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Microbiology > M26-Infective endocarditis > Flashcards

M26-Infective endocarditis Flashcards

1
Q

what is the peak incidence of infective endocarditis?

A

50+ age group

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2
Q

what is the mortality rate of infective endocarditis even if treated?

A

15-30%

-Without treatment - usually fatal

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3
Q

What is infective endocarditis caused by?

A

micro-organisms (bacteria/fungi) settling on heart valves

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4
Q

What do micro-organisms usually affect?

A

damaged valves (can affect normal ones)

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5
Q

what can also be affected in infective endocarditis?

A

other organs

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6
Q

What happens as patients get older?

A

infective endocarditis increases

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7
Q

What are the core concepts of infective endocarditis?

A

• 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

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8
Q

What has an effect on systemic disease?

A

periodontal health

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9
Q

What is the procedure of infective endocarditis?

A

• 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.

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10
Q

what complications are included?

A

stroke, meningeal reaction, brain abscess

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11
Q

why is there more damage caused if the species obtains intracellular access?

A

Able to hide from the immune system , bigger lesion forms and this can detach and move around the body

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12
Q

Name 4 clinical effects of infective endocarditis.

A

• 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

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13
Q

Name one remote embolic effect and describe it.

A
  • Osler’s nodes (finger pads)

- Red spots in peripheral part of blood where fragments block blood and cause build up

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14
Q

What is the problem with a remote embolic effect (palatal petechiae)?

A

Difficult to link this directly to infective endocarditis as it is also a cause of leukaemia, STD and viral infections such as infectious mononucleosis

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15
Q

What are the 2 spontaneous (intermittent and unpredictable) sources of bacteria?

A

Oral flora

Gut flora

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16
Q

What are the 3 induced (suspected to be result of procedures) sources of bacteria?

A
  • Gum margin manipulation (Extraction)
  • Bowel or genito-urinary tract procedures
  • Intravenous Drug Users
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17
Q

What staphylococci cause infective endocarditis?

A

– Coagulase negative (CNS)
• S. epidermidis (usually prosthetic valves)
• S. aureus (often normal valves)

Can cause rapid valve destruction

18
Q

what cocci species causes infective endocarditis ?

A
  • Streptococci (oral)

- Enterococci

19
Q

What species are in the culture negative : HACEK?

A

Haemophilus, Aggregatibacter, Eikenella, Coxiella, Bartonella & others

20
Q

What percentage is caused by streptococci (oral) ?

A

50%

21
Q

Describe the virulence.

A
  • Entry & circulate in Blood Stream
  • Adherence to host structure
  • Biofilm formation
  • Host-cell invasion
  • Aggressive damage/secretion of toxins
  • Intracellular persistence
22
Q

what surface adhesins does streptococcus gordonii express?

A
  • PadA

- Hsa

23
Q

Describe the virulence of streptococcus gordonii.

A

– 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

24
Q

What patients are at risk of infective endocarditis?

A
  • Individuals with damaged heartvalves (Rheumatic fever, congenital or degenerative heart disease)
  • Previous episode of IE
  • IVDU
  • Prosthetic valves
  • Cardiac surgery
  • Long intravascular lines
25
Q

What is the subacute presentation of infective endocarditis?

A

• 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

26
Q

Name symptoms of high index of clinical suspicion.

A
  • 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
27
Q

what happens in the diagnosis/ investigations of acute IE?

A

Blood culture X 2 sets within first 1hr (sustained bacteraemia) taken carefully

28
Q

what happens in the diagnosis/ investigations of subacute IE?

A

3 sets > 6hrs apart

29
Q

In terms of antibiotics , what are the principles of empiric therapy?

A
  • Cidal
  • Large doses (iv)
  • Long time (4-6 weeks)
30
Q

when does antibiotics start?

A

immediate start after blood culture

31
Q

when is antibiotics adjusted?

A

If laboratory confirms it

32
Q

what do antibiotics target for acute infection?

A

S. aureus

33
Q

Describe antimicrobial therapy?

A

• Beta-lactams:

  • amoxicillin
  • benzyl penicillin
  • flucloxacillin
34
Q

Describe the local antibiotic policy.

A

• Native valve acute/severe:
– Flucloxacillin
– increase in MRSA causing concern
• Native valve subacute: – amoxicillin & gentamicin
• Prosthetic valve:
– vancomycin, gentamicin & rifampicin
• MRSA:
– vancomycin, gentamicin & rifampicin

35
Q

Describe targeted therapy for fully sensitive strains (opposite of empiric prescribing).

A 
•  S. aureus MSSA
–  high dose flucloxacillin
•  Enterococci
–  high dose amoxicillin &amp; gentamicin
•  Viridans Group Streptococci
–  high dose penicillin
–  4 weeks for fully sensitive VGS
36
Q

Describe the follow up of treatment.

A
  • 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)
37
Q

Describe the prevention of IE for surgical procedures.

A
  • 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.
38
Q

what is the USA perspective of prophylaxis?

A

Prophylaxis only recommended for patients with underlying cardiac conditions associated with the highest risk of adverse outcome from infective endocarditis

39
Q

What are the arguments against prophylactic prescribing?

A
  • 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
40
Q

What are factors to consider when prophylactic prescribing?

A
  • Medical Status
  • Immunological status
  • Preceding infection at site
  • Invasiveness of procedure
  • Increase in IE cases since 2008
41
Q

What measures are taken for at risk patients and what does this reduce?

A

• 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

42
Q

Give the summary slide.

A

• 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

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