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4.1 Medical Microbiology > Infective Endocarditis > Flashcards

Infective Endocarditis Flashcards

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1
Q

What is infective endocarditis?

A

Infections of the endocardial surface of the heart:
- native heart valves
- prosthetic heart valves
- mural endocardium
- septal defect
-indwelling cardiac device

Vast majority affect the right side of the heart with left sided infection only really being seen in intravenous drug users

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2
Q

What is endocarditis a direct complication of and how?

A

Direct complication of bacteraemia

seeding of bacteria into bloodstream e.g. with oral flora or devices -> or foci infections

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3
Q

Comment on the mortality of IE
(4)

A

IE is relatively rare but remains life threatening

Mortality of 14-22% in hospital mortality

Up to 40% mortality in the first year of infection

The five year survival rate is worse than many common cancers

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4
Q

Comment on the burden of IE in Ireland

A

organisms often form biofilm -IE requires prolonged hospital admission for IV antibiotic treatment - could be up to 6 weeks treatment

High requirement for surgical intervention - removal of valves etc

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5
Q

What are the signs and symptoms of IE?

A

Fever
Fatigue
Weakness/malaise
Tachypnea
Tachycardia

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6
Q

Comment on the classification of IE

A

Used to be classified as either acute or subacute
- acute = rapid onset of symptoms e.g. S. aureus signs of infection etc etc
- subacute = more chronic, difficult to diagnose and treat

Now we classiy baased on infecting organism or the underlying anatomy
- native valve endocarditis
- prosthetic valve endocarditis
- cardiovascular implantable electronic device infection (CIEDI)

We use Modified Dukes Criteria 2023: positive blood culture + echocardiograph:
- definite
- possible
- rejected

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7
Q

Comment on the epidemiology of IE

A

Sharp increase in the incidence and mortality

Cases have more than doubled over last 30 years

It is the fourth most common life threatening infection

men have a much higher incidence but woman have higher mortality

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8
Q

How is the epidemiology of IE changing over the years?

A

Significant change in the profile of patients as well as the characterisitcs of the disease

Used to see a lot of younger people with IE caused by oral commensals such as GAS

Now seeing a lot of older patients with NVE or prostethic devices and heart valves

Would havae seen older people with rheumatic heart disease gettin IE but now were seeing more people without underlying issues

Seeing a major shift from oral flora IE to more HCA pathogens

Recent surge in IV drug use as weel causing a different cohort of pathogens

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9
Q

What are some cardiac risk factors for IE

A

Bicuspid aortic valve
Mitral valve prolapse
Rheumatic valve disease
Congenital heart disease
Prior infective endocarditis
Implanted cardiac devices
Prosthetic heart valves

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10
Q

What are some non-cardiac risk factors for IE

A

IV drug use
Long term haemodialysis
Chronic liver disease
Malignancy
Advanced age
Corticosteroid use
Poorly controlled D.M
Long term venous access
Immunocompromised state

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11
Q

What are the two ways IE can occur?

A

Path 1:
- Mucous membranes or other colonised tissue
- Trauma + local spread
- Bacteremia + spread to heart
- Adherence, colonisation and mature vegetation in heart

Path 2:
- Valvular endothelium + trauma/turbulence
- Platelt-fibrin deposition in heart
- Nonbacterial thrombotic endocarditis (NBTE)
- Adherence, colonisation, mature vegetation in heart

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12
Q

How do baceria colonise the heart to cause IE?

A

Adherence + division
Fibrin deposition (bacteria often form biofilm at this point)
Platelet aggregation
Extracellular proteases
Protection from neutrophils

Mature vegetation formed

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13
Q

What part of IE infection actually damages the heart??

A

The formation of bacteral vegetation on the valves

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14
Q

What are the four steps to vegetation formation?

A

normal healthy endothelium is resistant to pathogens

bacterial adhesion brought on by trauma or bacteraemia

inflammatory response by immune system recruits platelets to site of bacterial adhesion

thrombogenesis occurs - ie. fibrin deposited around biofilm (often in biofilm) to form vegetation on valves

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15
Q

What ae four risk factors for bacterial adhesion in the formation of vegetation?

