My last post cites a 2009 article that found:
“Faecal microbial flora of CFS patients and control subjects. The mean viable count of the total aerobic microbial flora for the CFS group (1.93×108 cfu/g) was significantly higher than the control group (1.09×108 cfu/g) (p<0.001). There was a significant predominance of Gram positive aerobic organisms in the faecal microbial flora of CFS patients. …This study confirms the previous observation (22), and those reported by other investigators (23) that there was a marked alteration of faecal microbial flora in a sub-group of CFS patients….. In this study the mean total count for Enterococcus and Streptococcus spp. for the CFS group was 52% of the total aerobic intestinal flora, which is significantly higher than the 12% seen in the control subjects (p<0.01). ” largely old hat to readers of this blog, a microbiome dysfunction.
But the study went on to some new interesting stuff, a possible mechanism:
“In this study the NMR-based metabolic profiles of the three intestinal micro-organisms, E. faecalis., S. sanguinis. and E. coli showed that the Gram positive bacteria (Enterococcus and Streptococcus spp.) produce more lactic acid than the Gram negative E. coli. Not surprisingly, these Gram positive bacteria were shown to lower the ambient pH of their environment in vitro as compared to that of E. coli. This suggests that when Enterococcus and Streptococcus spp. colonization in the intestinal tract is increased, the heightened intestinal permeability caused by increased lactic acid production may facilitate higher absorption of D-lactic acid into the bloodstream, henceforth perpetuating the symptoms of D-lactic acidosis. Increased intestinal permeability is also associated with endotoxin release from Gram negative enterobacteria, leading to inflammation, immune activation and oxidative stress, which are cardinal features in a large subset of CFS patients ”
This ties in well with observations, for example, some people getting relief by various breathing techniques intended to alter pH of the stomach and intestines.
So, putting on the blinkers and focusing solely on the overgrowth of Enterococcus and Streptococcus, how can someone impact this without getting antibiotics (in some countries, prescribing antibiotics for a condition that is not recognized as needing them, can cost a MD their license)?
- “Among the plants chloroform and isoamyl alcohol extracts of Cumin ( Cuminum cyminum), Clove (Syzygium aromaticum) and Turmeric (Curcuma long Linn) had significant effect against … Streptococcus pyogenes” 
- “Cortex phellodendri showed antimicrobial activity against Streptococcus mutans, while Radix et rhizoma rhei was effective against Streptococcus mitis and Streptococcus sanguis. Fructus armeniaca mume had inhibitory effects againstStreptococcus mitis, Streptococcus sanguis, Streptococcus mutans and Porphyromonas gingivalis in vitro.”  – most of these are Chinese/Japanese medicinal herbs
- “eight herbal extracts could inhibit the growth of Streptococcus sanguinis. Jasmine, jiaogulan, and lemongrass were the most potent,” 
- ” (common Fig) F. carica and (Olive leaf) Olea europaea leaves inhibited growth of… Streptococcus pyogenes” 
- “onion could inhibit E. coli, … Streptococcus faecalis  – not recommended because of impact on E.coli
- ” Lemongrass, oregano and bay inhibited all organisms” 
- “especially those of Origanum glandulosum and (Mediterranean thyme) Thymbra capitata with interesting minimum inhibitory concentration, biofilm inhibitory concentration, and biofilm eradication concentration values” 
Early post on treating Enterococcus cites: Azadirachta indica, Ocimum tenuiflorum, Monolaurin. Streptococcus is associated with excessive histamine, see earlier post. MedScape Article reveal no effective accepted treatment. A fuller article is (here JASN).
“… Recently, considerable progress has been made in the isolation of these strictly anaerobic butyric acid-producing bacteria from the human gut. It has been shown … that lactic acid, produced in vitro by lactic acid bacteria, is used by some strictly anaerobic butyrate-producing bacteria of clostridial cluster XIVa for the production of high concentrations of butyric acid (Louis & Flint, 2009). This mechanism is called cross-feeding …” [Source]
This implies that miyarisan (clostridium-butyricum) should be of benefit.
Supplement Approach – Thiamine (Vitamin B1)
100 mg every 12 hours is reported to reverse this for other conditions.
- “Thiamine replenishment at intravenous doses of 100 mg every 12 h resolved lactic acidosis and improved the clinical condition in 3 patients.” 
Cohen and Woods devised the following system in 1976 and it is still widely used:
- Type A: lactic acidosis occurs with clinical evidence of tissue hypoperfusion or hypoxia is likely what is seen in CFS. The hypoperfusion is well reported as a signature of CFS.
Word on Likely Dosage
The last article cited an article treating it. I noticed that often there was very high dosages. My gut feeling (no evidence to back it up) is that for any of the above, we may well be talking 8 – 16 “00” capsules per day of each one, with a possible change of the herb/spice every 7 days. Remember we are talking about reducing from 52% to 12%, not a walk in the park.
As always, consult with your knowledgable medical professional before starting or changing supplements.
Probiotics to avoid
L. delbrueckii bulgaricus (ATC 11842) has a 26:7 ration of D-Lactic acid to L-Lactic Acid [Source]