• Welcome to Phoenix Rising!

    Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of and finding treatments for complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia (FM), long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.

    To become a member, simply click the Register button at the top right.

Babesia Divergens: Red Cells deformability and vascular adhesion

Despite improvements with mold detoxification (Cholestyramine) and root canal/ cavitation removal, I still have periods when I slide backwards or get PEM from overexertion. The threshold is higher but still there

Back in 2009, I developed a typical lyme rash, but was told lyme is not in my area. I felt concerned enough to take cats claw for a month and seemed to be fine. But, it was still in back of my mind. My new local MD suggested the DNA Connexions test, which revealed Babesia divergens. Lucky, I ended up doing this test as very few if any test for the divergens type.

Atovaquone and azithromycin for now.

So, a red blood cell parasite. I wonder if there are other similar parasites that we are not testing for that affects RBCs. Instinctively, blood flow and RBC morphology is an important part for me.

This article is educational on the RBC impact:RBCs as targets of infection:Jeffrey McCullough1 ASH Hematology - The Education Program doi: 10.1182/asheducation-2014.1.404 ASH Education Book December 5, 2014 vol. 2014 no. 1 404-409 . I accessed this using Google Scholar.

Interesting excerpts:

The Babesia parasites alter the structure and function of RBCs in which they reside. The merozygotes attach to the RBC and invaginate the membrane to form a vacuole, causing the RBC to be more rigid. This is due partly to the presence of the abnormal nondeformable parasite within the RBC, but also there is some alteration of the RBC skeleton and membrane due to parasite-produced proteins.

Infected RBCs develop ridges that appear to be alterations of the RBC membrane skeleton, but are poorly understood. The parasite delivers proteins that associate with the underside of the RBC membrane and proteins that are exposed on the RBC surface. These poorly understood factors contribute to an adhesive effect of the RBC and parasitized RBCs become abnormally adhesive, including to vascular endothelial cells.

The accumulation of parasitized RBCs in the microvasculature leads to severe clinical complications such as cerebral babesiosis, respiratory distress, and multiorgan failure.

I found this to be a great article on RBCs and how they can be adversely affected by mycoplasma pneumonia, clostridia perfingens, and various viruses.