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CAM201 Microbiology > Infective endocarditis > Flashcards

Infective endocarditis Flashcards

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1
Q

Predisposing factors

A
  • Rheumaic heart disease
  • Congenital heart defects (e.g. VSD, coarctation of the aorta)
  • Degenerative heart lesions resulting in calcified lesions (calcified mitral annulus, for example)
  • IVDU
  • Healthcare-associated
    • Recent history of invasive procedure (wound care, haemodialysis)
    • Intravascular devices (central-venous catheters)
    • Implanted prosthetic valves
    • Implanted pacemakers; cardioverter defibrillators
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2
Q

The heart valves most commonly affected

A

Mitral > aortic > aortic and mitral valve > tricuspid valve (rarely)

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3
Q

Pathophysiology of IE

A

IE appears to require the simultaneous occurrence of several independent events

  • Endocardial (valve) surface damage: by various stressors, including differences in blood flow turbulence, or by direct action of the offending organism.
  • The surface damage results in the deposition of platelets, fibronectin, fibrin and other matrix proteins, forming so-called ‘sterile’ non-bacterial thrombotic endocarditis (NBTE) vegetations. NBTE vegetations are often seen in patients with underlying conditions (pancreatic, gastric or lung carcinomas; congenital heart-disease; uremia; and systemic lupus erythematous (SLE)).
  • The NBTE vegatations are then colonised by bacteria (transient or otherwise) which adhere to and invade the involved tissue, and are then able to persist (i.e. continuous bacteraemia).
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4
Q

Staphylococcus aureus IE

A

Most common cause of IE (mitral or aortic valve) in the developed world.

Increase identification of S. aureus induced IE amongst IVDUs, where it causes so called right-sided (tricuspid) IE.

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5
Q

Coagulase negative group IE

A
  • Staphlococcus epidermis
  • S. saprophyticus
  • S. lugdunensis

This group of orgnaisms is usually associated with prosthetic valves and are often acquired during health-care associated practices.

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6
Q

*Streptococci/ Viridians streptococci *IE

A

Historically responsible for the largest percentage of native valve endocarditis.

Part of the normal flora of the mouth and GIT.

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7
Q

Enterococci IE

A

These organisms are usual inhabitants of the GIT and anterior urethra.

Severe UTIs

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8
Q

Gram negative bacilli

A

Commonly acquired in the healthcare setting. Rarely seen in IE.

  • Salmonella spp. ( S. typhiumurium/ S. enteritidis)
  • Escherichia coli (E. coli)
  • Serratia marcescens
  • Pseudomonas aeruginosa: can also affect normal valves, surgery is often required because of poor prognosis.

GNB-associated IE common amongst IVDUs and patients with prosthetic valves

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9
Q

Fungal IE

A

Occur in the severely immunosuppressed.

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10
Q

HACEK group

A
  • Haemophilus
  • Aggregatibacter actinomycetecomitans
  • Cardiobacterium hominis
  • Eikenella corrodens
  • Kingella kingae

​These organisms cannot be cultured. They usually appear in the respiratory tract.

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11
Q

Clinical manifestations of IE

A

Onset can follow a subacute or chronic course. In some cases, patients will present with symptoms after a short incubation period (<2 wees) or often over 2-5 weeks.

Onset resembles flu-like illness (dry cough, body aches and pains and fatigue.

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12
Q

What factors influence the clinical picture?

A
  • Nature of the infecrious process (i.e. nature of valves infected)
  • Bland or septic emboli, which can affect any organ
  • Constant bacteraemia (with metastic foci of infection)
  • Circulaitng immune complexes
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13
Q

Common IE symptoms

A
  • Fever
  • Sweats
  • Cough
  • Stroke
  • Headache
  • Myalgia
  • Edema
  • Chest pain
  • Abdominal pain (nausea, vomiting)
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14
Q

Associated signs of IE

A
  • Heart murmur
  • Embolic (painful) lesions (fingers, or toes)
  • Skin or mucosal lesions
    • Soft palate petechiae
    • Subconjunctival petechiae
    • Haemorrhages within nail beds (splinter haemorrhages)
    • Painful, small subcutaneous nodules in the pads of fingers/toes (Osler’s node)
  • Janeway lesion (haemorrhagic nontender [painless] plaques on palms, soles)
  • Roth spot (retinal lesions)
  • Splenomegaly
  • Septic complications (pneumonia, meningitis)
  • Mycotic aneurysms
  • Clubbing
  • Renal failure (glomerulonephritis; abscess; infarction)
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15
Q

Diagnosis of IE

A

Diagnosis of IE requires laboratory and imaging findgings inc onjunction with clinical manifestations.

