CAM 20426

Fecal Analysis in the Diagnosis of Intestinal Dysbiosis

Category:Laboratory   Last Reviewed:October 2019
Department(s):Medical Affairs   Next Review:October 2020
Original Date:November 2001    

Intestinal dysbiosis may be defined as a state of disordered microbial ecology that is believed to cause disease. Laboratory analysis of fecal samples is proposed as a method of identifying individuals with intestinal dysbiosis.

The evidence for fecal analysis in patients who have suspected intestinal dysbiosis, irritable bowel syndrome, malabsorption or small intestinal overgrowth of bacteria includes several cohort and case control studies comparing fecal microbiota in patients with a known disease and healthy controls. Relevant outcomes are test accuracy and validity, symptoms and functional outcomes. No studies were identified on the diagnostic accuracy of fecal analysis versus another diagnostic approach or compared health outcomes in patients managed with and without fecal analysis tests. The evidence is insufficient to determine the effects of the technology on health outcomes.

Regulatory Status
Clinical laboratories may develop and validate tests in-house and market them as a laboratory service; laboratory-developed tests (LDTs) must meet the general regulatory standards of the Clinical Laboratory Improvement Act (CLIA). The Genova Diagnostics test is available under the auspices of CLIA. To date, the U.S. Food and Drug Administration has chosen not to require any regulatory review of this test.


  1. Fecal analysis by culture prior to fecal microbiota transplant (FMT) for the following microorganisms is considered MEDICALLY NECESSARY in accordance with the Food and Drug Administration:
    1. Extended spectrum beta-lactamase (ESBL)-producing Enterobacteriaceae
    2. Vancomycin-resistant Enterococci (VRE)
    3. Carbapenem-resistant Enterobacteriaceae (CRE)
    4. Methicillin-resistant Staphylococcus aureus (MRSA)
  2. Fecal analysis by nucleic acid amplification testing (NAAT) prior to fecal microbiota transplant (FMT) for the following microorganisms is considered NOT MEDICALLY NECESSARY:
    1. Extended spectrum beta-lactamase (ESBL)-producing Enterobacteriaceae
    2. Vancomycin-resistant Enterococci (VRE)
    3. Carbapenem-resistant Enterobacteriaceae (CRE)
    4. Methicillin-resistant Staphylococcus aureus (MRSA)
    5. Any other microorganisms not listed above
  3. Fecal analysis of the following components is considered NOT MEDICALLY NECESSARY as a diagnostic test for the evaluation of intestinal dysbiosis, irritable bowel syndrome, malabsorption or small intestinal overgrowth of bacteria:
    1. Triglycerides
    2. Chymotrypsin
    3. Iso-butyrate, iso-valerate, and n-valerate
    4. Meat and vegetable fibers
    5. Long chain fatty acids
    6. Cholesterol
    7. Total short chain fatty acids
    8. Levels of Lactobacilli, bifidobacteria, and E. coli and other "potential pathogens," including Aeromona, Bacillus cereus, Campylobacter, Citrobacter, Klebsiella, Proteus, Pseudomonas, Salmonella, Shigella, S. aureus, Vibrio
    9. Identification and quantitation of fecal yeast (including C. albicans, C. tropicalis, Rhodoptorul and Geotrichum )
    10. N-butyrate
    11. Beta-glucoronidase
    12. pH
    13. Short chain fatty acid distribution (adequate amount and proportions of the different short chain fatty acids reflect the basic status of intestinal metabolism)
    14. Fecal secretory IgA 

The human intestinal tract has a diverse and complex microbial community necessary for health and nutrition. The gut microbiome is estimated to consist of upwards of 1000 bacterial species (Guinane & Cotter, 2013; Ley, Peterson, & Gordon, 2006; Qin et al., 2010). The microbiota functions with the immune system to protect against pathogens. It also performs essential metabolic functions, extracting certain forms of energy and nutrients from food and providing a source of other essential nutrients and vitamins (Carding et al., 2015).

