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Robbin's Pathology says that vegetations of IE are more common on the atrial side in AV valves. In Liebmann Sack's Endocarditis, which is a sterile (non bacterial) type of endocarditis, the underside of the valve also has vegetations. Why is it so? If its just colonization of bacteria in IE, how does it matter where?

Does gravity matter in colonisation of bacteria!! ?

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With the bacterial IE, it would look like the vegetations tend to colonize the lower pressure sides of the valve structure (REF1). Something that was made clear that distinguishes the IE vegetations frm the Libman-Sacks vegetations was overall motility. Specifically, Libman-Sacks vegetations exhibit no independent motion and are largely sessile, whereas IE vegetations can be motile (REF2). In terms of where they attach I think this makes sense, the more motile vegetations colonize the less turbulent area, and the sessile vegetations seem to hold up in either scenario. Reference 1 also rather usefully points out that IE vegetations may be located anywhere on the valve structure as well, they just tend to be on the low-pressure side.

So being said i would argue that the motility of the organisms is a deciding factor.

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  • $\begingroup$ Robbins classifies IE as acute or subacute. Subacute IE is the one where flowing viridans bacteria stick to already damaged valves. Arrhythmia isn't mentioned as a risk factor or a predisposing factor. Rather valve damage/ prosthetics are. Could you suggest a further read regarding the Afib leading to endocarditis thing? $\endgroup$ – Polisetty Mar 4 '16 at 17:24
  • $\begingroup$ I'll be honest, I don't like that answer that I initially posted, so i'm going to rehaul it here $\endgroup$ – CKM Mar 4 '16 at 18:13
  • $\begingroup$ Thanks for the answer. Could you pls explain what 'motility' means in this context? The vegetations don't move themselves right? Like move with the valve?? $\endgroup$ – Polisetty Mar 4 '16 at 20:27
  • $\begingroup$ Motility meaning "are they capable of moving on their own or are they for the most part adhered to the structure?", in essence. $\endgroup$ – CKM Mar 4 '16 at 20:37
  • $\begingroup$ The Cleveland Cardiology review mentions Mural thrombi as a risk factor for bacterial endocarditis :) $\endgroup$ – Polisetty Oct 8 '16 at 20:46
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Infective endocarditis generally develops when there is a pre-existing valvular lesion. The location where the vegetation in infective endocarditis develops is based on the pressure of the surroundings. Bacteria tend to colonise places where the pressure is low.

'Where the pressure is low', depends upon what kind of a valve deformity is already present.

In mitral regurgitation, blood when pumped from the left ventricle enters the atria due to the patent bicuspid valve. Naturally, the pressure is more on the ventricular side than the atrial side. Hence, the bacteria settle on the top of the leaf. Moreover, the do so at the edges of the leaves. This is because, since the blood has to squeeze through, according to to bernoulli's theorem (Venturi effect). Hence they form on the edges of the atrial side of the valves

enter image description here

In case of an aortic regurgitation, since there is a backflow of blood from the aorta to the ventricles, the vegetations are found on the underside of the aortic valves.

Liebmann Sacks (which is non infective and happens in lupus) is common in the mitral valve though it can happen anywhere. I assume, since bacteria are living cells, the pressure constraint applies to them but not to sterile vegetations like the one in lupus.

I implore you to have a look at this wonderful video which explains it all. Picture credits and reference : Endocarditis by osmosis.org

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