A

Prosthetic valves
Cardiac implantable electronic devoce
Congenital heart disease
Intravenous drug use

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16
Q

What ae four risk factors for bacterial adhesion in the formation of vegetation?

A

Prosthetic valves
Cardiac implantable electronic devoce
Congenital heart disease
Intravenous drug use

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17
Q

What three things occur with IE?

A

Valve dysfunction
Abnormal blood flow
Heart failure

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18
Q

What are some complications of IE

A

Heart:
- Congestive heart failure
- Arrhythmias
- Myocardial abscess/infarction
- Murmurs

Cerebrum:
- Ischaemic stroke
- Abscess
- Intracranial haemorrhage/abscess
- Meningitis
- Infective intracranial aneurysms

Eye:
- Roth spots

Skin
- Janway lesions
- Osier nodes

Kidney:
- Acute kidney injury
- Glomerulonephritis
- Infarctino

Musculoskeletal:
- Osteomyelitis etc

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19
Q

What are some complications associated with emboli

A

Right sided IE can spead to lung and cause emboli here in IVDA

Left sided can spread to spleen, kidney, liver etc

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20
Q

What are roth spots?

A

Haemorrhages behind the eyes

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21
Q

What are roth spots?

A

Haemorrhages behind the eyes

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22
Q

What are the three classification of IE today

A

Native Valve Endocarditis

Prosthatic Valve Endocarditis

Cardiovascular Implantable electronic device (CIED)

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23
Q

Talk about the frequency of HCA IE

A

25% of IE are caused by HCA organisms in developed countries -> this incidence is increasing

These occurs across all classifications of IE

This increases burden on HC as well as HCAIE have considerably worse prognosis compared to CAIE

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24
Q

What is Native Valve Endocarditis?

A

This is where an individuals natural heart valves become infected

Associated with chronic sources of bacteraemia in conjuction with common predisposing factors