The gut is colonized at birth, but the intestinal microbiome changes rapidly during the first year of life. In adults, each individual’s unique population of gut microbiota is fairly stable over time; however, alterations in the microbiota can result from exposure to various environmental factors, including diet, toxins, drugs, and pathogens (Carding et al., 2015; Lozupone, Stombaugh, Gordon, Jansson, & Knight, 2012; Snapper & Abraham, 2019). This change in an individual’s normal microbiota is called “dysbiosis” (Johnston, 2017). Dysbiosis has been associated with obesity (Ley, Turnbaugh, Klein, & Gordon, 2006; Zhang et al., 2009) malnutrition (Kau, Ahern, Griffin, Goodman, & Gordon, 2011), systematic diseases such as diabetes (Qin et al., 2012) and chronic inflammatory diseases such as inflammatory bowel disease (IBD) (Frank et al., 2007; Guinane & Cotter, 2013). Both direct assessment of the gut microbiota (examination of bacteria levels) and indirect assessment (measurement of non-living markers such as pH or beta-glucoronidase) have been proposed for investigation of intestinal dysbiosis.

Microbial or microbial-derived components have also been cited as potential representations of dysbiosis. For example, short-chain fatty acids have been identified as a mechanism to regulate intestinal processes and, as such, may represent dysbiosis (Johnston, 2017). These fatty acids are the products of bacterial fermentation of fiber, and the concentrations of these fatty acids have been noted to decrease in IBD cases. Some fatty acids, especially butyrate, have been demonstrated to factor in signaling cascades that control immune function, which indicates a role in controlling intestinal inflammation (Parada Venegas et al., 2019). Ongoing research has uncovered many other potential links between intestinal metabolism and gut microbiota so many markers have been suggested as potential indicators of dysbiosis.

Many tests exist for the assessment of the gut microbiome. Due to the amount of conditions associated (or proposed to be associated) with gut microbiome balance, there are many corresponding tests, including screening measures intended for completely healthy individuals. These tests primarily revolve around nucleic acid amplification; microbial DNA or RNA is obtained from the sample, unique sequences are identified, and the nucleic acid is quantified (Raby, 2019). For instance, Viome offers a comprehensive screening panel that measures “all microorganisms” in the gut (including viruses, archaea, yeast, fungi, parasites, and bacteriophages). Those measurements are combined into a score for various issues, such as inflammatory activity, digestive efficiency, methane gas production, overall gas production, and more (Viome, 2019a). Viome also provides a list of nutritional recommendations, broken down into individual foods. Viome performs RNA sequencing with Illumina NextSeq and uses bioinformatics algorithms to classify taxonomic data (Viome, 2019b).

Some companies may offer companion products with their gut microbiome tests. BioHM provides a similar assessment of bacterial and fungal species in an individual’s gastrointestinal tract, but the company also offers a series of probiotics. These probiotics are intended for various purposes, such as colon cleansing or immunity (BioHM, 2018). Other companies offering a gut microbiome test include Thryve, GenCove, DayTwo, American Gut, and Genova (DNATestingChoice, 2019; Genova, 2019).

The potential clinical impact of imbalance in the intestinal microbiota suggests a need for standardized diagnostic methods to facilitate microbiome profiling. Documenting dysbiosis has traditionally relied on classical microbiological techniques and the ability to culture pure isolates for identification and classification; however, the ability to classify bacteria and archaea according to individual 16S rRNA sequences can now possibly provide a rapid and detailed means of profiling complex communities of microorganisms (Casen et al., 2015; Zoetendal, Akkermans, & De Vos, 1998).   Laboratory analysis of various fecal biomarkers have also been proposed as a method of identifying individuals with intestinal dysbiosis and may be useful in providing insight into the role of intestinal health and disease, and the development of non-gastrointestinal conditions associated with intestinal dysbiosis. However, there is a current lack of literature on the normal ranges of these biomarkers, which limit the applicability of these analyses in a general clinical setting (Bäckhed et al., 2012; Berry & Reinisch, 2013; Pang, Leach, Katz, Day, & Ooi, 2014).