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16
Q

Blood cultures for IE

A

Minimum of three blood cultures sets collected before abx therapya nd over the first 24 hours.

  • When common bacteria ARE present; first TWO cultures generally yielf the organisms >90% of the time.
17
Q

Fastigious organisms cultures

A

Require special growth media; serology and/or PCR and sequencing of DNA or RNA, for proper identification (and need to be requested from the laboratory).

18
Q

Culturing of common ‘sin contaminants’

A

e.g. *Propionibacterium, Corynebacterium, Bacillus, *Coagulase-negative staph.

  • One positive test = likely contamination
  • Need majority of 3 or more culture sets, collected at different time points (i.e. over 10 to 12 hours apart) for it to be considered possible cause of disease symptoms.
19
Q

Blood tests IE

A

These are relatively non-specific, often reveal:

  • Anaemia (low seurm iron concentration; low iron-binding capacity)
  • Thrombocytopenia
  • Leukocytosis
  • Elevated C-reactive protein (CRP)
  • Elevated erythrocyte sedimentation rate (ESR)
20
Q

Urinalysis

A

Is relatively non-specific and often reveals:

  • Proteinuria (excess [serum] protein in the urine)
  • Microscopic haematuria (presence of RBCs in urine)
  • Pyuria (elevated number of WBCs)
  • Bacteriuria (presence of significant numbers of bacteria in the urine)
21
Q

Echocardiography

A
  • Able to identify vegetations on all valves
  • Transthoracic echocardiography (TTE) and/or transesophageal echocardiography (TOE) can be used to visualise vegetation.
  • Positive findings are often used in conjunction with clinical presentation consistent with IE to decide if surgical intervention is required.
22
Q

CXR

A

May reveal evidence of septic pulmonary emboli, particularly in IE cases involving IVDUs.

23
Q

Definite Infective Endocarditis

A

Pathologic criteria

  • Microorganisms: shown by culture or histology in vegetation, o rin a vegetation that has embolised, or in an intracardiac abscess specimen; or
  • Pathologic lesions: vegetation or intracardiac abscess present, confirmed by histology showing active endocarditis.

Major and minor criteria

Presence of 2 major criteria; or

Presence of 1 major and 3 minor criteria; or

Presence of 5 minor criteria

24
Q

Possible IE

A

Presence of 1 major and 1 minor critera; or

Presence of 3 minor criteria

25
Q

Rejected IE

A
  • Firm alternative diagnosis explainaing evidence of IE; or
  • Resolution of IE syndrome with abx therapy for <4 days; or
  • No pathologic evidence of IE at surgery or autopsy after abx therapy for <4 days
26
Q

Major clinical criteria

A

1. Positive blood culture for IE

  • Typical microorganisms consistent with IE from 2 separate blood culture sets:
    • Viridians strepcocci
    • Streptococcus bovis
    • HACEL group
    • Community acquired *S. aureus or enterococci *in the absence of a primary focus; or
  • Persistently positive blood culture set for any organism (from at least 2 blood cultures sets drawn >12 hours apart); or
  • All 3 or a majority of 4 separate culture sets of blood positive (with first and last samples drawn at least 1 hours apart)

2. Single positive blood culture set for Coxiella burnetii or antiphase I-IgG antibody titre of >1:800

3. Evidence of endocardial involvement

  • Echocardiogram positive for IE
    • Oscillating intracardiac mass on valve or supporting structures, in the path of regurgitant jets, or on implanted devices, in the absence of an alternative anatomic explanation; or
    • Abscess; or
    • New partial dehiscence (movement of prosthetic valve)
  • New partial valvular regurgitation (worsening or changing of pre-existing murmur not sufficient)
27
Q

Minor clinical criteria

A
  1. Predisposition: predisposing heart condition or IVDU
  2. Fever: temperature >38 degrees
  3. Vascular phenomena: arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial haemorrhage, conjunctival haemorrhages, and Janeway lesions
  4. Immunologic pheomena: glomerulonephritis, Osler’s nodes, Roth’s spots, and rheumatoid factor.
  5. Microbiological evidence: positive blood culture but does not meet major criteria as above; or serological evidence of active infection with organism consistent with IE.
28
Q

Treatment IE

A

Blood cultures should be collected before the initiation of treatment.
Empiric therapy is usually initially instituted but must be modified once abx susceptibility patterns become known

The following abx (IV) may be considered

  • Benzylpenicillin plus di/flucloxacillin plus gentamicin; or
  • Vancomycin (alone)

Directed therapy ay be over long periods of time (>4 weeks, in some cases for some organisms)

Follow up testing ensure eradication or infection.

CAM201 Microbiology (7 decks)

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