I noticed today on facebook that someone posted a link to a NewScientist article Antibody wipeout found to relieve chronic fatigue syndrome (1 July 2015) dealing with the use of Rituximab. This is an anti-cancer drug. Since 2002, I have personally met physically several CFSers that went into full remission of CFS after treatment for cancer. The results are very believable that “Eleven of the 18 responders were still in remission three years after beginning the treatment, and some have now had no symptoms for five years”.
I know that cancer treatment results in a massive change of the microbiome (exactly what my model asks for!). For example:
- Chemotherapy-driven dysbiosis in the intestinal microbiome. “We found that faecal samples collected after chemotherapy exhibited significant decreases in abundances of Firmicutes (P = 0.0002) and Actinobacteria (P = 0.002) and significant increases in abundances of Proteobacteria (P = 0.0002) compared to samples collected before chemotherapy.”
- Effect of chemotherapy on the microbiota and metabolome of human milk, a case report. “Chemotherapy caused a significant deviation from a healthy microbial and metabolomic profile, with depletion of genera Bifidobacterium, Eubacterium, Staphylococcus and Cloacibacterium in favor of Acinetobacter, Xanthomonadaceae and Stenotrophomonas.”
- 16S rRNA gene pyrosequencing reveals shift in patient faecal microbiota during high-dose chemotherapy as conditioning regimen for bone marrow transplantation. ” Chemotherapy was associated with a drastic drop in Faecalibacterium and accompanied by an increase of Escherichia.”
- Oral microbiota distinguishes acute lymphoblastic leukemia pediatric hosts from healthy populations . “patients who developed subsequent bacteremia, or bloodstream infection exhibited decreased overall diversity and decreased abundance of taxa including Barnesiellaceae, Coriobacteriaceae, Faecalibacterium, Christensenella, Dehalobacterium, Desulfovibrio, and Sutterella. Using machine-learning methods, we developed a BSI risk index capable of predicting BSI incidence with a sensitivity of 90 % at a specificity of 90 % based only on the pretreatment fecal microbiome.”
- Fecal microbiota diversity in survivors of adolescent/young adult Hodgkin lymphoma: a study of twins . “Adolescent/young adult Hodgkin lymphoma survivors appear to have a deficit of rare gut microbes.”
- Also, very intersting: Lymphoma caused by intestinal microbiota. “While there are not a plethora of studies demonstrating a connection between microbiota and lymphoma development, we believe that animal models are a system which can be exploited in the future to enhance our understanding of causation and improve prognosis and treatment of lymphoma.”
So, we have Staphylococcus decrease and Escherichia increase – which is precisely the type of shift that I have been advocating….
What does PubMed say for CFS?
There are just 12 studies at the moment, newspaper reports tend to often tilt results to sell newspaper.
- “Recently, two clinical trials of B cell depletion therapy with rituximab (anti-CD20) reported convincing improvement in symptoms.” 
- “In a subgroup of ME/CFS patients, prolonged B-cell depletion with rituximab maintenance infusions was associated with sustained clinical responses.” 
- “The delayed responses starting from 2-7 months after Rituximab treatment, in spite of rapid B-cell depletion, suggests that CFS is an autoimmune disease and may be consistent with the gradual elimination of autoantibodies preceding clinical responses.” 
We have a drug that causes remission in a subset of CFS patients [Fact]. The drug causes multiple effects: B-lymphocyte depletion and shift of the microbiome. Which effect (or a third unknown one) is the cause of remission?
IMHO the shift of the microbiome is more likely, many people have reported on this site (and by private email), significant improvement of symptoms by shifting the microbiome by just probiotics and supplements. There is no apparent link to B-lymphocyte with that treatment.
The model also predicts that any treatment will only be effective on subsets because the success is determined by the effectiveness of the treatment against the very specific strains that a person has. This is what is reported in the above literature — effective for a subset.
If you can get this prescribed by your MD, covered by insurance, and you fully understand the risks (see official literature), then give it a try. For myself, I would exhaust the appropriate probiotics and appropriate antibiotic paths first.