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146 Cards in this Set

  • Front
  • Back
What is endocarditis?
inflamm of heart valves or endocardium almost always from infectious etiology
where is endocarditis likely to occur?
at area of turbulence, such as congenital heart lesions
at site of high P gradients across small orifices
the vegetations are downstream on low P side of gradient
pathgenesis of infective endocarditis?
microthrombi inplants in area of endocardial irregulartiy --> small sterile vegetation, which provides focus for bacterial seeding during transient bacteremia
Which organisms are most likely to adhere to sterile vegetations?
some strep viridans species (produce extracellular dextran which promotes adherence to platelet fibrin aggregates)
what are the organisms that can cause infective endocarditis?
strep viridans
staph aureus (coagulase + and -)
group D strep (esp S. bovis)
gram - rods (uncommon)
fungi (candida and aspergillus)
negative blood cultures
Which organism is the most common cause of subacute bacterial endo?
acute endo?
endo on prosthetic valve?
strep viridans
s. aureus (coagulase +)
s. aureus (coagulase -)
Which bacteria is commonly found in older men with endocarditis?
enterococci (from GU obstruction)
which bacteria is the marker organism for colon and other GI malig?
S. bovis (group D strep)
Which heart valves are commonly involved in SBE? acute?
M > A > T > P
A, and T (but variable)
Which type of endocarditis (acute or SBE) has emboli?
Neurologic findings?
what are some of the features of atypical presentation of endocarditis?
probs 2/2 embolism
renal failure (immune complex glomerulonephritis or renal infarction)
subarachnoid hemorrhage
meningitis (2/2 bacterial seeding)
brain abscess or epidural abscess
lab findings in endocarditis? (indicate which are acute and subacute)
anemia (more common in SBE, normochromic, normocytic)
high WBC in acute
ESR is hihg in SBE
microscopic hematuria (SBE)
How can endocarditis be detected?
TEE (transesophageal echo... detects vegetation in up to 90%)
how should treatment be initiated in acute endocarditis?
start AB after obtaining 2-3 blood cultures
SBE is less urgent, wait for cultures to become + before starting tx
what is the route of administration of AB in endocard?
how long shoul dtx be given for AB for endocarditis?
4-6 wks
SBE can be tx for 2 wks if organism is susceptable to penicillin
how is endocard therapy monitored?
serum bactericidal test (Schlicter test)
measures killing of pts organism based on leel of AB in pts blood
how is the Schlicter test performed? what is its utility?
dilute serum in serial fashion
greatest dilution that kills patient's bug = end point
it can predict bacteriologic but not clinical outcome
indications for surgical intervention of endocarditis?
progressive heart failure
valve dysfxn (perf cusp)
inability to control infecion
multiple or large emboli
fungal endocarditis (there are no cidal antifungal agents)
what is meant by "culture negative" endocarditis?
not detectable by conventional blood cultures, or can be noninfectious
how should culture negative endocarditis be tx?
don't tx empirically w/o ID consult
consider pts other illness
which organisms are "culture negative" in endo?
coxiella burnetti
what does a recurrence of fever indicate in endocard?
not d/t infection, can be from drugs
what is myocarditis?
inflamm process of cardiac muslce that may occur from organisms or the toxins they produce
si/sx of myocarditis?
many pts asymptomatic
can have arrhythmias, ekg abnormalities
fever/chest discomfort
elevated pulse, weak and thready
poor quality heart sounds
organisms that can --> myocard?
s. aureus
B. burgdorferi
rickettsia (RMSF)
Chagas disease (trypanosoma cruzi)
what viruses are most common for causing myocard?
coxsackie A and B
definition of pericarditis?
inflamm dz of pericardium that can be acute or chronic
pathogenesis of pericarditis?
hematogenous seedin gduring bacteremia or fungemia
direct extension from contiguous focus of infection
immune mech
viruses associated with pericarditis?
coxsackie B (most common)
coxsackie A
which BACTERIA are associated with pericarditis?
M. tuberculosis (2%, and esp in younger pts)
which fungi --> pericard?
which parasites --> pericard?
entameba histolytica (extension from amebic liver abscess)
ekg seen in pericarditis?
diffuse ST elevations
what is the best way to detect pericardial effusion?
what use is CXR in pericarditis?
may show enlarged cardiac silhouette if effusion is large
management of bacterial, fungal or parasitic pericarditis? (how to dx?)
get pericardial fluid for definitive dx (pericardiocentesis or open surgical procedure)
what causes constrictive percarditis?
late complication d/t scarring and shrinking pericardium
Definition of nosocomial FUO?
>38.3 C on several occassions
infection not present or incubating on admission
evaluation for 3 days
cultures for 2 days
if no dx, the FUO
HIV associated FUO?
>38.3 C on several occassions
+ HIV serology
Fever >4 weeks as outpt or 3 days in hospitalized pt
Definition of Neutropenic FUO?
>38.3 C on several occassions
Neutrophil count <500 or 1000 and dropping
Evaluation for 3 days
- cultures for 2 days
Which is the only type of fever that is treated empirically?
Neutropenic FUO because it can be deadly and is an EMERGENCY
all others... don't treat empircally b/c it can cause confusion
What is the fractional breakdown of FUO?
1/3 malignant
1/3 infectiion
