Infective Endocarditis JiTT 1

Infective Endocarditis (HzB)
This lecture was the micro side of infective endocarditis. For a clinical take, check out Dr. Dery’s lecture
in the next note set. Questions/corrections/comments or to discuss our mutual interest in panda cams:
[email protected].
I could watch this all day.
http://www.zooatlanta.org/1212/panda_cam
And a classic:
http://www.youtube.com/watch?v=EAcdvmnZ_GM
First, a few terms that may come back to haunt you in this note set and/or on the exam:
 IE= infective endocarditis
 SBE= sub-acute bacterial endocarditis slow onset, long duration, milder disease
 ABE= acute bacterial endocarditis rapid onset, short duration, fulminant disease
 NVE= native valve endocarditis
 PVE= prosthetic valve endocarditis
The Definition Is a Good Place to Start
Endocarditis is inflammation of the inner lining of the heart that affects valves.
Intro Block throwback: Don’t be scared of this. Yes, there are tons of highlighted bacteria. No, we do
not need to know each of their roles in endocarditis. The important take-homes:
 Lots of bugs can cause endocarditis (obviously), but gram-positives are usually the culprits.
 The theme is that all of these can cause bacteremia, and that’s how IE starts.
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Infective Endocarditis (HzB)
The Usual Suspects
Yes, a million things can cause IE, but you should just focus
on the usual causes with respect to major risk factors.
Generally speaking, bugs that cause IE can be found on the
skin or in the mouth, so you can imagine various ways they
get inside the body: PICC lines, dialysis catheters, IVDU,
dental work, prosthetic valves, pacemakers, and pretty much
anything else that could break them through those first line
epithelial barriers.
 The most common overall IE cause is Viridans Strep,
which is part of your normal mouth flora. It generally
results in SBE, though, so is less scary than some.
 Prosthetic valves: usually Staph aureus or coagulase
Endocarditis grossly. (Pun?)
negative Staph
 Pacemakers: S. epidermidis (Think biofilms! Then
think biofilms surgically implanted into your chest. Oh dear.)
 IVDU: nearly always Staph aureus, usually MRSA, and usually ABE. Primarily affects the
tricuspid valve, because that’s the first valve that makes contact with dirty venous blood.
 HACEK group: gram-negative bugs that are part of the normal mouth flora. Slow growing, so
might culture negative at first. They aren’t common IE agents in real life, but test life likes them.
I got the impression it would be crazy to memorize the specific names…but if you’re curious:
Haemophilus aphrophilus
Hi, my name is
Actinobacillus actinomycetemcomitans
Dario Hacek.
Cardiobacterium hominis
I come up in
Eikenella corrodens
bacterial Google
Kingella kingae
searches.
Starting Out the Infection
Like I said, IE generally starts with bacteremia….
1) Get into the body
2) Bacteremia
3) Adhere to heart valves. This part is a little more complicated. First off, the bugs can really only
bind abnormal/diseased valves, because healthy native valves don’t have the right receptors.
Lemme explain in the context of a couple major IE causes.
 Viridans Strep has adhesion receptors for fibrin, which wouldn’t be present en masse in
a normal valve.
But if the valve endothelium is damaged subendothelial collagen exposed platelet
plug + tissue factor and cytokine activation coagulation cascade fibrin sticks
Viridans able to join the party.
Summary: sticking to fibrin is an EC adhesion process.
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Infective Endocarditis (HzB)

Staph aureus weasels its way into heart valve cells via fibronectin receptors.
Damage, even microdamage integrins exposed integrins bind fibronectin Staph
aureus binds fibronectin with adhesion factors fibronectin sends signal to endothelial
cells to take up Staph aureus.
Summary: sticking to fibronectin results in IC uptake
 There are several other virulence factors important in IE adhesion: biofilms (Staph
epidermidis), coagulase (Staph aureus), teichoic acid (all gram-positives), and a few
other that she didn’t focus on. (On that note, there’s a great big table of adhesion
factors on slide 8. DON’T try to memorize it. FYI only.)
