Bartonella, Mold, Coagulation, Sepsis & More

Hey guys!

Recently, we discussed Dr M and Dr AC’s use of systemic proteolytic enzymes for their patients. They are treating primarily bartonella (Dr M) and Lyme/co/mold (Dr AC).

I just posed some questions on my COVID thread related to breathing, oxygen, and vasoconstrictors. That got me going down a rabbit trail, where I discovered this fascinating abstract on PubMed about Coagulation and Sepsis https://pubmed.ncbi.nlm.nih.gov/27886531/

Please take a look and if you can translate science into English, your thoughts would be greatly appreciated!!

Some short clips:
- “Severe sepsis is almost invariably associated with systemic activation of coagulation”
- “Inflammation not only leads to initiation and propagation of coagulation activity, but coagulation also markedly influences inflammation.”
- “At the same time, endothelial-associated anticoagulant pathways, in particular the protein C system, is impaired by pro-inflammatory cytokines.”
- “fibrin removal is severely obstructed by inactivation of the endogenous fibrinolytic system, mainly as a result of upregulation of its principal inhibitor, plasminogen activator inhibitor type 1 (PAI-1).”

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My interpretations of what little I comprehend are:

Bartonella/mold patients (believed to have hypercoagulation even if testing doesn’t look that bad) could be at higher risk for sepsis.

Bartonella/mold causes inflammation that leads to hypercoagulation.

The body apparently has a built in anticoagulation system that is endothelial related. Remember how Buhner emphatically emphasizes Japanese knotweed to protect the endothelium during Lyme and Bartonella?

The body’s Fibrin Removal gets obstructed, so systemic proteolytic enzymes can help remove the fibrin.

Know how bartonella and mold symptoms overlap extensively??? Maybe it’s because they dysregulate the same body processes. I am pretty sure that Dr AC, in that interview with Better Health Guy, mentioned mold patients among those she treats with systemic proteolytic enzymes. Something for mold folks to consider, in addition to those with bartonella or Lyme.

in general in bart its thought that infection drives a certain sort of inflammation response that triggers the fibrin depositing part of the coagulation system - but not necessarily all of the coagulation response. there are a great many factors and co-factors and pathways in the human coagulation system - 20-30 at least - so its a complex beast and it seems these stealth infections survive by manipulating it in subtle ways to their advantage

in fact in bart at least 50% of the time the normal markers of systemic inflammation
ESR( sedimentation rate - also a marker of coagulation ) is absolutely normal or even v low
C-Reactive protein - also low more often than not

this is related to the fact that bart must have inflammation reducing mechanisms that causes it to be able to live in the blood without triggering massive fever ( the normal response to even small amounts of bacteria in the blood)

this would not be a helpful survival strategy as it would kill the host before another arthropod had time to bite it and carry the bart off elsewhere to new hosts - hence the evolutionary pressure for bart to be a stealth pathogen with suppressed inflammatory response ( compared to most pathogens)

sepsis is something quite different - this is essentially a massive inflammatory response to the presence of foreign matter / microbes in the blood stream - it is a general response that occurs in response to many acute pathogens - including fungal species - eg candida.

in fact the actual pathogen is only identified in a minority of cases and the condition proceeds so quickly that it is fatal in a large proportion of cases.
normally there is some wound or lesion where the pathogen gains entry to the blood stream but this can be unseen, in the gut, an ear or a tooth for instance. once in the blood, it multiplies rapidly and triggers the dramatic inflammatory response - which runs out of control eventually triggering coagulation in the blood vessels organ damage/ death and necrosis. limbs are often lost due to the complete lack of blood flow due to coagulation.
in a way its the total opposite of what bartonella is trying to do.

the pathogens that case it are typically fast growing opportunistic or accidental infections - as opposed to these specifically parasitic infections like bart that can only survive by infecting suitable hots and keeping them alive

bartonella does cause a form of chronic low level hypercoagulation - the slides in the recent galaxy presentation show fibrin lining the blood vessels -
it is also immuno suppressive - so that could be reasoned to increase the risk of any other infections - including sepsis - but i don't think that is the main risk

its not clear yet what exactly the biofim is made of in chronic lyme patients
some LLMD's like Dr J are adamant that chronic lyme disease is a polymicrobial infection
and that the biofilms are polymicrobial colonies - and he is not talking about just borrelia, babesia and bartonella - but maybe 6-8 main species and dozens of lower level players - including fungal species and many opportunistic bacterial infections.

if this is the case it might be necessary to employ a wide variety of biofim disrupting agents as each species may contribute different substances to the mix
bartonella as far as we know does not itself make biofilm - but triggers the body to form fibrin deposits which have similar effects and is likely able to live in mixed biofilm colonies - borrelia certainly does make biofilm - Babesia may trigger fibrin also - Dr MacDonald stated around 90% of other bacteria do make biofilms

unfortunately, so far there seems to be very little agreement as to what exactly works best for these biofilms / deposits