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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
Q

Comment on the frequency of NVE

A

Relatively rare affecting onto 2 to 10 in every 100,000 people

Mostly affects hose >50

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26
Q

What are the three main risk factors for NVE

A

Rheumatoid vascular disease

Congestive heart disease

Age-related degenerative heart disease

*generally affects elderly -> wear and tear with old age -> degenerative heart diseases

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27
Q

What organisms are mostly associated with NVEs?

A

80% are gram-positive, 20% are HACEKs and others

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28
Q

Comment on the frequency of Gram positive NVE, how freuent is each pathogen

A

35-40% = S. aureus + CNS

40-45% = Streptococci + Enterococci
- oral streptococci = 20%
- S. gallolyticus = 10-15%
- Enterococci = 5%

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29
Q

What does HACEK stand for?

A

Haemophillus
Aggregatibacter
Cardiobacterium
Eikernella corrodens
Kingella

*Gram negatives that cause IE

30
Q

Comment on the frequency of NVE caused by gram negatives and others

A

<5% are caused by HACEKs

2% by Candida species
8% are polymicrobial (2+ organism)
2% are unidentified or other

31
Q

What are some complications associated with NVE?

A

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
Q

What is prosthetic valve endocarditis, how frequent are they, classify it?

A

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
Q

What is early onset PVE vs late onset PVE

A

PVE within 60 days of surgery = early

PVE >60 days atfer surgery = late

34
Q

How does early PVE compare to late PVE in terms of organisms?

A

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
Q

How can early-onset PVE be prevented?

A

Perioperative antibiotic prophylaxis
Strict infection control measures
Good surgical technique
Limiting the use of central venous catheters CVC

36
Q

How can late onset PVE be preventef

A

Maintenance of good oral hygiene
-> late PVE mostly caused by staphs and streps => prevent spread of oral commensals via dental work etc

37
Q

What is CIEDI

A

Cardiovascular Implantable electronic device infection

38
Q

How frequent is CIEDI, why is it challenging to diagnose and how is it treated?

A

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
Q

Across all classifications of IE what organism is most prevalent

A

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
Q

Comment on the organisms found in IE in the Mater study, give % of organisms in general

A

Viridans group strep (28.3%)
MSSA (25%)
Culture neg (18.4%)
Enterococci (11.8)
Miscellaneous(10.5%)
CNS (4.6%)
MRSA (1.3%)

41
Q

Comment on IE and IVDA, how do they impact epidemiology

A

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
Q

What are some general points on epidemiology changes in IE

A

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
Q

Talk about the detection of HACEKs

A

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
Q

What are some concerns with IVDA IE

A

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
Q

How does the aetiology of IVDA IE compare to the rest of IEs?

A

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
Q

How does the modified Dukes Criteria 2023 classify IE

A

Definite IE
Possible IE
Rejected

47
Q

How is a definite IE diagnosed under the modified dukes criteria 2023?

A

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
Q

How is a possible IE diagnosed under the modified dukes criteria 2023?

A

1 major and 1 minor clinical criteria

3 minor clinical criteria

49
Q

How is a query IE rejected under the modified dukes criteria 2023?

A

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
Q

What are the major criteria for IE under Dukes

A

Positive blood cultures

Endocardial involement by echocardiography

51
Q

What are the minor criteria for IE under Dukes

A

Predisposition
Fever
Vascular phenomena
Microbiologic evidence
Immunologic phenomena

52
Q

What qualifies as a positive blood culture under the modified dukes criteria?

A

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
Q

Give a walk through of a query IE where there is a positive blood culture

A

Confirm using MALDI

Culture -> microbe ID
- if culture negative go to serology then pcr

AST

54
Q

Give a walk through of a query IE where there is a negative blood culture

A

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
Q

What are the six most likely causes of a blood culture negative IE

A

Cloxiella Burnetti
Bartonella species
Aspergillus species
Legionella pneumophilia
Brucella species
Mycobacterium pneumoniae

56
Q

What is considered the hallmark and cornerstone of IE diagnostics

A

A sustained bacteraemia is the hallmark
Blood Cultures are the cornerstone of diagnosis

57
Q

What is our gold standard for detection of IE?

A

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
Q

What is our idea sample for query IE?

A

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
Q

How frequent is blood culture negative IE, why is this significant?
(4_

A

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
Q

Why might a positive IE be culture negative

A

Previous antibiotic administration

Fungi

Fastidious bacteria

Obligate intracellular organism

Specialised media might be required for slow growing organism

61
Q

In the lab what organisms are most likely causative of a negative BC, how do you work around this?

A

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
Q

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?

A

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
Q

What serology is available for culture negative IE?

A

Coxiella burnetti
Bartonella
Aspergillus
Mycoplasma pneumoniae
Brucella
Legionella pneumophila

64
Q

What specific PCR is available for BC negative IE?

A

Tropheryma whipplei
Bartonella species
Fungi (Candida species and aspergillus species)

65
Q

What broad spectrum PCR is available for culture negative IE, what are two improvements in this field?

A

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
Q

Talk about the use of serology for C. burnetti

A

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
Q

Talk about the use of serology for C. burnettir

A

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
Q

Talk about the use of serology for Bartonella species

A

Fastidious organism

Indirect immunofluorescence assays

Detect igM or igG

IgG titres of greater than 1:800 indicative of Bartonella

69
Q

In the future what might be a major benefit of sing molecular methods for detection of IE

A

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
Q

How does 16s rRNA PCR compare to positivity of blood cultures

A

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
Q

How do we treat IE

A

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
Q

What are some concerns in treatment of IE?

A

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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