3/22 Ch 14 Endocarditis Flashcards
∆ = difference
∆ between transient, intermittent and continuous bacteremia?
transient - occurs during normal daily activities (brushing teeth, bowel movements) or with manipulation of infected tissues
intermittent - occurs with infection and obstruction (e.g., pyelonephritis, cholecystitis), undrained abscesses
continuous “high grade”- occurs with endovascular infection: endocarditis, infected arterial aneurysm, infected grafts and shunts
Why get at least 2 sets of blood samples to determine if the patient has bacteremia?
for reasons of both sensitivity (higher volume of blood results in higher yield) and specificity (multiple positive cultures makes it more likely that a positive is a “true-positive”).
Normal skin flora (contaminants) in blood culture?
Coagulase-negative staphylococci (unless a FB is in place)
Bacillus spp.
Propionibacterium acnes
± viridans streptococci
When should you suspect contamination in a blood culture?
- clinical course is not suggestive of bacteremia
- a primary infection with the same organism(s) is absent
- predisposing factors absent (prosthetic devices, IDU, neutropenia)
- no leukocytosis or left shift in CBC
T/F True pathogens are often contaminants of blood.
False! True pathogens are rarely contaminants
Examples include Gram-negative bacilli Anaerobes S. aureus S. pyogenes (group A strep) S. pneumoniae
pathogenesis of endocarditis?
Endothelial damage results from turbulent flow, by trauma (e.g., catheters, particulate matter), or by chronic inflammation.
Localized thrombosis occurs, serving as a nidus for infection during transient bacteremia.
Platelet-fibrin layers form an effective barrier between embedded bacteria and circulating neutrophils (vegetation – an infected platelet-fibrin thrombus)
What is infective endocarditis?
a localized microbial infection of cardiac valves or mural endocardium
What are two types of infective endocarditis?
Acute endocarditis (ABE) Subacute endocarditis (SBE)
factors predisposing infective endocarditis?
Injecting drug use Mitral valve prolapse, especially if mitral regurgitation or thickened leaflets Degenerative valve disease Rheumatic heart disease Poor dental hygiene Long-term hemodialysis Previous endocarditis
Acute infectious endocarditis - definition?
Acute onset (within a week), rapidly progressive symptoms; occurs on normal or abnormal valves (often aortic + mitral)
etiology of acute infectious endocarditis?
virulent organisms
S. aureus most common
ß-hemolytic streptococci
Pneumococcus
presentation of acute infectious endocarditis?
High fever (vs. SBE)
Rigors (shaking chills) (vs. SBE)
Rapid development of CHF
Subacute infectious endocarditis - definition?
symptoms usually present for weeks-months before diagnosis; occurs on abnormal valves
etiology of Subacute infectious endocarditis?
“low grade” pathogens
Viridans streptococci most common
Coagulase-negative staphylococci - common; often associated with medical interventions
clinical presentation of Subacute infectious endocarditis?
Fever Anorexia, weight loss, malaise, night sweats Myalgias (40-50%) Splenomegaly Renal (hematuria, insufficiency) production of major emboli Stroke - results in - Amaurosis fugax - Abd pain, ileus, bleeding - Coronary emboli - splenic infarcts, splenic abscess
What is the classic presentation of endocarditis?
MUST KNOW EVERY SINGLE ONE
1) Fever (can be absent in patients with chronic diseases, antibiotics treatment, infections with less virulent organisms, elderly)
2) Roth Spots (white spots on retina surrounded by hemorrhage)
3) Osler nodes (tender, raised lesions on the finger/toe pads)
4) Murmur - reflects rapid valve destruction
5) Janeway Lesions (small, non-tender erythematous lesions on palm or sole)
6) Anemia
7) Nail-bed “splinter” hemorrhages
8) Emboli
“from jane”
Nonbacterial thrombotic endocarditis (“marantic endocarditis”) - definition?
sterile vegetations, seen in connective tissue diseases, malignancy
Nonbacterial thrombotic endocarditis (“marantic endocarditis”) pathogens?
NONE! actually seen in connective tissue diseases, malignancy
Culture-negative Endocarditis - definition?
endocarditis without etiology with negative cultures
Culture-negative Endocarditis - etiology?
1) recent antibiotic treatment
2) inadequate microbiological techniques
3) Fastidious organisms (many, but * are listed in FA)
- *Bartonella species (cat-scratch bacillus, trench fever)
- *Q fever (Coxiella burnetii)
- Nutritionally variant streptococci
- HACEK organisms
- Chlamydia species
- Legionella species
- Brucella species
- Fungi
What are HACEK organisms?
Haemophilus Actinobacillus Cardiobacterium hominis Eikenella Kingella
What must you do if you suspect Culture-negative Endocarditis?
special media
serologic testing
prolonged incubation of culture
IVDU endocarditis definition?
endocarditis in IV drug users; usually in people with no congenital heart disease
What valve is normally affected in IVDU endocarditis?
tricuspid
IVDU endocarditis pathogens?
S. aureus
Gram-negatives (esp. Pseudomonas)
polymicrobial
Candida albicans
clinical presentation of IVDU endocarditis?