4) Evade host immune response
5) Damage to the valve directly (eg toxins) or indirectly (eg hypersensitivity reaction). This is
when we really phase into endocarditis.
6) Exit the host
Those Elusive Symptoms
All of these carditises can be extremely hard to diagnose, even when they’re staring you in the face. That
said, here are the things that stare you in the face:
Mnemonic: FROM JANE
Fever
Roth’s spots (retinal hemorrhages with white centers made of up coagulated fibrin)
Osler’s nodes (painful swellings on the fingers and toes caused by immune deposits)
Murmur (due to valve vegetations)
Janeway lesions (painless petechiae on the palms and soles caused by septic emboli)
Anemia [of chronic disease]
Nail hemorrhage (nail bed splinter hemorrhages due to septic emboli)
Emboli (chunks of vegetation, can cause peripheral vascular occlusions and strokes)
But in many cases, you’re actually not “lucky” enough to get these symptoms, which is why it can be so
difficult to diagnose.
Roth’s spots
Splinter hemorrhages
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Infective Endocarditis (HzB)
Diagnosis?
If you do suspect IE, start with blood cultures to try and catch the bacteremia. The ideal strategy is to do
3-4 draws at different times and from different places, which can help avoid false positives from skin
bacterial contamination (because remember, many IE agents are normal skin flora). Usually, at least
two cultures should be positive—although sometimes you can make exceptions for really scary bugs
like MRSA and treat with one positive. But that’s more in the Dr. Dery lecture territory.
 Do the usual cultures to identify the bacteria: gram stain, catalase test, optochin test
(aka P-test), coagulase test, hemolysis pattern
 As I mentioned earlier, some bugs like HACEK won’t culture right away. Or maybe they
cultured negative because antibiotics were already given. Or maybe they have
fibronectin receptors and got sucked up into the valve cells. The point is that negative
cultures do not equal negative endocarditis.
…And the plot thickens.
This chart to the left is also not something you need to
memorize. The point is that desperate measures kick in fast once
you get a negative culture with suspected IE. (I mean, seriously,
“broad-range PCR for bacteria and fungi”…is just absurd.)
Treatment
Along with encephalitis/meningitis, acute endocarditis is one of
the two real ID emergencies and needs to be treated quickly
and aggressively. This is also one of the rare cases when you
really need to use bacteriocidal over bacteriostatic antibiotics,
because the bacteria are sheltered in vegetation and won’t be
fully removed unless they’re dead. (Remember that
bacteriostatic Abx stop bacterial growth but don't actually kill
them.) She didn’t get into specific drugs choices, though.
Staph lugdunensis: Know That It Exists
This guy is yet another coagulase-negative Staph strain that
causes IE. Although not a major concern at this time, it’s a hardto-treat emerging threat that will probably be much more
prevalent when we’re big kids.
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Infective Endocarditis (HzB)
Buzzwords! (Sometimes more like buzzconcepts…but whatever)
Duration
 SBA: Viridans Strep, CoNS, low virulence, mild, slow onset, long incubation
 ABE: Staph aureus, high virulence, fast onset, fulminant, short incubation
Culture results
 Positive: cultures positive after 24-48hrs, [usually] gram-positive, Pseudomonas aeruginosa
 Negative: cultures negative or positive after prolonged incubation, HACEK, intracellular bugs,
previous antibiotics
Heart side
 Right sided: IVDU, cardiac devices (eg pacemakers), Staph aureus
 Left sided: native or prosthetic valves, Staph aureus, Viridans Strep, CoNS, Enterococcus
Infection setting
 Nosocomial: Hospitals, inpatients issues (eg biofilms on plastic catheters and MRSA)
 Non-nosocomial: Dialysis, nursing homes
Valve type
 NVE: Staph aureus, Viridans Strep
 PVE: CoNS, Staph aureus, Enterococcus
And finally, the questions from lecture:
1) A 55-year-old man who recently emigrated from Tibet presents to the emergency department
with fever. He states that he has had recurring fevers over the past 3 weeks, associated with
chills, night sweats, and malaise. Today he developed new painful lesions on the pads of his
fingers, prompting him to come to the emergency department. His medical history is remarkable
for "being very sick as a child after a sore throat“. He is taking no medications. Skin examination
is remarkable for painful nodules on the pads of several fingers and toes. He has multiple
splinter hemorrhages in the nail beds and painless hemorrhagic macules on the palms of the
hands. Ophthalmoscopic examination is remarkable for retinal hemorrhages. A heart murmur
was heard on auscultation.