Falony et al analyzed “two independent, extensively phenotyped cohorts: the Belgian Flemish Gut Flora Project (FGFP; discovery cohort; N = 1106) and the Dutch LifeLines-DEEP study (LLDeep; replication; N = 1135).” These two sets were integrated with global data sets, combining to yield 3948 items. A “core” set of 14 genera was identified. 69 clinical and questionnaire-based covariates were found to be associated with microbiota compositional variation with a 92% replication rate. The authors noted that “stool consistency showed the largest effect size, whereas medication explained largest total variance and interacted with other covariate-microbiota associations, but early-life events such as birth mode were not reflected in adult microbiota composition” (Falony et al., 2016)

Zhernakova et al sequenced the gut microbiomes of 1,135 participants from a Dutch population-based cohort. The authors identified relations between the microbiome and “126 exogenous and intrinsic host factors, including 31 intrinsic factors, 12 diseases, 19 drug groups, 4 smoking categories, and 60 dietary factors”. “Significant” associations were found between the gut microbiome and various intrinsic, environmental, dietary, medication parameters, and disease phenotypes. The authors calculated that 18.7% of variation in microbial composition could be explained by these factors, and they observed that fecal chromogranin A was exclusively associated with 61 microbial species, totaling 53% of the microbial composition. A more diverse microbiome was associated with low CgA concentrations. The authors concluded that “these results are an important step toward a better understanding of environment-diet-microbe-host interactions” (Zhernakova et al., 2016).

Lo Presti et al profiled the fecal and mucosal microbiota of IBD and IBS patients. 38 IBD patients, 44 IBS patients, and 47 healthy controls were included, and overall, 107 fecal samples were provided. The authors found that “Anaerostipes and Ruminococcaceae were identified as the most differentially abundant bacterial taxa in controls, Erysipelotrichi was identified as [a] potential biomarker for IBS, while Gammaproteobacteria, Enterococcus, and Enterococcaceae [were identified] for IBD” (Lo Presti et al., 2019).

Malham et al investigated the microbiotic profile of pediatric IBD. 143 IBD patients and 34 healthy controls were included. A reduced “richness” in microbiotic profile was observed in IBD patients compared to healthy controls. In ulcerative colitis (UC), that reduced richness was associated with high intestinal inflammation and extensive disease. Nine species were “significantly” associated with a healthy microbiome, and three species were associated with IBD. The authors remarked that the microbiome composition could differentiate between Crohn’s Disease, UC, and healthy controls (Malham et al., 2019).

Danilova et al compared the gut microbiome composition of IBD patients to healthy controls. 95 IBD patients and 96 healthy controls were included. The authors noted an increase of Proteobacteria and Bacteroidetes bacteria and decrease of Firmicutes bacteria and Euryarchaeota archaea in IBD patients. Butyrate-producing and hydrogen-utilizing bacteria were observed to have lower representation in IBD patients. Short-chain fatty acids (SCFA) were also found to have a lower absolute content in IBD patients. The authors suggested that this finding may “indicate inhibition of functional activity and number of anaerobic microflora and/or an (sic) change in SCFA utilization by colonocytes” (Danilova et al., 2019).

Vaughn et al in reviewing the current status of intestinal dysbiosis and fecal transplantation found that “it is hypothesized that intestinal dysbiosis may contribute to the pathogenesis of many diseases, especially those involving the gastrointestinal tract. Therefore, fecal microbiota transplantation (FMT) is increasingly being explored as a potential treatment that aims to optimize microbiota composition and functionality (Vaughn, Rank, & Khoruts, 2018).” Holleran et al also found that fecal transplant is not recommended for use outside of Clostridium difficile infection (CDI) due to concerns regarding outcome and safety; however, several case series and randomized controlled trials have described its use in a research environment for a few gastrointestinal conditions related to intestinal dysbiosis, including ulcerative colitis (UC), Crohn's disease (CD) and irritable bowel syndrome (IBS). The most successful reports of the clinical efficacy of FMT in gastrointestinal conditions outside of CDI have been in treating UC (Holleran et al., 2018).