High fever, cough, chills, malaise
Pleuritic chest pain from septic pulmonary emboli is a hallmark R-sided infected endocarditis
prosthetic valve endocarditis - definition of early vs late? What is it usually associated with?
Early PVE – occurs within 2mo of surgery; usually acquired in the hospital
Late PVE – occurs >12 mo after surgery; usually “community-acquired”
Often associated with invasion of peri-vavular tissue, resulting in valvular
- abscesses
- obstruction
- dysfunction
- dehiscence (wound rupture)
What bugs are usually involved in prosthetic valve endocarditis?
Early PVE
S. aureus
coagulase-negative staphylococci
Late PVE
Streptococci
cardiac complications of endocarditis?
Valve damage causing CHF
- Extension of infection beyond the valve annulus (myocardial abscess)
- Extension into septum, causing heart block
Purulent pericarditis
neurologic complications of endocarditis?
embolic stroke in a patient with fever and underlying valvular disease
mycotic aneurysm leading to rupture and hemorrhage; early diagnosis by MRI scan or CT scan
most common site of endocarditis complications? how is it diagnosed?
Spleen the most common site (splenic abscess a common complication); diagnosed by CT scan
which pathogens have been implicated in the mortality of infective endocarditis?
Viridans streptococci: 4 – 16%
Enterococci: 15 – 25%
S. aureus: 25 – 47%
50% for gram-negatives, fungi
Factors Affecting Mortality in infective endocarditis?
1) Causative organism
2) Complications or coexisting conditions (e.g., CHF, neurologic events, renal failure)
3) Perivalvular extension
4) Appropriate surgical intervention
5) valve affected - much lower mortality rate from right-sided IE
how do you lower the risk of infective endocarditis?
prophylactic antibiotics given for patients at high risk (underlying valve disease), and when they undergo procedures that are likely to lead to bacteremia.
how is infective endocarditis diagnosed?
clinical picture, labs, ECHO, and clinical acumen
typical labs of infective endocarditis?
anemia, leukocytosis, abnormal urinalysis, elevated ESR and CRP
what is the hallmark of infective endocarditis?
“sustained bacteremia” - 3 separate venipunctures taken over several hours for SubacuteBE or over several minutes for Acute BE and inoculated in aerobic + anaerobic media
How method would you use to view vegetations?
Transthoracic ECHO (TTE) Transesophageal ECHO (TEE)
Pros/Cons of Transthoracic ECHO (TTE)?
Pros: rapid, non-invasive, cheap, high specificity (98%)
Cons: body habitus may preclude good study, sensitivity (60-70%)
Pros/Cons of Transesophageal ECHO (TTE)?
Pros: high sensitivity for vegetations (75-95%) without compromising specificity, especially useful for prosthetic valves, more likely than TTE to detect myocardial abscess
Cons: $$$, invasive
What criteria is used to ultimately determine if one has infective endocarditis?
Duke Criteria – don’t have to memorize; just know that it exists
Specificity said to be 99%
Negative predictive value 92%
What are basic principles guiding treatment of infective endocarditis?
Always obtain blood cultures first!
For SBE - delay treatment while awaiting culture results
For ABE - start treatment as soon as blood cultures have been obtained
followed by antibiotics (prolonged course of parenteral agents, high doses, and in-patient treatment until the patient has has responded)
When do you stop treating a patient with infective endocarditis?
until the patient has clearly responded (afebrile, repeat BCs negative) and the risk of complications has diminished
specific pathogens and treatments
Viridans streptococci treatment?
Penicillin G or ceftriaxone, 4 weeks
Streptococci with MIC
Penicillin for 4 weeks + gentamicin, 2 weeks
Enterococci, fastidious or resistant streptococci
Penicillin + gentamicin, 2-6 weeks
MSSA
Nafcillin, 4 weeks
MRSA
Vancomycin, 4 weeks
HACEK organisms
Ceftriaxone, 4 weeks
Prosthetic valves treatment for “sensitive” strep
gentamicin, 2 wks
Prosthetic valves treatment for “resistant” strep
gentamicin, 4-6 wks
Prosthetic valves treatment for MSSA, MRSA and coagulase-negative staphylococci (organisms that make biofilms)
gentamicin + rifampin
When is valve replacement surgery best done?
for both native and prosthetic valve endocarditis; best before severe CHF or spread of infection to peri-valvular tissue
Indications for valve replacement surgery?
1) persistent bacteremia despite appropriate therapy
2) perivalvular invasive disease (development of heart block)
3) moderate to severe CHF
4) recurrent major emboli (or one with a large vegetation)
5) large vegetations
6) specific organisms: Pseudomonas, fungi, highly resistant enterococci.
If you see these organisms, you should consider doing a valve replacement surgery
Pseudomonas
fungi
highly resistant enterococci
Risk of subsequent infective endocarditis with prosthetic valve?
Risk of infecting the new prosthetic valve is very low; can get superior outcomes with combined medical/surgical approach in the setting of poor prognostic factors, eg staphylococcal infection
