Diffentiating bacterial endocarditis causes

[WarriorMD]

Can anyone point me to a link or quickly summarize how to differentiate the bacterial causes for endocarditis.

My notes I made have conflicting info so now I'm all confused, but from what I can make sense of them this is a quick way to differentiate them:

S. Viridans - patient will have pre-existing damage to a heart valve
S. Aureus - IV Drug Users (can this be s. mutans as well?)
Enterococcus - ??

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[Myxedema]

S. viridans: Native, but damaged [alpha-hemolytic Streptococci, no groups, optochin resistant, not bile-soluble]
S. aureus: Native, non-damaged or damaged; especially seen in IV drug abusers (IVDA) [catalase-positive, coagulase positive, ferments mannitol, beta-hemolytic]
S. bovis: Native, assoc. w/ colorectal carcinoma [alpha- or non-hemolytic, Group D Streptococci, no growth in 6.5% NaCl]
Enterococci: Native, assoc. w/GI or genitourinary manipulation (Foley, colonoscopy, etc.) [alpha-, beta- or non-hemolytic, Group D Streptococci, grows in 6.5% NaCl]
HACEK group: Native; members of oropharyngeal flora, slow growing bacteria requiring high CO2, can cause "culture negative" endocarditis [Gram (-) bacilli]
S. epidermidis: Prosthetic [catalase-positive, coagulase-negative, novobiocin-sensitive]
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Apart from bacteria, fungi can infect both native (especially IVDA) and prosthetic valves

 

[sharklasers]

Is S. aureus the only one that is acute?

And how would you differentiate culture neg from non bacterial endocarditis. WBC count or something?

 

[Myxedema]

Is S. aureus the only one that is acute?

Not necessarily, other bacteria can also be found in acute IE (such as S. pyogenes), but it is the most common type of bacteria associated with acute IE.

And how would you differentiate culture neg from non bacterial endocarditis. WBC count or something?

I think this goes beyond the scope of Step I, but to mention it briefly, Duke criteria are used in the diagnosis of IE. There are two major criteria: (1) Positive blood culture [taken >12 hours apart, or 3 or more cultures positive with first and last drawn an hour apart], and (2) Evidence of endocardial involvement (for instance, positive echocardiogram). In addition, there are 5 minor criteria: (1) Predisposition, (2) Fever, (3) Vascular phenomena (emboli, infarcts, etc.), (4) Immune phenomena (glomerulonephritis, Osler's nodes, Roth spots, etc.) and (5) Microbiological evidence that fell short of first major criteria

In order to diagnose IE, either two major, or one major + 3 minor, or all 5 minor criteria would need to be present. So that brings us back to your question. An IVDA with a positive echo, fever and a new onset of glomerulonephritis with negative blood cultures ("culture negative") will be diagnosed as IE. A cancer patient without fever, but with a new onset of murmur and positive echo with negative blood cultures may be diagnosed as NBTE.

 

[MLT2MT2DO]

Can anyone point me to a link or quickly summarize how to differentiate the bacterial causes for endocarditis.

My notes I made have conflicting info so now I'm all confused, but from what I can make sense of them this is a quick way to differentiate them:

S. Viridans - patient will have pre-existing damage to a heart valve
S. Aureus - IV Drug Users (can this be s. mutans as well?)
Enterococcus - ??

Enterococcus- Guy/gal had a uro or some sort of colon surgery/biopsy
Bovis- Colorectal cancer
Strep Mutans is one of many organisms filed under Viridans strep, Dental sx is famous for this

 

[Pons Asinorum]

Not necessarily, other bacteria can also be found in acute IE (such as S. pyogenes), but it is the most common type of bacteria associated with acute IE.