2015 World Gastroenterology Organization (WGO) (Bernstein et al., 2016)
The WGO released their global guidelines for Inflammatory Bowel Disease in 2015 (published in 2016).  Their recommendations concerning stool examination and testing are as follows:

  • “Routine fecal examinations and cultures should be carried out to eliminate bacterial, viral, or parasitic causes of diarrhea.
  • Testing for Clostridium difficile (should be considered even in the absence of antecedent antibiotics) — should be carried out within 2 hours of passage of stools.
  • A check for occult blood or fecal leukocytes should be carried out if a patient presents without a history of blood in the stool, as this can strengthen the indication for lower endoscopy. Where lower endoscopy is readily available, these tests are rarely indicated.
  • Lactoferrin, α1-antitrypsin. The main reason for listing this test is to rule out intestinal inflammation, rather than using it as a positive diagnostic test. It may not be available in developing countries, but it can be undertaken relatively inexpensively and easily with rapid-turnaround slide-based enzyme-linked immunoassay (ELISA) tests.
  • Calprotectin — a simple, reliable, and readily available test for measuring IBD activity — may be better for UC than CD; the rapid fecal calprotectin tests could be very helpful in developing countries. If available, a home test may be useful as a routine for follow-up (Bernstein et al., 2016).”

2012 Rome Foundation Report (Simren et al., 2013)
An international Working Group convened in 2012 “to provide clinical guidance on modulation of gut microbiota in IBS” and released their findings on intestinal microbiota in functional bowel disorders: a Rome foundation report in 2013.  They state the following “Diagnostic and therapeutic general recommendations”:

  • “There is currently no clinically useful way of identifying whether the microbiota are disturbed in particular patients with irritable bowel syndrome (IBS).
  • Dietary evaluation and exclusion of possible sources of unabsorbable carbohydrates including fermentable oligo-, di- and mono-saccharides and polyols and excessive fibre could be beneficial in select patients.
  • Probiotics have a reasonable evidence base and should be tried, for a period of at least 1 month, at adequate doses before a judgement is made about the response to treatment.
  • The utility of testing for small intestinal bacterial overgrowth (SIBO) in the setting of IBS remains an area of uncertainty.
  • If SIBO is strongly suspected based on clinical presentation and testing is being considered, using stringent criteria for the glucose breath test or jejunal aspirate appear to be the best tests.
  • Consideration should be given to discontinuing proton pump inhibitors in those with SIBO.
  • There is emerging evidence that non-absorbable antibiotics may have the potential to reduce symptoms in some patients with IBS (Simren et al., 2013).”

European Society for Pediatric Gastroenterology, Hepatology, and Nutrition/European Society for Pediatric Infectious Diseases (ESPGHAN/ESPID)
These joint guidelines reviewed management of acute gastroenteritis (AGE) in children. In it, they note that AGE does not require a specific diagnostic workup and that “microbiological investigation is not helpful in most cases”. Fecal markers are also not recommended for differentiating viral and bacterial AGE. However, the guidelines observe that “microbiological investigations may be considered in children with underlying chronic conditions (eg, oncologic diseases, IBDs, etc), in those in extremely severe conditions, or in those with prolonged symptoms in whom specific treatment is considered” (Guarino et al., 2014).

World Gastroenterology Organisation Global Guidelines (WGO, 2013)
The WGO published guidelines on functional gastrointestinal (GI) symptoms. In it, they identify diagnostic tests for these symptoms. The basic diagnostic tests are as follows:

  • Complete blood cell count (CBC)
  • Erythrocyte sedimentation rate (ESR) / C-reactive protein (CRP)
  • Biochemistry panel
  • Fecal occult blood (patient aged > 50 y)
  • Pregnancy test
  • Liver function tests
  • Calprotectin or other fecal test to detect inflammatory bowel disease in patients thought to have IBS, but in whom inflammatory bowel disease (IBD) is a possibility; now routine in many primary care settings (in the United Kingdom)
  • Celiac serology; considered routine in areas with a high prevalence of celiac disease
  • Stool testing for ova and parasites

National Institute for Health and Care Excellence (NICE, 2017)
NICE updated their IBS guidelines in 2017. In it, they list the following items about diagnostic tests:

"In people who meet the IBS diagnostic criteria, the following tests should be undertaken to exclude other diagnoses:

  • full blood count (FBC)
  • erythrocyte sedimentation rate (ESR) or plasma viscosity
  • c‑reactive protein (CRP)
  • antibody testing for coeliac disease (endomysial antibodies [EMA] or tissue transglutaminase [TTG]).

