Intro To ID Flashcards
hallmark symptom of infection
fever
fever is what temperature
> 38C or 100.4 F
what is normal body temp
98-98.6 F
false positive causes of fever
drugs
-beta lactams
-sulfonamides
-anticonvulsants
false negative causes of fever
administration with antipyretics
(Tylenol, ibuprofen, ASA)
steroids
hypothermia
what drugs do we not give with antibiotics
antipyretics scheduled (can mask fever and response)
systemic signs of infection
blood pressure (SBP <90)
HR (tachycardia >90)
RR (>20)
increased/decreased WBC count
(>12k or <4k)
fever (>38C or <36C)
systemic inflammatory response syndrome (SIRS) warns us for risk of what
if 2+ criteria then risk of sepsis
what are the criteria for SIRS
HR
RR
fever
inc or dec in WBCs
why might WBCs be elevated
infection or non infection (leukemia/steroids)
mature neutrophils do what
most common WBC
fight infection
(first responders)
immature neutrophils are called what
bands
an increase in bands would indicate what
left shift
released by bone marrow
increased in infection
eosinophils are what
allergic reactions, parasites
(more specialized defense)
basophils are what
hypersensitivity reactions, release histamine
(alarm system)
lymphocytes are what
B and T cells
B cells do what
blueprint to create antibodies
T cells do what
assassins, kill affected cell
what are monocytes
macrophages, search for foreign material
(take out the trash)
leukocytosis is an increase in what
neutrophils +/- bands
leukocytosis indicates what kind of infection
bacterial
leukopenia is what
low WBC count, could be sign of overwhelming infection and poor prognosis
what is lymphocytosis
increased B and T cells
what kind of infection do we see lymphocytosis
viral, fungal, TB
what is an ANC
absolute neutrophil count
seggs + bands
what is neutropenia
ANC < 500
ANC < 100 is profound
when do we start to worry about opportunistic organisms with ANC decreasing
< 1000
what are the acute phase reactants we can use to check for infection?
ESR
CRP
procalcitonin
ESR normal values
male : 0-15 mm/hr
female: 0-20 mm/hr
CRP normal value
< 0.5mg/dL
can we use CRP and ESR to confirm infection
NO, non-specific
we use to monitor over time and check trends
procalcitonin normal value
< 0.05 mcg/L
procalcitonin used for what
more specific bacterial
serial measure every 1-2 days to assess response to therapy and de-escalate
when do we want to sample infected body materials?
before initiation of antibiotic therapy
what is contamination
introduction of an organism into the clinical specimen during sample collection or process
who do we want to obtain blood cultures in and how
all acutely ill febrile patients
1 set on each arm (aerobic and anaerobic)
preferably 1 hr apart
what would happen if organism grew in both aerobic and anaerobic
might be a contaminant
colonization vs infection
colonization is a potentially pathogenic organism presnet but not invading host andnot iliciting a response so NO symptoms
infection is damaging and eliciting a host response
what is MIC
minimum inhibitory concentration
lowest concentration that prevents visibile growth
what is a breakpoint
highest possible plasma concentration of drug that is safe
what does suseptible mean
MIC is less than the breakpoint, likely efficacious
what does intermediate men
MIC approaching the breakpoint, might be effective at higher doses
what does resistant mean
MIC greater than breakpoint
can’t achieve safe concentrations
what is non suseptible
does not respond to the antibiotic, no MIC
what is suseptible dose dependent
have to use higher doses than normal to achieve efficacy
gold standard for MIC testing
broth dilution
Kirby Bauer disk testing does what
can not show us MIC
measures zone of inhibition and we can see suseptibility
what can we find from gradient test strips
MIC
where ellipse intersects
(used with newer agents,expensive)
what is empiric therapy
targets the typical pathogens
before we have identification and suseptibility of organism
usually very broad
what is targeted or directed therapy
once we have identified the organism and suseptibility is known we switch the therapy
de-escalation
going from empiric to targeted
want the narrowest spectrum of activity
can be stepwise or all at once
what is a spectrum of activity
what bugs does the drug cover
definition of antibimrobial stewardship
interventions defined to improve appropriate use of antibiotics by promoting selection of optimal drug regimen, dosing, duration of therapy, and route of admin
what color is gram positive
purple
what color is gram negative
pink
characteristics of cell wall gram positive
thick cell wall
characteristics of cell wall gram negative
thin cell wall
how do atypical bacteria stain
they dont stain
what are acid fast bacilli
resistant to acids/ethanol
mycobacterium species
what is alpha hemolysis
partial hemolysis
what is beta hemolysis
full hemolysis
what is gamma hemolysis
no hemolysis
most medically important pathogens are what for gram positive
cocci
which bacteria form clusters
staphw
which bacteria form pairs/chains
strep + entero
what does catalase differentiate?
