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Step I Sickle Cell & Infections
Started by vsmedic
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Sickle cell patients undergo autosplenectomy (sp?), therefore they lose the ability to get rid of organisms by splenic macrophages. Normally, C3b or IgG would opsonize these organisms and send them to the spleen for destruction, but because the spleen is nonfunctional, they are unable to deal with organisms such as S.pneumoniae and H.influenza.
The autosplenectomy also results in formation of howell-jowell bodies which is a sign of a non-functional spleen. I think the reason for autosplenectomy is due to sickling of cells causing occlusion and subsequent ischemia, but I'm not 100% sure.
The autosplenectomy also results in formation of howell-jowell bodies which is a sign of a non-functional spleen. I think the reason for autosplenectomy is due to sickling of cells causing occlusion and subsequent ischemia, but I'm not 100% sure.
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spleen specifically clears encapsulated bugs
Well, there are a lot of different ways a body deals with infections. We have circulating neutrophils, macrophages, monocytes etc which can deal with "other forms" of organisms, since they have oxygen-dependent (MPO) and oxygen-independent (enzymes) methods of bacterial destruction, and they can do it right there and then, no need for spleen involvement . The only defense we have against encapsulated organisms is via opsonization and then ship them to the spleen for destruction by splenic macrophages. I hope that makes sense.
same
Actually, microinfarcts in the GI tract allow salmonella to enter the bloodstream and it is then by hematogenous spread that you get the osteomyelitis.
Actually, that would apply to any microvascular disease, not just sickle cell. Just because you read it in a book, does not mean you cannot think for yourself.
Relax, I wasn't trying to be confrontational. Not all isolates are Vi encapsulated strains of salmonella, so their functionally asplenic state doesn't always offer an explanation. I am only trying to give the full picture.
The point is that your explanation is incorrect and it ignores the absolute truth. The absolute reason is due directly to the lack of a spleen. The affinity of Salmonella, or E. coli or S. Aureus for their long bones is of secondary concern.
You can't disregard the mechanism by which the organism gets into the bloodstream. If not for that component, then there would not be a significant incidence of salmonella osteomyelitis. You have already acknowledged this, as have I that their asplenic state increases the likelihood that they will be infected with Vi encapsulated strains. I really don't see where the disagreement lies...
Your mechanism is incorrect. It doesn't explain why E Coli is the end leading cause.
What about the other encapsulated bacteria? Wouldnt there be a significant if not greater incidence of those (since Salmonella is less common to strep. pneumoniae and group b strep)?? Is it due to vaccination against many of the other encapsulated bacteria vs no vaccine for salmonella?
I haven't looked into it that much. I am sure that there is a reason for the affinity. At our level, though, it is more important to know about the function of the spleen and the most common bug for sickle cell patients.
I have yet to see a basic science source discuss the pathophysiology of it. That is beyond the scope of step I.
