Following up on that thread, here is another possibility to explain Froome's ET performance:
Schistosomiasis (Bilharzia) is known to result in a reduction of Hb/red cells. The mechanisms are still not clear, but probably there are several factors involved. Any reduction in red cells would trigger a homeostatic response in the body to increase EPO. So if Froome suffers from the disease, his natural EPO levels are getting a boost while he is symptomatic.
He supposedly has received treatment for the disease too keep it in check. Following treatment, his EPO and red cell levels should eventually stabilize. But during this period there would likely be a lag, in which the flatworms (or more precisely, their eggs, which seem to release the factors that reduce red cells) would be eliminated, but his EPO would remain elevated. The situation is somewhat analogous to the reported use of carbon monoxide as a PED. CO inactivates Hb, resulting in a stimulation of EPO. Again, the effect is only temporary, but the idea is that while the effect is there, the athlete will get a boost.
Treatment for schistosomiasis involves a single treatment with praziquantel once a year. Since it must be given annually, I assume the drug does not completely eliminate the organism's eggs, but merely suppresses them to a very low level. Under these conditions, I can well imagine a situation in Froome's body in which he could get the benefit of continual EPO stimulation from low levels of the antigens produced by the eggs. I would be very interested to see what his passport looks like. Since he and Sky have been very open about the effect of the disease on red cells, they must have seen some very dramatic changes in their levels. It makes me wonder how they were able to define a baseline at all.