The following tests are not necessary to confirm diagnosis in people who meet the IBS diagnostic criteria:

  • ultrasound
  • rigid/flexible sigmoidoscopy
  • colonoscopy; barium enema
  • thyroid function test
  • faecal ova and parasite test
  • faecal occult blood
  • hydrogen breath test (for lactose intolerance and bacterial overgrowth)” (NICE, 2017).

Infectious Diseases Society of America/American College of Gastroenterology/American Society for Gastrointestinal Endoscopy/American Gastroenterological Association/North American Society for Pediatric Gastroenterology, Hepatology and Nutrition (IDSA/ACG/ASGE/AGA/NASPGHAN)
These joint guidelines were sent to the FDA regarding recurrent Clostridium difficile infection (CDI). In it, the guidelines recommend screening donors for fecal microbiota transplantation (FMT) for C. difficile toxin B and performing a culture for enteric pathogens (IDSA/ACG/ASGE/AGA/NASPGHAN, 2013).

NASPGHAN published an FMT guideline for children in 2019, and the same analytes for screening (C difficile toxin B, culture for enteric pathogens) were recommended (Davidovics et al., 2019).

Food and Drug Administration (FDA)
The FDA has issued a guidance statement for fecal microbiota transplant (FMT) stating that it will exercise enforcement discretion regarding the investigational new drug (IND) requirements for the use of fecal microbiota for transplantation. In 2019, the FDA updated their guidance on FMT, stating that “FMT donor stool testing must include MDRO testing to exclude use of stool that tests positive for MDRO. The MDRO tests should at minimum include extended spectrum beta-lactamase (ESBL)-producing Enterobacteriaceae, vancomycin-resistant enterococci (VRE), carbapenem-resistant Enterobacteriaceae (CRE), and methicillin-resistant Staphylococcus aureus (MRSA). Culture of nasal or peri-rectal swabs is an acceptable alternative to stool testing for MRSA only. Bookend testing (no more than 60 days apart) before and after multiple stool donations is acceptable if stool samples are quarantined until the post-donation MDRO tests are confirmed negative (FDA, 2019).”

Fecal Microbiota Transplantation Workgroup (2011)
This Working Group published guidelines on FMT. Fecal donor screening recommendations were included. The following analytes were recommended to be screened:

  • “C difficile toxin B by PCR; if unavailable, then evaluation for toxins A and B by enzyme immunoassay (EIA)
  • Routine bacterial culture for enteric pathogens
  • Fecal Giardia antigen
  • Fecal Cryptosporidium antigen
  • Acid-fast stain for Cyclospora, Isospora, and, if antigen testing unavailable, Cryptosporidium
  • Ova and parasites
  • Helicobacter pylori fecal antigen (for upper gastrointestinal [GI] routes of FMT administration)” (Bakken et al., 2011).

American Gastroenterological Association (AGA, 2015)
The AGA published guidelines on FMT, including information on donor pathogen screening. C. difficile toxin B and culture for enteric pathogens were “suggested” to be screened for, Giardia, Cryptosporidium, Isospora and Cyclospora, Listeria, E. coli O157, Vibrio, and Norovirus should be “considered”, and Cytomegalovirus, Human T-cell lymphoma virus, Epstein–Barr virus, Dientamoeba fragilis, Blastocystis hominis, Strongyloides stercoralis, Entamoeba histolytica, H. pylori, Schistosoma, JC virus, Vancomycin-resistant enterococci, and Methicillin-resistant Staphylococcus aureus should “maybe” [term used by authors] be screened (Kelly et al., 2015).