1/3 collagen vascular dz/vasculitis
What is the most common ccause of a prolonged fever?
that they don't really have a fever at all... their body temp is just set higher than most
What is the least common cause of prolonged fever?
familial mediterranean fever
What are dry eyes associated with?
What is conjunctivitis associated with?
Cat Scratch
What are conjunctival petechiae associated with?
What is conjunctival suffusion associated with?
What are Roth spots associated with?
what are subconjunctival hemorrhages associated with?
infectious endocarditis
what is uveitis associated with?
What are Roth spots?
hemorrhagic lesions in fundus
What are WBC scans and what are they used for?
Remove pts WBC, tag them with radio isotopes and see where it goes... does it go to an abscess???
What does an increased alk. phos point to?
some sort of bone or liver dz
How to dx FUO?
Fever chart
If persists for 3 weeks, than FUO
D/c all nonessential meds, if it resolves = drug fever, if persists for >3 days, continue w/u
do abdominal CT and WBC scan; if no focus, is infectious endocarditis suspected? If no, do venous doppler
If -, is status deteriorating?
If not, just follow pt, if yes, do liver bx and laparotomy
What is sepsis?
Clinical evidence of infection and systemic response to the infection
What is Systemic Inflammatory Response Syndrome (SIRS)?
2+ of the following:
HR > 90 bpm
RR > 20/min
WBC > 12,000
What does + blood culture indicate?
indx of failure of host defenses to contain infection at primary focus
index of failure of dr to remove, drain, or otherwise tx infection
What is the indirect way taht bugs enter bloodstream?
What is the direct way?
through lymphatics
IV catheters, prosthetics, self injection (IV drug users)
When is clearing of organisms impaired?
if infection is overwhelming or if it has an intravascular foci
how do crticosteroids affect clearing of microorganisms?
don't affect clearing from blood, but they enhance the entry of organisms from tissue into blood b/c they suppress phagocytic cells at primary site of infection
Which cells are most important in clearing infection?
fixed macrophages in liver and spleen
Is unimicrobial or polymicrobial bacteremia more common?
who commonly gets polymicrobial bacteremia?
pts with intraabdominal infections and/or bowel obstruction and non-hematologic malignancies
Which bacteremia very commonly causes a transient pattern?
Acute bacterial meningitis
What can cause continuous bacteremia?
infective endocarditis, or some other endovascular infection
suppurative thrombophlebitis
infected aneurysm
early typhoid fever or brucellosis
What is the main source of bacteremia/fungemia?
IV catheter
What are hte 2 most common organisms of bacteremia/fungemia?
E coli
Which organisms if found in blood are likely just contaminants?
coagulase - staph
strep viridans
How much blood should be drawn to culture for bacteremia? Why?
20-30 ml for adults
The more blood you draw the more likely you are to get bacteria in the sample
1-5 ml in an infant
How to make a lab dx of bacteremia and fungemia?
2 blood cutlures (2 separate venipunctures)
A single culture will only detect 80-90% of episodes
A single culture that grows common skin flora is uninterpretable clinically
How should you culture for FUO?
2 blood cultures, if - after 48 hrs, repeat 2x more
How should cultures be given if endocarditis is suspected?
if acute, 3 BC over 1 hr, then start tx
If subacute, 3 BC of 24 hr, if - after 48 hrs, repeat 2x
What % die from bacteremia?
What are some of the risk factors for death in bacteremia/fungemia?
>70 yo
Fungi or enteric GNR (not E. coli)
Source in lungs, bowel or unknown
malignancy, AIDS, renal failure
No fever
Prescribing inappropriate antibiotics
Clinical syndrome of shock?
hypotension (systolic BP <80-90)
weak, thready pulse
cool, clammy skin
peripheral cyanosis
altered respiration (hyperventilation early, followed by hypoventilation)
change in mental status
What are some of the mediators of septic shock?
What are some of the endotoxins involved in septic shock?
most are from GNR, so LPS/lipoprotein outer membrane
Lipid A is very active
In animal models, endotoxin alone can ==> manifestations of septic shock
What do endotoxins do?
activate complement cascade
activates coagulation --> DIC
activates fibrinoloysis --> DIC
activates kinin system --> hypotension
pathophysiology of septic shock?
nidus of infections (caused by endogenous toxins or by activating endogenous mediators) --> activates various cytokines --> effects on myocardium itself (depression or dilatation) or effects on vasculature with both vasodiliatation and vasoconstriction --> maldistribution of blood flow
what is the prognosis of someone in septic shock?
50% recover
50% have multi organ failure and die
what are some of the skin manifestations seen in septic shock?
intense vasoconstriction in extremities which can lead to acrocyanosis --> gangrene
esp with gram(-)rods: can get these raised necrotic looking lesions called ecthymic gangronosum
- Some will go on to develop a diffuse white out of the lung called ARDS
What is Activated protein C? Side effects?
When should it be used?
antithrobotic, antiinflamatory and fibrinolytic activity; bleeding = major side effect
Only works if used EARLY!
What are the tx options in septic shock?
What are the criteria for acute meningitis?
Chronic meningitis?
Recurrent meningitis?
Onset w/i hrs-days, <4 wks duration, bacterial (septic) or aseptic

