M26-Infective endocarditis Flashcards
what is the peak incidence of infective endocarditis?
50+ age group
what is the mortality rate of infective endocarditis even if treated?
15-30%
-Without treatment - usually fatal
What is infective endocarditis caused by?
micro-organisms (bacteria/fungi) settling on heart valves
What do micro-organisms usually affect?
damaged valves (can affect normal ones)
what can also be affected in infective endocarditis?
other organs
What happens as patients get older?
infective endocarditis increases
What are the core concepts of infective endocarditis?
• Predisposing lesion on valve – area of endocardial injury
• Attracts layer of platelets/fibrin
• Makes the surface ‘sticky’
• Circulating bacteria attach – Specific adhesins
• Incorporated into ’vegetation’
• Infection develops
– Type of infecting agent can influence disease
– S. aureus can gain access to cytoplasm of valve endothelium with increased damage & inflammation
What has an effect on systemic disease?
periodontal health
What is the procedure of infective endocarditis?
• Pathogen gains temporary access to the bloodstream
– Route important
• Pathogens rapidly adhere via
platelet fibrin deposition
• Some species obtain intracellular access
• Proliferation of microbes formation of vegetation
• Embolization or haematogenous spread leading to range of complications.
what complications are included?
stroke, meningeal reaction, brain abscess
why is there more damage caused if the species obtains intracellular access?
Able to hide from the immune system , bigger lesion forms and this can detach and move around the body
Name 4 clinical effects of infective endocarditis.
• Bacteraemia:
– diagnosis now largely linked to positive blood culture
• Damage to valve by growing vegetation :
– Mitral/aortic (IVDU = right sided valve)
– Valve can rupture
• Emboli: bits flake off & lodge in small vessels:
– Seeding bacteria around the body
– From remote embolic effects to stroke, meningitis & abscess formation
• Immune complex effects:
– Stimulates humoral & cellular immunity
– Systemic deposition of complement/immune complexes – e.g. Glomerulanephritis
Name one remote embolic effect and describe it.
- Osler’s nodes (finger pads)
- Red spots in peripheral part of blood where fragments block blood and cause build up
What is the problem with a remote embolic effect (palatal petechiae)?
Difficult to link this directly to infective endocarditis as it is also a cause of leukaemia, STD and viral infections such as infectious mononucleosis
What are the 2 spontaneous (intermittent and unpredictable) sources of bacteria?
Oral flora
Gut flora
What are the 3 induced (suspected to be result of procedures) sources of bacteria?
- Gum margin manipulation (Extraction)
- Bowel or genito-urinary tract procedures
- Intravenous Drug Users
What staphylococci cause infective endocarditis?
– Coagulase negative (CNS)
• S. epidermidis (usually prosthetic valves)
• S. aureus (often normal valves)
Can cause rapid valve destruction
what cocci species causes infective endocarditis ?
- Streptococci (oral)
- Enterococci
What species are in the culture negative : HACEK?
Haemophilus, Aggregatibacter, Eikenella, Coxiella, Bartonella & others
What percentage is caused by streptococci (oral) ?
50%
Describe the virulence.
- Entry & circulate in Blood Stream
- Adherence to host structure
- Biofilm formation
- Host-cell invasion
- Aggressive damage/secretion of toxins
- Intracellular persistence
what surface adhesins does streptococcus gordonii express?
- PadA
- Hsa
Describe the virulence of streptococcus gordonii.
– Surface located proteins associated with platelet adhesion & aggregation
– PadA & Hsa
– Key virulence proteins
– Candidates for Vaccine
– Lactobacillus lactis expressing N-terminal cell wall binding domain
What patients are at risk of infective endocarditis?
- Individuals with damaged heartvalves (Rheumatic fever, congenital or degenerative heart disease)
- Previous episode of IE
- IVDU
- Prosthetic valves
- Cardiac surgery
- Long intravascular lines
What is the subacute presentation of infective endocarditis?
• Malaise,night sweats,rigors, weightloss, headaches, shortness of breath
• Pyrexia
• Heartmurmur
– new or changing
• Embolicmanifestations
– in renal, lung, spleen, brain
– 30% - often 1st sign
•Immune complex disease in kidney, small vessels – Glomerulanephritis
• Likely microbes are Streptococci or Enterococci
Name symptoms of high index of clinical suspicion.
- Fever & new murmur – 38 ̊C
- Fever & known heart lesions
- Fever & recent bacteraemia, heart failure, stroke
- Unexplained embolic events
- Night sweats,malaise, anorexia in a cardiac risk
- Unexplained positive blood culture
- Related to lines if blood culture positive < 72 hours after removal
what happens in the diagnosis/ investigations of acute IE?
Blood culture X 2 sets within first 1hr (sustained bacteraemia) taken carefully
what happens in the diagnosis/ investigations of subacute IE?
3 sets > 6hrs apart
In terms of antibiotics , what are the principles of empiric therapy?
- Cidal
- Large doses (iv)
- Long time (4-6 weeks)
when does antibiotics start?
immediate start after blood culture
when is antibiotics adjusted?
If laboratory confirms it
what do antibiotics target for acute infection?
S. aureus
Describe antimicrobial therapy?
• Beta-lactams:
- amoxicillin
- benzyl penicillin
- flucloxacillin
Describe the local antibiotic policy.
• Native valve acute/severe:
– Flucloxacillin
– increase in MRSA causing concern
• Native valve subacute: – amoxicillin & gentamicin
• Prosthetic valve:
– vancomycin, gentamicin & rifampicin
• MRSA:
– vancomycin, gentamicin & rifampicin
Describe targeted therapy for fully sensitive strains (opposite of empiric prescribing).
• S. aureus MSSA – high dose flucloxacillin • Enterococci – high dose amoxicillin & gentamicin • Viridans Group Streptococci – high dose penicillin – 4 weeks for fully sensitive VGS
Describe the follow up of treatment.
- Essential
- May be blood cultures/repeat ECHO
- High risk of recurrence
- Education of patients re alert healthcare staff of their condition
- Prevention (good oral hygiene)
Describe the prevention of IE for surgical procedures.
- Historically dental procedures such as extraction considered high risk for IE.
- Prophylatic use of penicillin prior to procedure – 3g of Amoxycillin or 600mg Clindamycin
- NICE guidelines amended(2008) &reviewed(2015) to recommend prophylactic Antibiotics are not to be used.
what is the USA perspective of prophylaxis?
Prophylaxis only recommended for patients with underlying cardiac conditions associated with the highest risk of adverse outcome from infective endocarditis
What are the arguments against prophylactic prescribing?
- Brushing teeth twice per day for 1 year estimated to expose 154K x more bacteria than tooth extraction
- No evidence prophylactic prescribing effective or ineffective for at risk patients
What are factors to consider when prophylactic prescribing?
- Medical Status
- Immunological status
- Preceding infection at site
- Invasiveness of procedure
- Increase in IE cases since 2008
What measures are taken for at risk patients and what does this reduce?
• Advice on good oral hygiene:
-Reduces need for extractions
-Reduces risk of bacteraemia if Rx is needed
-Reduces spontaneous bacteraemia
• Education re symptoms of IE
• GDP should remain up to date, while not prescribing should communicate symptoms /complications to patient
Give the summary slide.
• Uncommon but increasing
– Unclear why? & some consideration of high risk patients
• Beware of condition in otherwise healthy heart valves
– Patients medical history
• Predisposingfactors
– History, Age, drug use, immune system,
• Can present as a subtle clinical course
• Acute and rapid onset
• High index of suspicion
– Be aware of classical symptoms