clusters from chains/pairs
(staph from strep)
what does coagulase differentiate
staph aureus from CoNS
alpha hemolysis represents which flora
oral flora
beta hemolysis represents which flora
skin, pharynx, genitourinary
gamma hemolysis represents which flora
GI
what can oxidase test do
distinguish enteric vs non
what are fastidious organisms
slow growers
require special supplemental media
gram positive cell wall structure
thick cell wall
periplasmic space
gram negative cell sructure
thin cell wall
lipopolysaccharides
porins
what are penicillin binding proteins
vital for cell wall synthesis, shape, structure
ex. transpeptidases
what do transpeptidases do
final cross linking in the peptidoglycan structure
what do lipopolysaccharides do
mediator of immune response
what do porins do
hydrophillic channels that permit diffusion of essential nutrients and hydrophillic molecules
what does the periplasmic space do
bacterial protien secretion, folding
where is the periplasmic space
gram +: between cell wall and cell membrane
gram - : between cell membrane and outer membrane
mechanisms of intrinisc resistnace
absence of target site
bacterial cell impermeability
mechanisms of acquired resistance
mutation in bacteria
acquisition of new DNA
what is a plasmid
DNA that is transferable between organisms
what is a transposon
move from plasmid to chromosome
what is a phage
virus that can transfer DNA from organism to organism
what is conjugation
trade bracelets
most common
direct contact
what is transduction
transver of genes between bacteria by phages
(give a bracelet and run away)
what is transformation
picks up DNA from environment
pick up a bracelet
4 mechanisms of antibiotic resistance
efflux pumps
decreased porin production
drug inactivating enzyme
modified drug target
what are beta lactamases
enzyme tht hydrolyze the beta lactam by splitting amide bond and opening the ring
types of beta lactamases
serine and metallica
Ambler class A beta lactamases
ESBLs
serine carbapenemases
Ambler class B beta lactamase
metallo beta lactamase
Ambler class C beta lactamase
cephalosporinases
Ambler class D beta lactamases
OXA- type
examples of beta lactams
penicillins
cephalosporins
carbapenems
cephamycins
monobactams
clavams
ESBL enzyme
CTX-M-15
serine carbapenemase enzyme
KPC
metallo beta lactamse enzyme
NDM-
cephalosporinase enzyme
amp-c
OXA-type enzyme
OXA-48
ESBLs most prevalent in which bacteria
e. coli
Klebsiella pnemoniae / oxytoca
proteus mirabilis
treatment for ESBLs
carbapenems
carbapenemase most prevalent in which bacterias
Klebsiella pneumoniae / oxytoca
e. coli
proteus mirabilis
e. coloacae
e. aerogenes
treatment for carbapenemase
meropenem + bactam
metallo beta lactamases treatment
aztreonam + ceftazidine /avibactam
very limited, we cant inhibit with beta lactamase inhibitors
cefiderocol is trojan horse
OXA- type found in what bacteria
acinetobacter aumannii
pseudomonas aeruginosa
treatment for OXA type
cefiderocol
sulfabactam
treatment for ESBL urinary
piperacillin/tazobactam
which beta lactamase is inducible
AmpC
AmpC inducer organisms
Hafnia alvei
Enterobacter cloacae
Citrobacter freundii
Klebsiella aerogenes
Yersinia enterocolitica
Serratia marcescens
Morganella morganii
Aeromonas hydrophila
heck yes maam
which common drug is high risk suseptibility to AmpC hydrolysis
ceftriaxone
what do we give if stably depressed mutants? if initially suseptible and then resistant
cefepime 1st
carbapenem
non beta lactams
aminoglycoside resistance happens how
aminoglycoside modifying enzymes
acetylation
nucleotidylation
phosphorylation
impairs cellular uptake and binding
vancomycin resistance looks like what on a test
Van A or VanB present
produces vancomycin resistant enterococccus (VRE)
treatment for vancomycin resistant enterococcus
linezolid
daptomycin
how does vancomycin resistance work
altered target site
penicillin binding protein resistance happens how
decreased affinity of PBPs for antibiotic or decreased PBPs produced by bacteria
would a beta lactamase inhibitor help with penicilinn binding protein resistance
no since it is an altered target not an enzyme
how would we know if someone had methicillin resistance staph aureus?
mecA or PBP2A gene
what does the mecA gene mean
MRSA
treatment for MRSA
ceftaroline
ceftobiprole
vancomycin
linezolid
daptomycin
efflux resistance important for what
pseudomonas aeruginosa against carbapenems
sterp nerumonia against macrolides
porin channel resistnace important for what
seen in enterobacterales and carbapenem resistnt pseduomonas aeurginosa
bacteriocidal
bacteria actively being killed
bacteriostatic
inhibiting bacterial replication without killing the organism
which classes exhinit PAE (post antibiotic effect)
concentration dependent
(aminoglycosides and fluroquinolones)
also vanc
aminoglycosides activity measured how
Cmax/MIC
AUC/MIC
fluroquinolones activity measured how
AUC/MIC
optimal dose of aminoglycosides found how
high dose and extended interval
therapeutic drug monitoring
which drug classes are time dependent
beta lactams
which drug classes are concentration dependent
aminoglycosides
fluroquinolones
how are time dependent drugs optimized
fT>MIC
time above MIC
do beta lactams have PAE
no, time dependent
dosing optimization for carbapenems
> 40%
dosing optimization for penicillins
> 50%
dosing optimization for cephalosporins
> 60%
how can we maximize ft>MIC
increase the dose and keep same interval
same dose shorter interval
continuous infusion
prolonged infusion
is vancomycin time dependent or concentration dependent
both - more time dependent tho
PD target for vanc
AUC/MIC
what is the PAE like for vancomycin
very long for gram positivw
prolonged and elevated AUC in vancomycin patients can lead to what
nephrotox