4+ wks duration

Multiple acute episodes w/i <4 wks
What is acute meningitis?
inflammation of the meninges
infecction of subarachnoid space
exudate over spinal cord and brain
CSF w inflammatory changes
Roles of CSF?
maintains constant IC pressure
protects against sudden pressure changes
possesses antibacterial properties
How do pathogens enter CSF?
paracellular passage
transcellular transport
invasionw/i WBCs during diapedesis
What are the most common organisms for acute bacterial meningitis?
Strep pneumoniae
N. meningitidis
Listeria monocytogenes
H. influenza B
Group B strep
gram - enterics
which organism is the primary pathogen in acute meningitis in adults?
in children?
Strep pneumoniae

N. meningitidis (also associated with outbreaks and increased incidence of infection in household contacts)

Broup B beta hemolytic strep
which form of menignitis has a vaccine against it?
H. influenza B
When is the most common time of the year to get meningitis (and for which organism)?
Strep pneumonia (winter)
N. meningitidis (spring and winter peak, but year-round)
Which meningiits organism has the highest mortality rate?
Strep pnuemonia (30%)
What is the most common way that acute bacterial meningitis spreads w/i body?
direct spread/extension less common (usually post-surgical or cranial injury, 2/2 congenital malformation, and est neighboring infection)
what is the portal of entry for acute bacterial meningitis? wHY?
nasopharynx from bacteria in URT
Nasopharyngial mucosal epithelium provides local immunity and is the attachment site for bacteria
How does N. menigitidis breach host defenses?

How do encapsulated organisms do it?
makes IgA protease and escapes phagocytosis by capsular polysaccharide

inhbiit neutrophil phagocytosis and complement mediated killing
What are hte host defense mech against menigitis?
alternative complement pathway (merely the presence of the microbe activates complement)
describe how the CNS gets infected in acute bacterial meningitis?
replication of organism in subepithelial tissue
hematogenous spread to CNS
seeding of meninges by organism via choroid plexus
penetration of BBB
development of inflammatory response (--> brain edema and increased intracranial pressure/brain ischemia)
What is the time frame of stage 1 of neutrophil migration into CSF?

when does it occur?
1-2 hrs
cytokine release w/i CSF in response to bacterial replication or lysis --> enhanced binding of neutrophils and enodthelial cells
What is stage 2 of neutrophil migration into CSF?
cytokine stimulation --> IL8 release by vascular endothelium --> neutrophil diapedesis and entry into CSF
What is stage 3 of neutrophil migration into CSF?
CSF cytokines activate neutrophils --> degranulation --> release of vasoactive lipid autacoids and toxic O2 metabolites --> impairment of BBB with leakage of albumin into CSF --> increasd perm of BBB --> brain edema
What are the different types of brain edema?
Vasogenic edema (disruption of BBB and leakage of capillary vessels)
Cytotoxic edema (increased intracellular fluid from cell injury)
Interstitial edema (purulent exudate in arachnoid space interferes with reabsorption of CSF and obstruction of flow, with mov't of fluid from ventricular system to parenchyma)
What bacterial products --> bacterial meningitis?
teichoic acid
what are the cellular mediators in acute bacterial meningitis?
Arachidonic acid
What causes the decreased cerebral perfusion?
WBC get activated, which --> endothelial injury --> coag cascade activation --> thrombosis --> decreased cerebral blood flow
What are the pathologic features of acute bacterial meningitis?
purulent exuddate over brain, spinal cord and in ventricles
spinal root/nerve inflammation
hydrocephalus (arachnoid thickening at base of brain)
thrombosis/occlusion of cerebral vessels
Subdural effusions
What are the clinical features of acute bacterial meningitis?
life threatening emergency
acute and fulminant presentation
fever, neck stiff, abnormal consciousness
Brudzinski and Kernig sign
photophobia, lethargy
bulging frontanelle (in infants) and headache in adults
What is Brudzinski sign?
Kernig sign?
flex neck will arch their leg (spinal cord extends all the way to the back and its very stiff so it can bend the knee)