  1. Bäckhed, F., The Wallenberg Laboratory, U. o. G., Sahlgrenska University Hospital, Göteborg, Sweden 41345, Institute for Genome Sciences at the University of Maryland School of Medicine, B., MD 21201, USA, Ringel, Y., Division of Gastroenterology and Hepatology, D. o. M., University of North Carolina at Chapel Hill, NC 27599, USA, Dairy & Food Culture Technologies, C., CO 80122, USA, . . . (2012). Defining a Healthy Human Gut Microbiome: Current Concepts, Future Directions, and Clinical Applications. Cell Host & Microbe, 12(5), 611-622. doi:10.1016/j.chom.2012.10.012
  2. Bakken, J. S., Borody, T., Brandt, L. J., Brill, J. V., Demarco, D. C., Franzos, M. A., . . . Surawicz, C. (2011). Treating Clostridium Difficile Infection With Fecal Microbiota Transplantation. Clinical Gastroenterology and Hepatology, 9(12), 1044-1049. doi:10.1016/j.cgh.2011.08.014
  3. Bernstein, C. N., Eliakim, A., Fedail, S., Fried, M., Gearry, R., Goh, K. L., . . . LeMair, A. (2016). World Gastroenterology Organisation Global Guidelines Inflammatory Bowel Disease: Update August 2015. J Clin Gastroenterol, 50(10), 803-818. doi:10.1097/mcg.0000000000000660
  4. Berry, D., & Reinisch, W. (2013). Intestinal microbiota: a source of novel biomarkers in inflammatory bowel diseases? Best Pract Res Clin Gastroenterol, 27(1), 47-58. doi:10.1016/j.bpg.2013.03.005
  5. BioHM. (2018).
  6. Carding, S., Verbeke, K., Vipond, D. T., Corfe, B. M., & Owen, L. J. (2015). Dysbiosis of the gut microbiota in disease. Microb Ecol Health Dis, 26. doi:10.3402/mehd.v26.26191
  7. Casen, C., Vebo, H. C., Sekelja, M., Hegge, F. T., Karlsson, M. K., Ciemniejewska, E., . . . Rudi, K. (2015). Deviations in human gut microbiota: a novel diagnostic test for determining dysbiosis in patients with IBS or IBD. Aliment Pharmacol Ther, 42(1), 71-83. doi:10.1111/apt.13236
  8. Danilova, N. A., Abdulkhakov, S. R., Grigoryeva, T. V., Markelova, M. I., Vasilyev, I. Y., Boulygina, E. A., . . . Abdulkhakov, R. A. (2019). Markers of dysbiosis in patients with ulcerative colitis and Crohn's disease. Ter Arkh, 91(4), 17-24. doi:10.26442/00403660.2019.04.000211
  9. Davidovics, Z. H., Michail, S., Nicholson, M. R., Kociolek, L. K., Pai, N., Hansen, R., . . . Kellermayer, R. (2019). Fecal Microbiota Transplantation for Recurrent Clostridium difficile Infection and Other Conditions in Children: A Joint Position Paper From the North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition and the European Society for Pediatric Gastroenterology, Hepatology, and Nutrition. J Pediatr Gastroenterol Nutr, 68(1), 130-143. doi:10.1097/mpg.0000000000002205
  10. DNATestingChoice. (2019). Microbiome Testing.
  11. Falony, G., Joossens, M., Vieira-Silva, S., Wang, J., Darzi, Y., Faust, K., . . . Raes, J. (2016). Population-level analysis of gut microbiome variation. Science, 352(6285), 560-564. doi:10.1126/science.aad3503
  12. FDA. (2019). Fecal Microbiota for Transplantation: Safety Communication- Risk of Serious Adverse Reactions Due to Transmission of Multi-Drug Resistant Organisms.
  13. Frank, D. N., St Amand, A. L., Feldman, R. A., Boedeker, E. C., Harpaz, N., & Pace, N. R. (2007). Molecular-phylogenetic characterization of microbial community imbalances in human inflammatory bowel diseases. Proc Natl Acad Sci U S A, 104(34), 13780-13785. doi:10.1073/pnas.0706625104
  14. Genova. (2019). Organix® Dysbiosis Profile. Retrieved from
  15. Guarino, A., Ashkenazi, S., Gendrel, D., Lo Vecchio, A., Shamir, R., & Szajewska, H. (2014). European Society for Pediatric Gastroenterology, Hepatology, and Nutrition/European Society for Pediatric Infectious Diseases Evidence-Based Guidelines for the Management of Acute Gastroenteritis in Children in Europe: Update 2014. 59(1), 132-152. doi:10.1097/mpg.0000000000000375
  16. Guinane, C. M., & Cotter, P. D. (2013). Role of the gut microbiota in health and chronic gastrointestinal disease: understanding a hidden metabolic organ. Therap Adv Gastroenterol, 6(4), 295-308. doi:10.1177/1756283x13482996
  17. Holleran, G., Scaldaferri, F., Ianiro, G., Lopetuso, L., Mc Namara, D., Mele, M. C., . . . Cammarota, G. (2018). Fecal microbiota transplantation for the treatment of patients with ulcerative colitis and other gastrointestinal conditions beyond Clostridium difficile infection: an update. Drugs Today (Barc), 54(2), 123-136. doi:10.1358/dot.2018.54.2.2760765
