ICL 3.1: Clinical: Endocarditis and Other Cardiac Infections

Question 1

what is infective endocarditis?

Answer 1

infection of the endocardial surface of the heart or heart valves

infection can occur with bacterial or nonbacterial pathogens

previously called acute endocarditis or subacute endocarditis (SBE)

Question 2

what are the 2 types of infective endocarditis?

Answer 2

1. native valve endocarditis

• left sided
• right sided –> primarily PWID

2. prosthetic valve endocarditis

Question 3

how common of infective endocarditis?

Answer 3

in the US, approximately 450,000 cases from 2000 to 2010

1/1000 hospitalizations and Incidence is rising especially with increased IV drug use = increased right sided endocarditis

fatal without treatment!! this is because your body can’t fight the infection on it’s own and it’s in the heart so you can’t tolerate an infection in this site

Question 4

what is the pathophysiology of infective endocarditis? aka how does it happen?

Answer 4

1) injury to the endocardial surface –> can occur from turbulent blood flow, inflammation or direct injury to the surface
2) collagen is exposed and in direct contact with the blood stream and there is a STERILE platelet-fibrin-thrombus formation at the site of injury = marantic endocarditis
3) sterile thrombi provide a surface for the bacteria to adhere to
4) bacterial adherence to the platelet-fibrin-thrombus complex with bacterial growth and host response

Question 5

how susceptible is the endothelium to bacterial adhesion?

Answer 5

normal cardiac endothelium is HIGHLY resistant to bacterial adhesion!!

like normal tooth brushing releases bacteria into the bloodstream but it does not result in IE in healthy patients

however, if the surface of the endocardium gets roughed up/damaged then sterile platelet-fibrin-thrombi form on the exposed collagen on the surface of the cardiac endothelium which provide a place for bacteria to adhere!

Question 6

how well to bacteria adhere to sterile thrombi in the endocardium following endothelial damage?

Answer 6

some bacteria are intrinsically “stickier” to the thrombus

ex. strep and staph are “stickier” then E. coli because of extracellular dextran –> gram (+) are “stickier”!

Question 7

what are the 2 mechanisms by which bacteria enter the bloodstream?

Answer 7

1. direct inoculation

2. indirect entry

Question 8

what is direct inoculation of bacteria into the bloodstream?

Answer 8

bacteria are mechanically placed into blood stream

ex. tooth brushing, catheter placement into a vein through the skin (PWID, hemodialysis, IV line) can all result in transient bacteremia

Question 9

what is indirect entry of bacteria into the bloodstream?

Answer 9

bacteria breach local defenses and anatomic barriers and cause a bacteremia

ex. cellulitis with bacteremia

Question 10

can virulent organisms directly adhere to the endocardium without prior injury?

Answer 10

yeah…..scary

for example, staph aureus may be able to directly injure the endocardium and adhere to underlying collagen

in fact, about 50% of cases of acute S. aureus bacterial endocarditis (especially in PWID) occur in the absence of heart disease

Question 11

what happens once bacteria binds to the thrombus on the damaged heart tissue?

Answer 11

infected thrombus continues to grow due to bacteria - platelet - fibrin interaction and the fibrin matrix inhibits macrophage killing

host attempts to kill the bacteria are ineffective and actually backfire because they result in many of the clinical manifestations that are seen with IE:

antibodies are produced against circulating bacterial Ag
Immune complexes of Ab:Ag form and are deposited in a variety of organs (eg - spleen, skin) and are deposited in/ cleared by glomerulus –> a few PMN’s are deposited on thrombotic lesions –> cytokine release results in systemic symptoms

Question 12

what are the risk factors that increase your chance for infective endocarditis?

Answer 12

1. > 60 years old = more degenerative valvular disease
2. male (probably because of HTN)
3. PWID
4. dialysis (indwelling line)
5. poor dentition (bacteria get into the bloodstream)
6. structural heart disease
7. prosthetic valve/implanted material

these generally represent the ways in which the valve gets roughed up and/or bacteria get into the blood stream

Question 13

which structural heart conditions increase your risk for infective endocarditis?

Answer 13

CONGENITAL
1. unprepared cyanotic heart disease

2. bicuspid aortic valve

ACQUIRED
1. history of infective endocarditis –> because your heart valves are damaged from previous bought

2. valve regurgitation in heart transplant

Question 14

which bacteria are most likely to cause infective endocarditis?

Answer 14

bacteria with extracellular dextran are stickier = gram (+)

1. staph aureus (30%)
2. viridian’s strep (17%)
3. non-viridans strep (12%)
4. enterococci and coagulation negative staph (11%)

Question 15

which other bacterial outside the most common ones can cause IE?

Answer 15

1. HACEK = haemophilus, aggritatebacter, cardiobacterium, eikenella, kingella (2%)
2. polyicrobial infections are actually really rare….only 1%, so it’s usually only 1 organism causing IE
3. true culture negative endocarditis (8%) –> you can’t easily recover the microorganisms

Question 16

what are HACEK organisms?