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25
Comment on the frequency of NVE
Relatively rare affecting onto 2 to 10 in every 100,000 people Mostly affects hose >50
26
What are the three main risk factors for NVE
Rheumatoid vascular disease Congestive heart disease Age-related degenerative heart disease *generally affects elderly -> wear and tear with old age -> degenerative heart diseases
27
What organisms are mostly associated with NVEs?
80% are gram-positive, 20% are HACEKs and others
28
Comment on the frequency of Gram positive NVE, how freuent is each pathogen
35-40% = S. aureus + CNS 40-45% = Streptococci + Enterococci - oral streptococci = 20% - S. gallolyticus = 10-15% - Enterococci = 5%
29
What does HACEK stand for?
Haemophillus Aggregatibacter Cardiobacterium Eikernella corrodens Kingella *Gram negatives that cause IE
30
Comment on the frequency of NVE caused by gram negatives and others
<5% are caused by HACEKs 2% by Candida species 8% are polymicrobial (2+ organism) 2% are unidentified or other
31
What are some complications associated with NVE?
Permanent valve damage Mitral and aortic valve incompetence Congestive heart failure due to damaged heart valves causing inadequate blood pumping Myocardial abscesses in heart muscle - arrhythmia Metastatic infection Neurological complications Heart failure and permanent heart damage
32
What is prosthetic valve endocarditis, how frequent are they, classify it?
Life threatening infection of a valve prosthesis Mechanical valve infection Very rare, not many people have mechanical valves, but well recognised as a complication of valve replacement and repair Classified as eithe early onset PVE or late onset PVE
33
What is early onset PVE vs late onset PVE
PVE within 60 days of surgery = early PVE >60 days atfer surgery = late
34
How does early PVE compare to late PVE in terms of organisms?
Early PVE is caused by perioperative acquisition of organisms so we see more HCA organisms and skin commensals e.g. CNS, S. aureus, GNBs, Candida, Streps and Ents, Corynebacterium Late PVE has similar organisms to NVE i.e. mostly gram pos
35
How can early-onset PVE be prevented?
Perioperative antibiotic prophylaxis Strict infection control measures Good surgical technique Limiting the use of central venous catheters CVC
36
How can late onset PVE be preventef
Maintenance of good oral hygiene -> late PVE mostly caused by staphs and streps => prevent spread of oral commensals via dental work etc
37
What is CIEDI
Cardiovascular Implantable electronic device infection
38
How frequent is CIEDI, why is it challenging to diagnose and how is it treated?
Incidence ranges from 0.8% to 19.9% Diagnosis challenging due to the low sensitivity and specificity of the modified duke criteria for this population removal of the device is recommended
39
Across all classifications of IE what organism is most prevalent
Staphylococci, then streps, then enterococci - slight variation in relative percentages when you break them down to each classes but this trend still remains the same
40
Comment on the organisms found in IE in the Mater study, give % of organisms in general
Viridans group strep (28.3%) MSSA (25%) Culture neg (18.4%) Enterococci (11.8) Miscellaneous(10.5%) CNS (4.6%) MRSA (1.3%)
41
Comment on IE and IVDA, how do they impact epidemiology
Opioid epidemic in US plas a huge part in this Marked increase in S. aureus, candida species, gram negative bacteria and polymicobial ie polymicrobial due to constant introduction of new bacteria Candida thought to be due to lemon + drug mixture, acidic conditions that candida thrive on
42
What are some general points on epidemiology changes in IE
Health care associaed IE increasing Escalating CDIE Declining S. viridans worlwide Enterococcus faecalis CAIE increasing - associated with older male patients with underlying GI or GU tract abnormalities
43
Talk about the detection of HACEKs
relatively low numbers <5% of cases Used to rarely be detected as they needed special investigations but are now detected routinely -> improvements in blood culture media
44
What are some concerns with IVDA IE
More common tricuspid valve involvement (right side) High incidence of spetic emboli Frequent comorbid infections already (HIV/HCV etc) as well as other sites of infection Withdrawal symptoms and pain management needs Poor long-term outcomes Concern for recurrent infection of prosthetic valves High readmission rates Require follow up with addiction team, valve specialists and infectious disease specialists
45
How does the aetiology of IVDA IE compare to the rest of IEs?
Incidence of S. aureus infection is double but CNS much lower, nearly 70% are S. aureus Incidence of Streps and Ents less common Polymicrobial infections more common Fungal infections, particularly candida more common
46
How does the modified Dukes Criteria 2023 classify IE
Definite IE Possible IE Rejected
47
How is a definite IE diagnosed under the modified dukes criteria 2023?
Evidence of lesions/vegetation on histology or microorganism on culture or histology 2 Major clinical criteria 1 major and 3 minor clinical criteria 5 minor clinical criteria
48
How is a possible IE diagnosed under the modified dukes criteria 2023?
1 major and 1 minor clinical criteria 3 minor clinical criteria
49
How is a query IE rejected under the modified dukes criteria 2023?
Firm alternative diagnosis Resolution of clinical manifestations in ess than 4 days of antibiotic therapy No pathologic evidence of IE on tissue sample after antibiotic therapy for less than 4 days Clinical criteria for definite or possible IE not met
50
What are the major criteria for IE under Dukes
Positive blood cultures Endocardial involement by echocardiography