  18. IDSA/ACG/ASGE/AGA/NASPGHAN. (2013). Current Consensus Guidance on Donor Screening and Stool Testing for FMT.
  19. Johnston, R. (2017). An overview of the innate immune system.
  20. Kau, A. L., Ahern, P. P., Griffin, N. W., Goodman, A. L., & Gordon, J. I. (2011). Human nutrition, the gut microbiome and the immune system. Nature, 474(7351), 327-336. doi:10.1038/nature10213
  21. Kelly, C. R., Kahn, S., Kashyap, P., Laine, L., Rubin, D., Atreja, A., . . . Wu, G. (2015). Update on Fecal Microbiota Transplantation 2015: Indications, Methodologies, Mechanisms, and Outlook. Gastroenterology, 149(1), 223-237. doi:10.1053/j.gastro.2015.05.008
  22. Ley, R. E., Peterson, D. A., & Gordon, J. I. (2006). Ecological and evolutionary forces shaping microbial diversity in the human intestine. Cell, 124(4), 837-848. doi:10.1016/j.cell.2006.02.017
  23. Ley, R. E., Turnbaugh, P. J., Klein, S., & Gordon, J. I. (2006). Microbial ecology: human gut microbes associated with obesity. Nature, 444(7122), 1022-1023. doi:10.1038/4441022a
  24. Lo Presti, A., Zorzi, F., Del Chierico, F., Altomare, A., Cocca, S., Avola, A., . . . Guarino, M. P. L. (2019). Fecal and Mucosal Microbiota Profiling in Irritable Bowel Syndrome and Inflammatory Bowel Disease. Front Microbiol, 10, 1655. doi:10.3389/fmicb.2019.01655
  25. Lozupone, C. A., Stombaugh, J. I., Gordon, J. I., Jansson, J. K., & Knight, R. (2012). Diversity, stability and resilience of the human gut microbiota. Nature, 489(7415), 220-230. doi:10.1038/nature11550
  26. Malham, M., Lilje, B., Houen, G., Winther, K., Andersen, P. S., & Jakobsen, C. (2019). The microbiome reflects diagnosis and predicts disease severity in paediatric onset inflammatory bowel disease. Scand J Gastroenterol, 1-7. doi:10.1080/00365521.2019.1644368
  27. NICE. (2017). Irritable bowel syndrome in adults: diagnosis and management.
  28. Pang, T., Leach, S. T., Katz, T., Day, A. S., & Ooi, C. Y. (2014). Fecal Biomarkers of Intestinal Health and Disease in Children. Front Pediatr, 2. doi:10.3389/fped.2014.00006
  29. Parada Venegas, D., De la Fuente, M. K., Landskron, G., Gonzalez, M. J., Quera, R., Dijkstra, G., . . . Hermoso, M. A. (2019). Short Chain Fatty Acids (SCFAs)-Mediated Gut Epithelial and Immune Regulation and Its Relevance for Inflammatory Bowel Diseases. Front Immunol, 10, 277. doi:10.3389/fimmu.2019.00277
  30. Qin, J., Li, R., Raes, J., Arumugam, M., Burgdorf, K. S., Manichanh, C., . . . Ehrlich, S. D. (2010). A human gut microbial gene catalogue established by metagenomic sequencing. Nature, 464(7285), 59-65. doi:10.1038/nature08821
  31. Qin, J., Li, Y., Cai, Z., Li, S., Zhu, J., Zhang, F., . . . Kristiansen, K. (2012). A metagenome-wide association study of gut microbiota in type 2 diabetes. Nature, 490(7418), 55-60. doi:10.1038/nature11450
  32. Raby, B. (2019). Tools for genetics and genomics: Polymerase chain reaction.
  33. Simren, M., Barbara, G., Flint, H. J., Spiegel, B. M., Spiller, R. C., Vanner, S., . . . Zoetendal, E. G. (2013). Intestinal microbiota in functional bowel disorders: a Rome foundation report. Gut, 62(1), 159-176. doi:10.1136/gutjnl-2012-302167
  34. Snapper, S., & Abraham, C. (2019). Immune and microbial mechanisms in the pathogenesis of inflammatory bowel disease - UpToDate. Retrieved from
  35. Vaughn, B. P., Rank, K. M., & Khoruts, A. (2018). Fecal Microbiota Transplantation: Current Status in Treatment of GI and Liver Disease. Clin Gastroenterol Hepatol. doi:10.1016/j.cgh.2018.07.026
  36. Viome. (2019a, 03/28/2019). Demo Two. Retrieved from
  37. Viome. (2019b). Recommendations. Retrieved from
  38. Zhang, H., DiBaise, J. K., Zuccolo, A., Kudrna, D., Braidotti, M., Yu, Y., . . . Krajmalnik-Brown, R. (2009). Human gut microbiota in obesity and after gastric bypass. Proc Natl Acad Sci U S A, 106(7), 2365-2370. doi:10.1073/pnas.0812600106
  39. Zhernakova, A., Kurilshikov, A., Bonder, M. J., Tigchelaar, E. F., Schirmer, M., Vatanen, T., . . . Fu, J. (2016). Population-based metagenomics analysis reveals markers for gut microbiome composition and diversity. Science, 352(6285), 565-569. doi:10.1126/science.aad3369
  40. Zoetendal, E. G., Akkermans, A. D., & De Vos, W. M. (1998). Temperature gradient gel electrophoresis analysis of 16S rRNA from human fecal samples reveals stable and host-specific communities of active bacteria. Appl Environ Microbiol, 64(10), 3854-3859.