What is the likely diagnosis?
What are some common predisposing factors to this disease?
Which factor is most likely in this patient?
Which infectious agents could cause this?
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Infective Endocarditis (HzB)
2) A 60 y/o woman presents to the clinic with a 7-day history of malaise, nausea, and loss of
appetite. 10 years previously, her aortic root and valve were replaced. She has been quite well
until now, although she is a poor complier and it has been difficult to stabilize her anticoagulate
therapy. On exam she has fever (38ºC), is flushed and unwell. Her pulse is 110/min and her BP is
80/60 mm hg. A prosthetic valvular click and a systolic murmur are heard on auscultation. Her
chest is otherwise clear, and abdominal exam is unremarkable. What is the probable diagnosis?
a. Acute IE of native heart valve
b. Subacute IE of native heart valve
c. Subacute IE of prosthetic heart valve
d. Acute IE of prosthetic heart valve
3) Cultures of the above identify an organism that’s gram-positive, catalase negative, coagulase
negative, nonhemolytic, and don’t grow in bile esculin and 6.5%NaCl. What is it?
a. Enterococcus faecalis
b. Haemophilus aphrophilus
c. Staphylococcus aureus
d. Streptococcus bovis
e. Viridans streptococcus
4) A 24 y/o man presents to the ER with a fever, chills, night sweats, malaise, and fatigue that
started 3 days ago. In the past day he has also become short of breath. He admits to using IV
drugs regularly. At presentation, the patient is shaking and appears pale. A systolic murmur is
heard on auscultation. The patient states that he never had anything wrong with his heart
before. Which pathogen is most likely responsible for this patient’s condition?
a. Enterococcus faecalis
b. HACEK group
c. Staphylococcus aureus
d. Streptococcus bovis
e. Viridans streptococcus
5) A 60 y/o man was diagnosed clinically with subacute IE. Routine blood cultures failed to grow
any organisms and the infection was initially described as culture-negative. However, after 14
days of culture, organisms that are part of the normal mouth flora were isolated from the blood.
A gram stain is shown below. With which group of organisms is he most likely infected?
a. Coagulase-negative Staphylococci
b. Fungi
c. Enterococci
d. HACEK group
e. Viridans group Streptococci
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Infective Endocarditis (HzB)
6) A patient had surgery several months ago to put in a pacemaker. He felt fine initially, but over
the past month, he has been feeling worse. He is running a low-grade fever, tires easily, and has
worsening heart murmurs. Which of the following coagulase negative, catalase positive, grampositive organisms is a major cause of health care associated endocarditis and the most likely
causative agent in this case?
a. Staphylococcus aureus
b. Coxiella burnettii
c. Enterococcus faecalis
d. Staphylococcus epidermidis
e. Streptococcus bovis
Answers:
1) What is the likely diagnosis? Untreated infective endocarditis, an infection of the cardiac valves
What are some common predisposing factors to this disease?
 presence of abnormal cardiac valves related to rheumatic heart disease
 mitral valve prolapse with an audible murmur
 congenital heart disease
 prosthetic valve
 prior endocarditis
 Injection drug use
Which is most likely in this patient? The patient's history of significant illness as a child after a
sore throat suggests the possibility of rheumatic heart disease.
Which infectious agents are most likely to be involved? Gram-positive bacteria, including
Viridans Streptococci, S. aureus, and enterococci
2)
3)
4)
5)
6)
d
e
c
d
d
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