51
What are the minor criteria for IE under Dukes
Predisposition Fever Vascular phenomena Microbiologic evidence Immunologic phenomena
52
What qualifies as a positive blood culture under the modified dukes criteria?
The isolation of an organism that commonly causes IE in 2 or more separate blood culture sets The isolation of an organism that occassionally or rarely causes IE in 3 or more seperate blood culture sets Positive PCR or other NAATs for Coxiella burnetti or Bartonella species IFA for IgM or IgG antibodies for Bartonella species
53
Give a walk through of a query IE where there is a positive blood culture
Confirm using MALDI Culture -> microbe ID - if culture negative go to serology then pcr AST
54
Give a walk through of a query IE where there is a negative blood culture
if high clinical suspicion go to serology methods - if negative do broad spectrum PCR to ID bac/fungi etc - if positive do specific PCR e.g. Cloxiella PCR AST
55
What are the six most likely causes of a blood culture negative IE
Cloxiella Burnetti Bartonella species Aspergillus species Legionella pneumophilia Brucella species Mycobacterium pneumoniae
56
What is considered the hallmark and cornerstone of IE diagnostics
A sustained bacteraemia is the hallmark Blood Cultures are the cornerstone of diagnosis
57
What is our gold standard for detection of IE?
Our Blood culture automated continuous monitoring systems such as the BacTec - Ideal for Staph, streps, ents, HACEKs and Candida species, all will grow in standard 5 day incubation period -> used to extend for query endocarditis but we dont do this anymore
58
What is our idea sample for query IE?
3 sets of blood cultures taken over a 12 hour period At least 2 sets of optimall filled BC if theres a sustained bacteramia and very high level of concern -> mightny be able to wait to give antibiotics
59
How frequent is blood culture negative IE, why is this significant? (4_
Up to 24% of all IE are culture negative -> similar rates across all 3 classes 18% of cases in ireland are culture negative This proves considerable diagnostic and therapeutic dilemmas - major delays Increased risk of morbidity and mortality
60
Why might a positive IE be culture negative
Previous antibiotic administration Fungi Fastidious bacteria Obligate intracellular organism Specialised media might be required for slow growing organism
61
In the lab what organisms are most likely causative of a negative BC, how do you work around this?
Coxiella burnetti Bartonella species Carry out serology for both - if positive confirm with histology to diagnose IE - if negative then culture, gram and retain histo tissue for molecular testing
62
If you have a blood culture negative, C. burnetti and Bartonella serolog negative query IE, what molecular testing shouhld you carry out/what next steps?
16s rRNA gene PCR or 18s for fungal - if negative do species specific PCR e.g. C. burnetti PCR on valve Special staining such as PAS-D If no evidence of inflammation or organism he consider non-infectious etiology
63
What serology is available for culture negative IE?
Coxiella burnetti Bartonella Aspergillus Mycoplasma pneumoniae Brucella Legionella pneumophila
64
What specific PCR is available for BC negative IE?
Tropheryma whipplei Bartonella species Fungi (Candida species and aspergillus species)
65
What broad spectrum PCR is available for culture negative IE, what are two improvements in this field?
16S and 18S ribosomal ribonucleic acid (rRNA) - need tissue sample FISH combined with 16s rRNA-gene PCR and sequencing improved the diagnosis in 30% of cases NGS of plasma microbial cell-free DNA may facilitate a rapid diagnosis of IE in the future
66
Talk about the use of serology for C. burnetti
Needed as it is a facultative intracellular organism Accounts for 37-43% of BC negative IE IgG titre of 1 to 800 (1:800) is indicative of C. burnetti
67
Talk about the use of serology for C. burnettir
Needed as it is a facultative intracellular organism Accounts for 37-43% of BC negative IE IgG titre of 1 to 800 (1:800) is indicative of C. burnetti
68
Talk about the use of serology for Bartonella species
Fastidious organism Indirect immunofluorescence assays Detect igM or igG IgG titres of greater than 1:800 indicative of Bartonella
69
In the future what might be a major benefit of sing molecular methods for detection of IE
We have to culture both our positive and negative BCs in order to do sensitivity Molecular methods are now getting ot the point where they can detect resistance -> work around having to culture positives just for AST
70
How does 16s rRNA PCR compare to positivity of blood cultures
55% of BC positive but 75% were PCR positive if priot antibiotic exposure then only 11% were BCP and 76% were PCR positive 61% of BCN were PCR positive => increased sensitivity with 16sPCR especially for antibiotic usage and BCNs
71
How do we treat IE
IV antimicrobials for an extended period of time >6weeks usually Emperic treatment with IV Vancomycin and Ceftriaxone Review post culture positive and switch to narrow spectrum Prophylaxis only for very specific treatments i.e. dental work - very weak evidence to support Valve replacement but usually dont work very well afterwards, significant regurgitation and haemodynamic compromise
72
What are some concerns in treatment of IE?
There are limited options for culture negative IE, especially if serology negative and no tissue available for PCR -> what do we do then? For really sick patients there can only be a maximum wait time of 48 hours between each step i.e. 48hours for culture, if negative then serology, if negative then PCR etc etc

4.1 Medical Microbiology (30 decks)

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