flex hip and knee and you will see the neck flex
what are some of the more serious late complications of acute bacterial meningitis?
focal neurologic signs
CN palsies
papilledema is unusual
what is papilledema? why is it rare?
bulging of optic disc
occurs when a pt is about to herniate, so not an acute sign
what are some features that would suggest N. meningitidis?
Strep pneumonia?
petechiae, non blanching, red, flat
respiratory infections (ear/sinus)
clinical presentation of neonates with acute bacterial meningitis?
non-specific findings
poor feeding
increased sleeping
decreased urine output
Normal CSF:
# cells/mm3
type of cells
Bacterial meningitis CSF:
# cells/mm3
type of cells
TB meningitis CSF?
# cells/mm3
type of cells
low (20-40)
hihg >150
fungal meningitis
# cells/mm3
type of cells
low (20-40)
+ india ink
Viral meningitis CSF:
# cells/mm3
type of cells
what is nml CSF blood glucose in relation to blood glucose?
2/3 of blood glucose, any less is a problem
what happens if the lumbar puncture is traumatic (hits a BV)?
can cause increased CSF protein (falsely)
what population normally has a high CSF protein?
Where else should be cultured?
petechial scrapings (if N. meningitidis)
tympanocentisis in otitis media (strep. pyogenes)
what is the most important thing to keep in mind with treatment of bacterial meningitis?
must achieve bactericidal concentrations of AB in CSF
What should be used to treat an unknown cause of bacterial meningitis?
Vanco + 3rd generation cephalosporin for broad spectrum coverage (get more specific later)
other than with meds, how should a pt with meningitis be treated?
24 hr isolation in first 24 hrs of AB tx (for HiB and N. meningitidis)
steroids given before abx to reduce deafness from Hib
Supportive care
Tx of other infection sites and predisposing condition
What is the mortality of bacterial meningitis in adults? infants?
infants are higher
Which is the most common permanent sequelae of acute bacterial meningitis in children?
Which organisms for bacterial meningitis have vaccines?
N. meningitidis
Strep pneumoniae
When are the vaccines given for Hib?
What is used for post-exposure proph?
2 months

(given to members in household under 5 yo)
What is the postexposure proph for N. meningitidis?
rifampin or ciprofoxdacin or ceftriaxone
given to household and close contacts, sometimes given to index case
Who gets vaccinated against N. meningitidis?
military recruits
travellers to some areas
college freshman
Who gets vaccinated against Strep pneumonia?
Infants, starting at 2 months
Which bacterial meningitides have post-exposure proph?

Which don't?
N. meningitidis

Strep pneumonia
Gram - bacilli
Which organism for bacterial meningitis has no immunization?
Gram - bacilli
What is the leading cause of aseptic meningitis?
What are others viruses associated with aseptic meningitis?
Enterovirus (echo and coxsackie B)

Arbovirus (insect vector)
LCV (rare, from rodent exposure)
when does LCV normally occur?
winter and fall
what are the bacterial causes fo aseptic meningitis?
partially treated bacterial infection
M. tubuerculosis
Brain abscess
Parameningeal focus
Non viruses/bacteria --> aseptic meningitis?
pathophysiology of viral meningitis?
mucosal colonization
escapes host defences, and disseminates and invade CNS
how does viral meningitis spread?
Hematogenous spread after replication at specific site s
CNS invasion of BBB and indirect invasion via peripheral or CN (polio or HSV)
What happens after the body is seeded with virus in meningitis?
inflammatory response --> alteration ofo BBB (--> introduction of serum proteins and local Ig synthesis)
Eradication of infection requires intact host immune response and T cell function
Clinical features of viral meningitis?
presents with fever, ha, stiff neck
Changes in mental status suggest concurrrent encephalitis
URI sx
myalgias, arthralgias
which virus has a severe and fatal meningitis?
Which is mild and insidious?
Which has association with myalgias/arthralgias?
which has rashes?
Non-polio enteroviruses
LCV, leptospirosis
mumps, enterovirus, HSV, EBV, leptospirosis
what is arbovirus?
ARthropod BOrne vector
Treatment for viral meningitis?
symptomatic tx
antivirals not indicated EXCEPT for HSV
IVIG for immunocompromised
Treat children with acetominophen (not aspirin --> Reye's) to control fever
Prevention of viral meningitis?
MMR prevents mumps as cause of meningitis