Bacteremia and Endocarditis

Brief bacteria in the blood
Asymptomatic
Occurs during normal daily activities: tooth brushing, bowel movements
Manipulation of infected tissues

Symptomatic
Occurs with infection and obstruction
(like pyelonephritis, cholecystitis)
or undrained abscesses

Endovascular infection
Endocarditis, infected arterial aneurysm, infected grafts and shunts

Skin prep w/ EtOH, iodophor, chlorhexadine
10-20 mls of blood
anaerobic and aerobic cultures

Best to get at least two sets better for sensitivity and specificity

Normal skin flora are usually contaminants
True pathogens are rarely contaminants

Contaminents are less likely to be found in multiple cultures, also more likely to be found in a clinical situation which does not finish

Localized microbial infection of cardiac valve or mural endocardium

Infected platelet rich thrombus

Caused by invasive organisms
Rapidly progressive

Caused by low-grade pathogens
Symptoms usually present for weeks to months before diagnosis

Sterile vegetations
Seen in connective tissues diseases, malignancy

Normal or abnormal valves
Acute onset, hectic pace, early complications
Virulent organisms (S. aureus, beta-hemolytic strep, pneumococcus)

Usually occurs at abnormal valves
Subacute onset over months
Insidious course
Less virulent organisms: viridans strep, coagulase-neg staph

2-6/100K person-years
M>W, 50% older than 55

Predisposing risk factors
IDU
Mitral valve prolapse
Degenerative valve disease
Rheumatic heart disease
Poor dental hygiene
Long term hemodialysis
Previous endocarditis

Damaged endocardial surface
High velocity flow
Passage of blood from high pressure to low pressure
Localized thrombosis ensues serving as a nidus for infection during transient bacteremia
Platelet-fibrin layers form barrier between bacteria and neutrophils
Allows for bacterial growth

Viridans strep
S. aureus
especially in nosocomial , IDU
Coagulase neg staph - often iatrogenic
Enterococci esp w/ bladder outset obstruction

Polymicrobial = IDU

Community acquired - strep viridans > staph species

IDU - Staph majority
also sometimes see fungi

<12 months out - coag-neg staph
>12 months out - strep viridans

Not common
Usually seen after recent antibiotic use

Sometimes difficult to culture organisms
Bartonella - cat scratch, trench
Q fever
Abiotrophic strep
HACEK orgnanisms
Chalmydia
Legionella
Brucella
Fungi

Hemophilus
Actinobacillus
Cardiobacterium hominis
Eikenella
Kingella

Fever in 95% of pts

Anorexia, weight loss, malaise, night sweats
Myalgias - 50% of patients
Heart murmur
Embolic stimata
Splenomegaly

Splinter hemorrhages (red -->brown)
Conjunctive petichiae
Osler's nodes - painful subq nodules often on pulp of thenar eminence
Janeway lesions - nontender erythematous lesions on palms or soles
Petichiae

Sign of SBE
Retina - oval white areas surrounded by hemorrhage

Emboli
Stroke
Monocular blindness
Acute abdominal pain
Coronary syndrome
Splenic infarct/abscess
Renal
Microscopic hematuria
Renal insufficiency

Monocular blindess from thrombus to retinal artery

Abrupt onset
High fever
Rigors common
Prominent cutaneous manifestations
Emboli common
Rapidly changing murmur
Rapid development of CHF

Usually normal valves
Staph aureus, polymicrobial, fungi

High frequency of tricuspid involvement
High fever, cough, chills, malaise
Pleuritic chest pain from septic pulmonary emboli is hallmark of right sided IE

Often associated with perivalvular invasion
Valve-ring abscesses
Valvular dysfnc
Valve dehisence

Can get obstruction/abnormal fnc

Hallmark is sustained bacteremia

Take a different sites over hours in SBE
Take multiple sites right away in ABE

Each into aerobic and anaerobic

Rapid, noninvasive
98% specific for vegetations
60-70% sensitive

Body habitus may limit

75-95% sensitive for vegetions
Highly specific
Can also see myocardial abscesses

Invasive, expensive

3 major or 1 + 3 or 5 minor

Major:
Organism on 2+ blood cultures
New murmur/+ECHO

Minor
Risk factors
Fever
Vascular phenomenon
Immunologic phenomenon
Not persistent, but positive BC

glomerulonephritis
RF
Osler's nodes
Roth spots

Specificity said to be 99%
NPV - 92%

25-35% do

Increased risk w/
Community acquired
Absence of primary focus
Presence of metastatic sequelae
Fever/bacteria lasting >3 days after removing cat

(Increased risk for needing valve replacement)
Persistent bacteremia/fever
Recurrent emboli
Heart block - abscess hindering conduction
CHF
New heart murmur

Valve damage causing CHF
Myocardial abscess
Extension into septum causing heart block
Purulent pericarditis

20-40% frequency
Mostly emboli -- stroke
Also mycotic aneurysm can rupture and hemorrhage
Risk during anticoag for valve replacement

Treatment rapidly decreases risk

Cultures first
High doses of parenteral agents
4+ weeks for native valve
6 weeks for prosthetic

Inpatient until clear response (afebrile, repeat negative blood cultures)

Based on cultures

Pen if you can
Nafcillin/Vanco
add rifampin

Fever should be gone in a week
CRP fall in 1-2 weeks

Indicated in 25-40% of native and 45% of prosthetic
Best to do before development of CHF or spread to perivascular tissue

Low risk of infecting new valve

Persistent bacteremia
Perivalvular invasive disease
Mod/severe CHF
Recurrent emboli
Large vegetations
Pseudomonas, fungi, resistant enterobacter

4-16% - viridans strep
15-25% with enterococci
25-50% with staph
>50% for gram negs, fungi

Theory is to give high risk pts antiobiotics prior to events likely to cause bacteremia
Unproven

Highest risk: previous endocarditis, prosthetic valves, cyonotic heart malformations

Times: dental work, surgery