This test is most useful if any of these apply to you.
A stool Streptococcus result combines bacteria with different origins and different roles. Some may have arrived from your mouth, some can live in your intestine, and others come from fermented foods. The total cannot distinguish those possibilities.
Research has linked particular stool streptococci to coronary artery calcium, inflammatory bowel disease, and several other conditions. This remains an exploratory biomarker: there are no validated clinical cutpoints for the pooled genus, and using this result to guide prevention or treatment has not been shown to improve health.
Streptococcus is a genus containing many species. These include common mouth bacteria such as S. salivarius and S. parasanguinis, the yogurt starter S. thermophilus, and species capable of causing infections. Their effects depend on the species, strain, and location in the body.
This stool test estimates the abundance of the genus from bacterial DNA. Detection does not establish that the bacteria are alive, have permanently colonized your gut, or are causing disease. A genus-level result also cannot identify which species account for the total.
Much of the research below used DNA sequencing to measure relative abundance. Relative abundance is the share of detected microbes assigned to a particular group. That share can rise when other bacteria fall, even without an increase in the group's actual number. Research percentages, species-specific results, and counts from different methods are not interchangeable with this result.
You swallow mouth bacteria throughout the day. Stomach acid and conditions inside the intestine influence which survive. In a study of 144 community-dwelling adults, about 73% had at least one matching bacterial DNA sequence in saliva and stool. S. salivarius and S. parasanguinis were prominent among the shared bacteria. The shared sequences usually made up a small fraction of the gut community, a median of about 0.14%, though a few people had much more. Older age and more dental plaque were associated with a larger total amount of these shared sequences in stool.
Matching sequences support a connection between the two sites, but they do not prove that most stool streptococci came from the mouth or that the organisms established lasting colonies. Streptococci also colonize the healthy gut early in life. Research tracing infant strains has identified maternal stool as one possible source.
A separate analysis of 22,710 human microbiome samples developed a score combining several kinds of oral bacteria found in the gut. That score was associated with multiple diseases. It is a different measurement from total stool Streptococcus, and neither result directly measures whether the intestinal lining is leaking.
A study of 8,973 Swedish adults without previously diagnosed cardiovascular disease compared stool bacteria with coronary artery imaging. Sixty-four species were associated with coronary artery calcium after accounting for standard risk factors: 51 tracked with more calcium and 13 with less. S. anginosus and S. oralis had the strongest associations, and several associated species also tracked with blood markers of inflammation. Because the measurements were taken at the same stage of the study, they show an association with existing calcium, not how quickly calcium was accumulating.
A systematic review covering 67 studies also found that stool Streptococcus was often more abundant in people with cardiovascular disease. These studies differed in their populations and methods, and disease, medication, and diet can all influence the microbiome.
One study compared 189 people with acute stroke against 55 people without stroke, then followed the stroke patients for about two years. S. anginosus was enriched in the gut of stroke patients, and in that group it was associated with roughly fivefold higher rates of death and major cardiovascular events. The estimate was imprecise. It concerned one species, so it cannot be translated into a risk estimate from your total Streptococcus abundance.
These findings support further study of specific bacteria in cardiovascular disease. They do not establish that gut streptococci cause artery disease, or that this stool result improves decisions about cholesterol treatment or coronary imaging.
Different species can move in opposite directions. In a study spanning people with low cardiovascular risk through those with an acute heart attack, S. thermophilus became less common as risk increased. A smaller study found lower total stool Streptococcus in infants with eczema. Gestational diabetes studies point both ways: some found less Streptococcus, others found more, and a systematic review found no consistent microbial pattern.
Those observations do not establish that increasing these bacteria would prevent disease. They show why a single interpretation such as 'less is healthier' does not work across this genus. Even identifying a species leaves questions about its strain, activity, and role in the surrounding microbial community.
The best-known colorectal cancer association concerns the S. bovis/S. equinus complex, which includes S. gallolyticus. In a systematic review, people with colorectal cancer had about twice the odds of carrying these particular bacteria in stool or intestinal samples. The analysis did not establish a clear association with adenomas. That uncertainty does not prove that carriage is absent during the precancerous stage.
Bloodstream infection is a separate finding with a stronger clinical implication. Infection involving this bacterial complex was associated with a higher likelihood of colorectal cancer, and S. gallolyticus bloodstream infection or endocarditis warrants evaluation for a colorectal source. A pooled genus-level stool DNA result does not carry the same meaning.
Other studies have examined stool Streptococcus in gastric and pancreatic cancer, including comparisons involving cancer that had spread to the liver. A research model combining stool Streptococcus with Lactobacillus showed some ability to distinguish gastric cancer cases from healthy controls. These were comparisons involving people with known disease, not proof that a standalone Streptococcus test detects cancer early in otherwise healthy people.
This measurement has not been validated to detect or rule out colorectal cancer, gastric cancer, pancreatic cancer, or precancerous growths.
Studies of Crohn's disease and ulcerative colitis have found increased stool streptococci, including oral-associated species such as S. parasanguinis. Research using paired saliva and stool samples has also grown live streptococci from both sites. Culture provides evidence of living organisms in those samples; DNA abundance alone does not.
These patterns are being studied as part of the wider microbial changes accompanying inflammatory bowel disease. Total stool Streptococcus has not been validated to distinguish inflammatory bowel disease from irritable bowel syndrome or to measure disease activity. Fecal calprotectin has an established role in assessing intestinal inflammation.
A small study of people with alcohol-related liver disease found more stool Streptococcus in those with cirrhosis and associations with blood markers of liver injury. It did not establish a reliable way to grade liver damage from this bacterium.
A meta-analysis also found higher Streptococcus abundance in nonalcoholic fatty liver disease. More recent research into metabolic dysfunction-associated steatotic liver disease found enrichment mainly in participants who were not lean. These associations cannot separate the effects of liver disease from accompanying differences in medication, diet, and metabolism.
Certain stool Streptococcus species were more abundant in a study of chronic obstructive pulmonary disease, and two of them correlated with lower lung function. A review of lupus studies described lower oral and higher intestinal Streptococcus abundance. Those opposite patterns do not by themselves demonstrate movement of the same strains between sites.
A small study of children with Kawasaki disease found greater relative stool Streptococcus abundance than in healthy children. Findings from an acute childhood illness do not establish a useful interpretation for preventive testing in adults.
Repeated measurements under similar conditions can document whether the reported abundance changes. There is no validated amount of change that establishes improvement or deterioration in health. A falling total can also conceal different changes among the species included in it.
Streptococcus is best interpreted alongside these tests.
Streptococcus is included in these pre-built panels.
See what your gut microbes are actually doing, not just whether your digestion feels off, and track the balance over time.