Welcome to my blog post Desulfovibrio: What You Need To Know
You may like to also read my blog Hydrogen Sulphide: The Good, the bad, and the misunderstood.
What Is Desulfovibrio?
Desulfovibrio are sulfate-reducing bacteria that are ubiquitously present in the environment and as resident commensal bacteria within the human gut. Though they are minor residents of the healthy gut, Desulfovibrio are ‘opportunistic pathobionts’ that may overgrow in the setting of various intestinal and extra-intestinal diseases.
An increasing number of studies have demonstrated a positive correlation between Desulfovibrio overgrowth and various human diseases. (source) One of the known mechanisms explaining this correlation is due to the fact that they produce hydrogen sulfide gas (H2S).
While the relationship between Desulfovibrio overgrowth and disease pathology has not been clearly established, mounting evidence suggests a causal role for these bacteria in disease development.
Within a healthy human host, DSV localise to the pH neutral, distal colon where they represent ~66% of all colonic SRB.
What Causes An Overgrowth?
In anaerobic environments with low redox potential, other anaerobic bacteria directly compete with desulfovibrio for hydrogen, including those that convert hydrogen to methane (methanogens) or acetate (acetogens), with the presence of sulfate being crucial to this competition. (source).
So we can conclude that an aerobic environment, with poor redox potential that is high in the presence of sulphate may lead to an overgrowth of desulfovibrio.
Desulfovibrio bacterial strains
There are more than 30 proposed species including:
- D. desulfuricans.
- D. vulgaris.
- D. salexigens.
- D. africanus.
- D. gigas.
- D. baculatus.
- D. sapovorans.
- D. baarsii.
- D. thermophilus.
- D. fairfieldensis
- D. gabonensis.
- D. piger.
- D. profundus.
- D. aosterae.
- D. burkinensis.
- D. longus.
- D. orale.
- D. aespoeensis.
Conditions Associated With Desulfovibrio
There are a number of diseases that are associated with desulfovibrio overgrowth. These include conditions that not only affect the gut but also affect parts of the body outside of the gut.
There are case reports that frame desulfovibrio as an agent of bacteremia (bacteria in the blood), including in the context of sepsis, renal cyst infection, liver abscess, acute cerebral infarction, and ulcerative colitis.
Among these reports, D. desulfuricans and D. fairfieldensis are usually described as the predominant species responsible for infections. (source)
Intestinal Bacterial Overgrowth
The majority of evidence points toward a positive association between desulfovibrio overgrowth and disease pathology – further research is needed to fully understand this connection. Below, I summarise intestinal and extra-intestinal disorders that are linked to desulfovibrio overgrowth. (source)
Inflammatory Bowel Disease
Inflammatory bowel disease, including Crohn’s disease and ulcerative colitis, is characterised by chronic inflammation of the gastrointestinal tract. It is widely known that IBD patients have dysbiosis (an imbalance in gut bacteria). Multiple studies have identified that desulfovibrio are enriched in IBD. Colon mucosal biopsy samples obtained from ulcerative colitis patients revealed a significant increase in desulfovibrio in acute and chronic ulcerative colitis when compared to healthy controls. In a separate study, a higher number of desulfovibrio, specifically D. piger, were isolated from faeces of patients with IBD compared to healthy subjects. (source)
A longitudinal study of UC patients conducted over a period of 1 year revealed a positive correlation between DSV with high clinical activity indices and worse sigmoidoscopy scores. In UC patients, desulfovibrio abundance was not only correlated with intestinal disease but also with anxiety and depression. (source)
It was also found that the small intestinal transit time was prolonged in IBD patients, suggesting that intestinal transit may be dysregulated in IBD patients. Moreover, an increase in the production of hydrogen sulfide has also been linked to IBD. The role of desulfovibrio in causing slowing of intestinal transit was demonstrated. (source)
DSV overgrowth has also been linked to Parkinson’s disease. (source) While the cause of Parkinson’s disease is still not fully understood, it has recently been proposed that it may originate in the gut. The gut microbiome profile in Parkinson’s disease patients has been found to have significantly increased levels of DSV compared to controls. (source)
Furthermore, one study compared desulfovibrio from Parkinson’s disease patients to that of healthy controls. They found that isolates from Parkinson’s disease patients were more potent than similar DSV isolates from healthy controls when it came to α-syn aggregation – a hallmark of the disease.