Answer 16

organisms previously associated with culture negative endocarditis

Ⓗaemophilus aphrophilus

Ⓐctinobacillus actinomycetemcomitans

Ⓒardiobacterium hominis

Ⓔikenella corrodens

Ⓚnigella king

Question 17

what is right sided native valve endocarditis?

Answer 17

often seen in people who inject drugs

usually associated with intravascular devices

most commonly cause by staph aureus (70%) and then streptococci and enterococcus cause 30%

Question 18

what kind of IE is associated with people who use drugs?

Answer 18

90% of patients with right sided IE are PWID

S aureus is really commonly the cause BUT you need to consider additional contaminants like drug diluents such as saliva or tap water, contaminated equipment –> this would include bacteria like pseudomonas, fungi, or oral flora

Question 19

what is prosthetic valve endocarditis?

Answer 19

EARLY: due to intraoperative contamination or hematogenous spread in the post-op period

<2 months post-op, S. aureus and coagulation negative staph are most common cause –> 2-12 months post-op coat neg staph is the most common cause

LATE: >12 months post-op

microbiology and pathophysiology similar to native valve endocarditis

Question 20

what are the 3 main characteristics of IE?

Answer 20

clinical signs occur slowly over weeks/months (SBE) or days (acute endocarditis)

1. presence of vegetations
2. consistent/persistent bacteremia –> seeding and infection of distant sites
3. immunologic phenomenon

Question 21

how does the presence of vegetations in IE effect heart function?

Answer 21

1. cardiac abnormalities due to increasingly dysfunctional valve (veggies don’t let the valve close and interfere with the functioning of the heart)
2. embolic phenomenon occur as parts of the expanding, infected thrombus break off and enter the blood stream –> septic pulmonary emboli or cerebral emboli

Question 22

what is the immunologic phenomenon that happens with IE?

Answer 22

immune complex (AB:Ag) deposition in kidneys –> glomerulonephritix

Question 23

what patient presentation should immediately make you think infective endocarditis?

Answer 23

fever and murmur!

mitral regurg or aortic regurg murmurs common

some of the “classic” manifestations of endocarditis are not commonly seen today because they are late stage/end stage manifestations of IE which we don’t see because we usually diagnose it prior to seeing the “classics”

Question 24

what are the early clinical manifestations of IE?

Answer 24

early signs and symptoms are usually non-specific with insidious onset over days, not hours unless acute IE/S. Aureus

1. rigors/chils
2. fatigue
3. myalgia
4. arthralgia
5. night sweats
6. stroke symptoms
7. weight loss
8. fever ( >90%)
9. murmur

may recall a precipitating event like dental work or a h/o underlying heart disease

Question 25

what are the late stage clinical manifestations of IE?1.

Answer 25

1. splenomegaly up to 50%

2. petechia stroke, altered mental status, visual change, seizures, encephalopathy

Question 26

what are some of the classic signs of IE?

Answer 26

1. Janeway lesions
2. Oslers nodes
3. CHF, arrthymias, pericarditis
4. diffuse glomerulonephritis with uremia or renal infarction with hematuria

Question 27

what are Janeway lesions?

Answer 27

small, non-tender,erythematous lesions on palms and soles(?emboli)

sign of IE

Question 28

what are Osler nodes?

Answer 28

small, red, tender lesions on palmsor soles (?emboli or immune complex)

sign of IE

Question 29

how do you diagnose IE?

Answer 29

usually done by clinical manifestations, positive blood cultures and echos

get blood cultures BEFORE antibiotics are given –> three sets of blood cultures drawn from separate venipuncture sites in patients who have not received antibiotics will detect bacteremia in 98% of patients with IE because consistent, persistent bacteremia is a hallmark of IE

Question 30

what kind of echo do you do to diagnose IE?

Answer 30

transthoracic echocardiogram (TTE) is performed for all cases of suspected IE

transesophageal echocardiogram (TEE) has higher sensitivity for abscess around the valve ring, smaller lesions, leaflet perforations

Question 31

what lab values will you see in someone with IE?

Answer 31

1. anemia>70%
   normocytic,normochronic
2. thrombocytopenia
3. ESR elevated in >90%
4. proteinuria, hematuria common
5. leukocytosis <20%

Question 32

how do you treat IE?

Answer 32

directed antibiotic therapy used once the organism and antibiotic sensitivities are known

blood cultures are repeated every 48 hours tilbacteremia is cleared (document negative blood cultures)

duration of therapy is calculated from the day of first negative blood cultures

therapy is usually 4 to 6 weeks from that time

use bactericidal antibiotics because this isn’t an infection your body can help you clear up

Question 33

what are the pearls for IE?

Answer 33

1. Prosthetic valve IE (PVE) –> infection at site of surgical attachment of valve to heart tissue (annulus) can lead to a ring abscess and often requires surgery for treatment
2. polymicrobic IE is rare
3. fungal IE usually needs valve replacement
4. NVS = nutritionally variant streptococci
   GPC like Abiotrophia defective
5. Group D streptococci IE –> do a colonoscopy to rule out underlying neoplasm
6. valve replacement surgery for native valve IE –> early surgery preferred, urgent surgery required for arrthymia, CHF,emboli