Dysbiosis

Dysbiosis is an imbalance in the microbial ecology of a part of the body, usually the gut.

Psychological stress
Psychological stress can alter the gut microbiota, decreasing numbers of Bifidobacteria and Lactobacilli.

Antibiotic use
Antibiotics negatively alter the healthy combination of phyla within the gut microbiota, e.g. by reducing the ratio of Firmicutes to Bacteroidetes, and increasing levels of Proteobacteria. The antibiotics ciprofloxacin, vancomycin, ampicillin, cefazolin and cefoperazone reduce the diversity of gut microbiota, although in one study ciprofloxacin increased rather than decreased the Firmicutes to Bacteroidetes ratio. Combination antibiotics cause more severe dysbiosis than using a single antibiotic.

Lifetime antibiotic use alters the gut microbiome and is a proposed risk factor for ME/CFS.

Long-term probiotic use
Degirolamo et al (2014) states that Bifidobacterium and Lactobacillus probiotic strains may provide additional good bacteria, reducing the harm from antibiotics, but in long term use may also disturb the balance of gut microbiota.

ME/CFS
There is evidence that dysbiosis or an imbalance in the microbial ecology of the gut plays a role in the symptoms of ME/CFS. On average, ME/CFS patients have lower levels of Bifidobacteria, Escherichia coli and higher levels of aerobic bacteria, in particular Enterococcus and Streptococcus species. The latter produce D-lactate, a form of lactic acid only produced by non-human cells that is poorly metabolized in humans. D lactate is associated with a wide variety of cognitive and neurological symptoms, such as in patients who suffer from D-lactic acidosis. A study found that higher levels of Enterococcus bacteria in CFS patients were associated with more severe neurological and cognitive dysfunction.

"In one study researchers were able to classify 83% of the ME/CFS patients correctly based on their dysbiosis in gut and increased inflammatory markers in blood as a consequence of microbial translocation (13)."

CFS patients may suffer from small intestinal bacterial overgrowth (SIBO) at higher rates.

One hypothesized consequence of dysobiosis is an overproduction of hydrogen sulfide (H2S) by pathogenic bacteria. H2S can inhibit mitochondrial respiration by blocking cytochrome c oxidase.

Sheedy et al. (2009) studied Norwegian and Belgian ME/CFS patients and found significantly decreased proportions of Firmicutes genera Holdemania and increased proportions of bacteroidetes genera Alistipes in the Norwegian but not the Belgian sample. Significantly increased proportions of Firmicutes genera Lactonifactor were found in both.

Notable studies

 * 2003, Chronic fatigue syndrome: lactic acid bacteria may be of therapeutic value - (Full text)
 * 2007, Normalization of the increased translocation of endotoxin from gram negative enterobacteria (leaky gut) is accompanied by a remission of chronic fatigue syndrome - (Full text)
 * 2007, Increased serum IgA and IgM against LPS of enterobacteria in chronic fatigue syn- drome (CFS): indication for the involvement of gram-negative enterobacteria in the etiology of CFS and for the presence of an increased gut-intestinal permeability - (Full text)
 * 2009, Increased d-lactic Acid intestinal bacteria in patients with chronic fatigue syndrome - (Full text)
 * 2013, High-throughput 16S rRNA gene sequencing reveals alterations of intestinal microbiota in myalgic encephalomyelitis/chronic fatigue syndrome patients - (Full text)
 * 2015, Increased expression of activation antigens on CD8+ T lymphocytes in Myalgic Encephalomyelitis/chronic fatigue syndrome: inverse associations with lowered CD19+ expression and CD4+/CD8+ ratio, but no associations with (auto) immune, leaky gut, oxidative and nitrosative stress biomarkers - (Abstract)
 * 2015, Changes in gut and plasma microbiome following exercise challenge in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) - (Full text)
 * 2016, The role of microbiota and intestinal permeability in the pathophysiology of autoimmune and neuroimmune processes with an emphasis on inflammatory bowel disease type 1 diabetes and chronic fatigue syndrome - (Full text)
 * 2016, A role for the intestinal microbiota and virome in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) - (Full text)
 * 2016, The association of fecal microbiota and fecal, blood serum and urine metabolites in myalgic encephalomyelitis/chronic fatigue syndrome - (Full text)
 * 2016, Reduced Diversity and Altered Composition of the Gut Microbiome in Individuals With Myalgic Encephalomyelitis/Chronic Fatigue Syndrome - (Full text)
 * 2017, Fecal Metagenomic Profiles in Subgroups of Patients With Myalgic Encephalomyelitis/Chronic Fatigue Syndrome - (Full text)
 * 2018, The Emerging Role of Gut Microbiota in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): Current Evidence and Potential Therapeutic Applications - (Full text)
 * 2018, A role for a leaky gut and the intestinal microbiota in the pathophysiology of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) - (Thesis - Full text)
 * 2020, The “Leaky Gut”: Tight Junctions but Loose Associations? - (Full text)
 * 2020, Mitochondria and immunity in chronic fatigue syndrome - (Full text)
 * 2021, The Emerging Role of Gut Microbiota in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): Current Evidence and Potential Therapeutic Applications - (Full text)
 * 2021, Tryptophan Metabolites, Cytokines, and Fatty Acid Binding Protein 2 in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome - (Full text)
 * 2022, The Gut Microbiome in Myalgic Encephalomyelitis (ME)/Chronic Fatigue Syndrome (CFS) - (Full text)