These data suggest that some factor(s) in the PD gastrointestinal environment may change certain Desulfovibrio spp. to make them more pathogenic. (source)
Many studies have reported an increase in the abundance of DSV in context of autism. For instance, it was found that children with ASD had more desulfovibrio when compared to healthy children. Additionally, severity of ASD appears to be proportional to DSV abundance. Despite this strong correlation, studies aiming to understand the mechanistic link between DSV overgrowth and ASD are lacking. Some studies have suggested a few mechanisms by which DSV may be responsible for ASD. (source)
One study found low iron bioavailability caused by DSV due to its production of hydrogen sulphide. By binding iron, hydrogen sulfide forms iron sulfide, resulting in iron deficiency, a feature of autism. (source)
Another mechanism by which DSV may contribute to autism is through their production of LPS endotoxin. (source) This is supported by findings that show increased endotoxin (LPS) concentrations in autism patients when compared to healthy controls. LPS may contribute in ASD by causing neuroinflammation. (source)
Several studies have reported an increase in DSV in cancer patients when compared to healthy control groups. This has been observed in cases of rectal cancer, adenomatous polyps, colorectal cancer, gastric cancer, breast cancer, and lynch syndrome. (source)
The main player in DSV-induced cancer phenotypes appears to be the hydrogen sulphide produced by these bacteria. Hydrogen sulphide is known to cause DNA damage and contributes to colorectal cancer.
The role of hydrogen sulphide in mitochondria has also been discussed in context of cancer. (source)
Many studies have reported a positive correlation between DSV and obesity and other metabolic syndrome phenotypes. A high abundance of desulfovibrio was observed in obese patients. Testing has revealed an abundance of DSV in Type 2 diabetes (T2D).
My Interview with Dr. Greg Nigh
How To Reduce Desulfovibrio
Various therapies aimed at treating human cancer patients and animal models have shown that desulfovibrio abundance can be successfully suppressed with probiotic treatments. (source)
In another study, oral administration of Bifidobacterium reduced the abundance of DSV and improved dextran sodium sulfate (DSS)-induced colitis and colon cancer in rats. (source) While I can’t find the exact strain a good bifido blend is Probiota Bifido.
Similarly, Lactobacillus coryniformis MXJ32 administration decreased desulfovibrio and ameliorated azoxymethane/DSS-induced colitis-associated colorectal cancer, enhanced tight junction proteins, and downregulated proinflammatory cytokines. (source)
At gut microbial level, L. acidophillus decreased the abundance of DSV. While I can’t find the exact strain a good lacto blend is Acidophilus Ultra.
Additionally, both diet (consisting of pre- and pro-biotics as well as whole grains) and feral microbiota transplant have been shown to control blood glucose and blood pressure levels in T2D patients while also significantly decreasing desulfovibrio and other sulphate reducing bacteria.
In another study, consumption of high dietary fiber reduced T2D and DSV in Chinese patients . In other interventional studies in pre-clinical models, various compounds have been shown to have a protective effect against T2D and to decrease the DSV load. (source)
A high-fat, high-fructose corn syrup-based, high-cholesterol western-style diet was found to cause obesity, dyslipidemia, and systemic insulin resistance in juvenile Ossabaw swine pigs compared to control pigs. (source)
Additionally, it was found that exercise improved Western diet (WD)-induced atherosclerosis by modulating gut microbiota, including diet-induced increase in desulfovibrio.
In contrast to a high fat diet, a diet rich in fiber showed a negative association with DSV abundance. In a cross-sectional and a longitudinal study involving Chinese patients, it was shown that high fiber intake among diabetes patients lowered the abundance of DSV. (source)
For example, a high-fiber diet ameliorated T2D serological and psychiatric outcomes in a randomized control study, with these outcomes correlating with a decrease in DSV abundance. (source)
The prebiotic GOS.
The bifido blend Probiota Bifido.
The lacto blend Acidophilus Ultra.