I think most of the micro-clots are very small (the dots in the images) but able to induce platelet activation which adhere to RBCs. RBCs carrying platelets around would slow their passage in capillaries.
The larger aggregates shown in the fluorescence studies might be an artefact of their preparation, rather than representing their in vivo state. Eg does adding the Thioflavin T that binds to the anomalous amyloid (fluorescence) cause clumping?
ETA: Of course even more likely, they may clump as a result of the spin-down to form the platelet-poor plasma.
This is a good point, the microclots were elicited from the plasma in Dr. Pretorius's study by adding something to make them clot, so you wouldn't see microclots under the microscope if you drew blood and looked at it. It seems the formation/deposition of the microclots is actually in the microcirculation, so hard to visualize and access.
Microclots can be visualized on autopsy in COVID patients in the lungs and other organs. Their presence can be inferred by tissue perfusion MRI, CT, or SPEC scan and by altered venous blood gas readings. The tendency to microclot can be measured through a TEG test
However, to distinguish typical microclots from Long-Covid type resistant microclots
you have to use the method described by Dr. Pretorius in her paper
or examine them after removal by HELP apheresis for the hallmarks of resistant microclots (altered-fibrinogen structure, high alpha-antiplasmin, high serum amyloid, and resistance to breakdown from trypsin).
I think microclots would also contain platelets since they are basically very small thrombi, but they didn't in Dr. Pretorius's study because she elicited the clotting in platelety poor plasma.
Is the above your understanding as well? Two brains are better than one
Still, when it comes to Ron Davis's "Something in the Blood", since that experiment was carried out measuring the ability of WBC in ME/CFS serum to produce energy (and not in a microvasculature environment), it seems the something would have been an exosome (with miRNA which can epigenetically modify other cells), or an unknown signaling molecule.
To me it seems that clots, serum amyloid A, or primed clotting factors would have been spotted and probably wouldn't have the direct impact on intracellular energy production seen in the experiment. Here is a nice summary: https://www.virology.ws/2019/12/16/...grath-on-ron-davis-on-something-in-the-blood/