I think this goes beyond the scope of Step I, but to mention it briefly, Duke criteria are used in the diagnosis of IE. There are two major criteria: (1) Positive blood culture [taken >12 hours apart, or 3 or more cultures positive with first and last drawn an hour apart], and (2) Evidence of endocardial involvement (for instance, positive echocardiogram). In addition, there are 5 minor criteria: (1) Predisposition, (2) Fever, (3) Vascular phenomena (emboli, infarcts, etc.), (4) Immune phenomena (glomerulonephritis, Osler's nodes, Roth spots, etc.) and (5) Microbiological evidence that fell short of first major criteria

In order to diagnose IE, either two major, or one major + 3 minor, or all 5 minor criteria would need to be present. So that brings us back to your question. An IVDA with a positive echo, fever and a new onset of glomerulonephritis with negative blood cultures ("culture negative") will be diagnosed as IE. A cancer patient without fever, but with a new onset of murmur and positive echo with negative blood cultures may be diagnosed as NBTE.

Dude, who the hell are you? Your explanations for questions like this and in the complicated concepts thread are amazing. I'm not sure where you are in your training or if you're just a dude with T1 line to Wikipedia headquarters, but your explanations are always clear, sourced, and clinically relevant. Thanks man. I'm planning on studying for my IM shelf by just reading your old posts.

 

[sharklasers]

Dude, who the hell are you? Your explanations for questions like this and in the complicated concepts thread are amazing. I'm not sure where you are in your training or if you're just a dude with T1 line to Wikipedia headquarters, but your explanations are always clear, sourced, and clinically relevant. Thanks man. I'm planning on studying for my IM shelf by just reading your old posts.

LMAO i was just about to post something like this... myxedema has been a god send for me.

Incredible explanations for every single question that has come up since I have seen him post.

Myxedema, when are you taking step 1? You need to take it ASAP to put all your knowledge to use haha.

 

[tiedyeddog]

There is a uworld question on this, you need to be able to differentiate S. viridans and Enterococci based on which one can grow in 6.5% salt. Both are G+, catalase - and both grow (or atleast don't die) in bile.

Enterococci can thrive in 6.5%, Viridans cannot. Also, from this same poorly written question, you can get endocarditis from Enterococci from procedures in the groin region (cytoscopy, putting in a catheter... etc.) f UW sometimes...

 

[sharklasers]

There is a uworld question on this, you need to be able to differentiate S. viridans and Enterococci based on which one can grow in 6.5% salt. Both are G+, catalase - and both grow (or atleast don't die) in bile.

Enterococci can thrive in 6.5%, Viridans cannot. Also, from this same poorly written question, you can get endocarditis from Enterococci from procedures in the groin region (cytoscopy, putting in a catheter... etc.) f UW sometimes...

i missed this question because i didnt associate Enterococci with GU procedures...

 

[tiedyeddog]

i missed this question because i didnt associate Enterococci with GU procedures...

Yup, me too.

 

[Trogghunter]

Recent studies have shown that s. Aureus is the most common cause in acute and chronic in native and prosthetic valves FYI. This is fairly recent and may not be updated on step 1 but it is important.

Staphylococcus aureus is one of the most common causative pathogens of bloodstream infections (BSIs). In approximately one-half of patients with S. aureus BSI, no portal of entry can be documented. This group of patients has a high risk of developing septic metastases. Similarly, patient populations at high risk of S. aureus BSI and BSI-associated complications include patients receiving hemodialysis, injection drug users, patients with diabetes, and patients with preexisting cardiac conditions or other comorbidities. One of the most severe complications of S. aureus BSI is infective endocarditis, and S. aureus is now the most common cause of infective endocarditis in the developed world. Patients with methicillin-resistant S. aureus BSI or infective endocarditis have higher rates of mortality, compared with patients with methicillin-susceptible S. aureus infection. Nasal carriage is the most important source of S. aureus BSI. Better eradication and control strategies, including nasal decolonization and more-active antibiotics, are needed to combat S. aureus BSIs.

 

[Myxedema]

Thank you all for your kind words. I'm glad if what I've written has been useful. I'm an IMG and I plan on taking the exam (hopefully) within the next three months.