetrate the blood brain barrier to access the CSF
what is infective arthritis
inflammatory reaction within joint space associated with purulent effusion
when is infective arthritis most common
young children, elderly, rheumatoid arthritis
what is osteomyelitis
inflammation of bone, especially the marrow
when is osteomyelitis most common
can affect any bone, persons of all age
classifications of infectious arthritis
- duration of illness (acute <7 days, chronic >7 days)
- mechanism of infection
- microbiologic etiology (gonococcal, nongonococcal)
- number of joints affected (monoarticular, polyarticular)
- native or prosthetic joint
classifications of osteomyelitis
- duration of illness (acute: recent onset symptoms for 1 week, chronic longer than 1-4 weeks/initial infection relapse)
- mechanism of infection
- presence or absence of peripheral vascular disease (PVD) and vascular insufficiency
- portion of bone affected
- patient’s physiologic status
- local environment
hematogenous
infection that results from spread through the bloodstream
direct inoculation
infection that results from a source outside the body
contiguous spread
infection that results from progressive spread from an adjacent site (soft tissue infection to bone, or bone to joint)
______ is a risk factor for osteomyelitis
peripheral vascular disease (PVD) that causes decreased vascular supply
name the mechanisms of infection of infectious arthritis
- usually by hematogenous spread– highly vascular synovial tissue, no basement membrane, easy access for pathogens
- also by direct inoculation with a deep penetrating wound, intra-articular steroid injections, arthroscopy, prosthetic joint surgery
- may be acquired by contiguous mechanism– contiguous osteomyelitis expansion into joint (neonates)
most infective arthritis infections are ____articular
monoarticular
what is the most common site of infective arthritis
knee
name the mechanisms of infection of osteomyelitis
- 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
- direct inoculation from penetrating wound, open fractures, invasive orthopedic procedures (surgery)
- contiguous spread from injected tissue adjacent to bone (multiple bones may be affected if PVD involved)
what are the most common bacterial pathogens of infectious arthritis in adults
mostly: staph aureus, strep
less often gram negative: E. coli (most common), pseudomonas aeruginosa (PWID), neisseria gonorrhoeae (adults in developing countries)
what is the most common bacterial pathogen of infectious arthritis in children <3 years old
K. kingae
what is the most common bacterial pathogen of infectious arthritis in children >4 years old
S. aureus
most common etiologies of osteomyelitis
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
clinical presentation of infectious arthritis
painful swollen joint in absence of trauma, restriction of joint motion, warmth at joint, fever (children), tenderness/ redness/ effusion at the joint
clinical presentation of osteomyelitis
pain, tenderness, swelling, restriction of motion in the area of the affected bone
fever, chills, malaise
lab/diagnostic tests for infectious arthritis
-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
lab/diagnostic tests in osteomyelitis
-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
general approach to treatment for infectious arthritis or osteomyelitis
early and appropriate empiric antibiotic therapy– typically initiate empiric therapy before pathogen identified
pearls for empiric therapy for infectious arthritis
empiric selection based on gram stain of synovial fluid. combination therapy for prosthetic joint infection often includes rifampin
general points for antibiotics for osteomyelitis or infectious arthritis
-start with high dose IV– oral therapy only after resolving signs/symptoms in select patients
what is associated with failures and complications such as loss of limb or life
compromised immune systems/vascular supply and short courses
how to achieve source control for infectious arthritis
joint drainage
how to achieve source control for osteomyelitis
surgical debridement of bone
duration of therapy for infectious arthritis
3-4 weeks in adults
10 days in children with normalized CRP
duration of therapy for osteomyelitis
4-6 weeks in adults, 8 weeks for MRSA.
in acute hematogenous osteomyelitis in children 3 weeks minimum (some still do 4-6 weeks)
ways to classify necrotizing fasciitis
- by anatomy
-fournier’s gangrene: perineum
-ludwig’s angina: submandibular space
-cervical - by depth of involvement
-superficial fascia
-subcutaneous/adipose tissue
-fascia - by microbial source (Type I-IV)
what depths are NOT necrotizing fasciitis
dermis, muscle (myonecrosis)
Type _ necrotizing fasciitis is the most common
I
accounts for 80% of all necrotizing soft tissue infections
what happens in type I
anaerobes and facultative bacteria act synergistically to cause destruction of fat and fascia
what happens in type II
streptococcal gangrene; flesh eating bacteria— rapidly extending necrosis (24-72 hr) of sc tissues/skin, gangrene, severe local pain, systemic toxicity
type II is highly associated with ___
early onset shock, organ failure
increasing MRSA
type III involves _____
skeletal muscle
type III how common?
less than 5% of all NSTIs
Type __ necrotizing fasciitis is the most rare
IV
what is the etiology of type IV
fungal (candida)– traumatic wounds, burns, severe IC
type I is ____microbial
poly
what are the risk factors for type I
DM, PVD, PWID, HIV, ETOH abuse, obesity, kidney failure, abscess, insect bite, surgery, GI perforation, cirrhosis, immune compromise
possible bacterial etiologies of Type I
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.
type II is ____microbial
mono
what pathogens cause type II
Group A strep (GAS- strep pyogenes)
S. aureus (often MRSA)
risk factors for type II
trauma, PWID, surgery, childbirth, burns, exposure
type III is ___microbial
mono
what pathogens cause type III
clostridium spp (C. perfringens)
vibrio vulnificus (salt water, seafood)
aeromonas spp (water, soil, wood)
risk factors for type III
trauma, surgery, PWID
clinical presentation of necrotizing fasciitis
difficult to differentiate early from cellulitis: hot, swollen, erythematous without margins, often shiny, exquisitely tender and painful
where does necrotizing fasciitis occur
any area but typically abdomen, perineum, lower extremities
what contrasts necrotizing fasciitis from cellulitis?
- severe pain, disproportional to clinical findings
- 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
necrotizing fasciitis requires _____ management
surgical!
IMMEDIATE/AGGRESSIVE debridement of all necrotic tissues is ESSENTIAL
if surgical debridement of necrotic tissue >14 hours after diagnosis–> Increased _____
patient mortality
non-surgical treatments of necrotizing fasciitis
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
