Hi there,
Thanks for your questions. After I read the KDM paper which stated that patients with CFS have more strep and enterococci bacteria in stool samples than healthy people, and these bacteria produce d-lactic acid, and the symptoms of CFS were strikingly similar to d-lactic acidosis, I became more interested in looking at d-lactic acidosis.
I believe strep bacteria could cause most of the symptoms you mention, strep throat is a known medical condition, and it contagious. If you have a build up of lactic acid, you become sore, so I think it is possible for d-lactic to cause PEM, however in patients with d-lactic acidosis, they are treat urgently, so this has not been documented.
I found this on the 25 ME group Organisation which mentions the KDM study.
Bacteria in your Guts?
Various gastrointestinal and neurological problems that are common in people with ME/CFS are surprisingly similar to the symptoms of “D-lactic acidosis”. This condition arises from bacterial fermentation of carbohydrates in the gastrointestinal tract, leading to increased lactic acid levels in the blood. Could there be an overgrowth of Gram-positive anaerobic lactic acid bacteria in the guts of ME/CFS patients too?
Scientists at the University of Melbourne in Australia examined the faeces of 108 ME/CFS patients and 177 healthy controls for the presence of the most common of the 500 different bacterial species that inhabit the human gut.
Their recent paper in the journal ‘In Vivo’ reported significantly increased levels of aerobic Gram-positive intestinal bacteria in the ME/CFS group than the controls, particularly Enterococcus and Streptococcus species which are the common aerobic bacteria in humans.
Moreover, the organisms found in the patients produced significantly more lactic acid (p<0.01) than those from the healthy subjects, indicating that acidosis was at least a possibility in ME/CFS.
The researchers postulate that increased colonisation by Enterococcus and Streptococcus could heighten intestinal permeability, assisting the absorption of D-lactic acid into the bloodstream. Increased gut permeability might also aid the release of endotoxins from the bacteria themselves, leading to inflammation, immune activation and oxidative stress, which are prominent features in a large subset of ME/CFS patients.
While the cause of the increased colonization remains unclear, the researchers point out that eradication of all bacteria is not the answer; indigenous bowel microflora has both positive and negative impacts on health, and the balance of “good” to “bad” bacteria is important. And their next experimental step is to measure D- and L-lactic acid accumulation in the biofluids of ME/CFS patients to confirm whether D-lactic acidosis really is a factor. If so, existing interventions, such as short-course antibiotics, alkalinizing agents, a low carbohydrate diet or dietary glucose restriction might prove to be useful.
Here is a link to the full article, which you might have already read.
http://www.cfids-cab.org/rc/Sheedy.pdf
D-lactic acidosis is not taught to anyone other than gastroenterologist's and biochemist's, and they only recognise it as a consequence of a shortened bowel. It needs a specific test, and does not show up in routine testing, although in short bowel patients there is usually an increase in the anion gap. It can occur without this increase however, making testing just about impossible, see below. If you take a look on the Latest Research section, I have put a thread there about d-lactic acidosis, if you are interested.
Second, metabolic acidosis may be present without a rise in the plasma anion gap. In
this latter setting, either the D-lactate anion was retained in the
lumen of the GI tract (with the H being absorbed or titrated by
bicarbonate in the lumen of the GI tract), or it was excreted in the
urine, but in either case, the cation lost with it was Na and/or K
ion [671 (not a H or NH4 ion, lower right portion of Fig. 6).
This latter type of metabolic acidosis is akin to the over-production
of hippuric acid in glue sniffers [68]. Since D-lactate anions
are reabsorbed by the kidney much less readily than is L-lactate
[54, 69, 70], as time progresses, the anion gap may decline without
resulting in a rise in the plasma bicarbonate concentration-that is,
D-Iactate is excreted as its Na or K salt (Fig. 6). Hence there
are a number of mechanisms that may contribute to the presentation
whereby the rise in the plasma anion gap might not match
the fall in the plasma bicarbonate concentration. Not only might
this lead to a diagnostic problem, it has implications for therapy
because, once the organic anions are excreted as their Na or
salts, these anions are no longer available for metabolism to
regenerate bicarbonate, and the patient might have developed a
deficit of Na and/or K4.
This article below talks about d-lactic in calves and states "The mechanism is likely similar to that documented for D-lactic acidosis in SBS in humans
except the etiology of the malabsorption is viral infection–induced villous atrophy rather than surgical removal of the small intestine." It goes on to say "There is a possibility, although it has not been described, that a similar scenario could occur in diarrheic monogastrics, including humans. Villous atrophy and malabsorption certainly occur in humans suffering from viral diarrhea, but whether there is sufficient fermentation to cause excess D-lactate to accumulate is not known. Metabolic acidosis was identified in human rotaviral diarrhea, and was attributed to carbohydrate malabsorption; however, the identity of the acids was not determined."
http://jn.nutrition.org/content/135/7/1619.full
Given the KDM study, I think more investigation needs to be done in this regard, and I thought the poll might help me and others who might be interested, to see whether the two conditions are more strongly linked, and if we a missing an important part in diagnosing CFS.
Hope this helps.
Glynis