A few years ago, a section on the gut for CFS and its bacteria would have been just a sentence and not a chapter. The involvement of the gut would likely be a description of poor absorption of nutrients only. Recent studies have suggested that the gut’s bacteria or microfloras may play a major, possibly dominant role, in CFS. Microbiota has a role in immune regulation, and changes in gut microbiota may be the basis for an increased incidence of autoimmune diseases and asthma in developed countries[663]. microfloras do impact stress response.

A 2010 study alters the relationship between microfloras and disease greatly. The study found that metabolic profiles based on bacterial structural components and metabolites are disease-specific. In other words, the pathogens determine different microfloras mixtures. The mixture is almost a fingerprint for the pathogen! Each microfloras produces different mixtures of amino acids, inflammatory chemicals, etc. Some specific microfloras convert food more efficiently than others and thus have been associated with obesity[665] [666]. Other microfloras impact the respiratory immune system and appear to be seeded by the birth process (quasi-inherited). Fecal transplants are most successful when the donor is a blood relative.

Of special interest to CFS patients, is the association of microfloras changes with sleep disorders, as well as behavioral changes in IBS. 92% of CFS patients in one study had IBS. We are not talking about minor changes of microfloras, but large shifts in microfloras populations.

Each person has a unique microfloral signature

We should note that we are talking about many different types and species of bacteria. A total of 947 Bacteroides and 745 Clostridium strains were isolated from 67 healthy and 94 anti-microbial treated children in one study. For each family, over a thousand strains may be seen. Eliminating the harmful ones and encouraging the helpful ones is a task for researchers for decades to come. Shift of strains percentage in a species may be a significant factor that has only been lightly explored. There are more than a 1000 species that commonly live in and on the healthy human body. Each person harbors around 150 species, mostly in the gut (Nature, Volume 464, p. 56,18 March 2010). This unique profile is being investigated as equivalent (or better) than a fingerprint (New Scientist, Volume 215, no. 2875, p. 36, 28 Jul 2012). Identical twins who can rarely be distinguished by DNA are easily distinguished by the use of skin bacteria. A very old Dr.Who episode, used as a story-device, a scanner that determined who was the last person holding an object. This was science fiction then; today it has been demonstrated that a skin bacteria fingerprint will remain, and be detected for up to two weeks on computer mice, keyboards, and tables (Proceeding of the National Academy of Science, Volume 107 p. 6477).

CFS microfloras

Our current knowledge on CFS microfloras is limited, but there are many shifts of families of microfloras from those seen in controls.

  • High Enterobacter species (240%)
  • High Fungi
  • High Gram positive D/L lactate producing bacteria
  • High Klebsiella/Enterobacter
  • High Streptococcus
  • Low Escherichia coli[698](50% less) in 62% of CFS Patients
  • Low Bacteroides species in 25% of CFS Patients
  • Low Bifidobacterium species (30%)
  • Low Lactobacillus species.

This was done from a sample of CFS patients, and these individuals are expected to have different shifts depending on their pathogens (and their genes). This simple model explains the wide variety of laboratory manifestations and symptoms seen in CFS. The pathogens, microfloras, and genes determine the clinical manifestations.

Microfloras encourages pathogens

The triggering event for CFS may be changes of the microfloras that ended up activating pathogens altering microfloras further. Consider a change of microfloras that decreases lysine and increases arginine production: this combination is known to reactivate some herpes viruses. Over production of trypsin reactivates influenza viruses. microfloras and pathogens are a two way street. Pathogens alter microfloras; microfloras reactivates pathogens.

A second route arises from a surprising finding about the high incidence of viral RNA found in stomach samples compared to controls. The viral RNA becomes incorporated with your native microfloras, producing harmful mutations.

Translating this into Remission Modelling

During my research for a forthcoming book, I came across similar information in several studies. The information result in a model that appears to be consistent with CFS/FM/IBS being an alteration of microfloras that persisted.

In probability modelling there are semi-stable processes that are have a random chance of  occurring. A good example is radio-active decay. The pattern that I saw was similar and would be consistent with alteration of microfloras by virus RNA.

The reported data when people with acute onset were followed is shown below. The conditions were technically different, but the onset rates for CFS were surprisingly similar. If we take a view that the infection RNA enters the stomach and result in microfloras mutations, then these mutations will be eliminated over time for most people — however some mutations take a long time to eliminate.

Ross River Virus 11% [583]
Lyme Disease 10-20%[2390]
EBV 11-13% [1651] [1652]
Sarcoidosis 47% [160]
Giardia 50% [1653]
Acute bacterial enteritis patients 7- 33% of IBS [1801]

Some studies tracked people after acute EBV and reported the following rates of these patients moving into CFS. Failure to recover rates for EBV over time

6 months 11%-12%-13%
12 months 7%-9%
24 months 4%

Applying a little mathematical curve fitting to this data, we end up with the result shown below.

6 – 12 Months ~ 50% ~14%
12 – 24 Months (2 yrs) ~ 50% ~7%
24 – 48 Months (4 yrs) ??? 50% ~4%
48 – 96 Months (8 yrs) ??? 50% ~2%
96-192 Months (16 yrs) ??? 50% ~1%

Does this directly helps treat CFS? No — but it suggests that intentional attempts to destabilize microfloras may be beneficial.

(c) 2012 Ken Lassesen