Coding Section 

Codes Number Description
CPT  82239  Bile acids, total 
  82542  Column chromatography, includes mass spectrometry, if performed (eg, HPLC, LC, LC/MS, LC/MS-MS, GC, GC/MS-MS, GC/MS, HPLC/MS), non-drug analyte(s) not elsewhere specified, qualitative or quantitative, each specimen (used to test for short-chain fatty acids) 
  82710  Fat or lipids, feces; quantitative (used to test for fecal triglycerides) 
  82715 Fat differential, feces, quantitative (used to test for fecal cholesterol)
  82725  Fatty acids, nonesterified (used to test for long-chain fatty acids) 
  82784  Gammaglobulin (immunoglobulin); IgA, IgD, IgG, IgM, each 
  83520  Immunoassay, for analyte other than infectious agent antibody or infectious agent antigen; quantitative, not otherwise specified (used for eosinophil protein X) 
  83630  Lactoferrin, fecal; qualitative 
  83986 pH; body fluid, not otherwise specified (used to measure fecal pH) 
  84311  Spectrophotometry, analyte, not elsewhere specified (used twice, once each to test for stool Bglucuronidase and chymotrypsin) 
  87045  Culture, bacterial; stool, aerobic, with isolation and preliminary examination (eg, KIA, LIA), salmonella and shigella species 
  87046  Culture, bacterial; stool, aerobic, additional pathogens, isolation and presumptive identification of isolates, each plate 
  87075  Culture, bacterial; any source, except blood, anaerobic with isolation and presumptive identification of isolates 
  87102  Culture, fungi, isolation, with presumptive identification of isolates: other source (used for fecal culture for fungi) 
  87177  Ova and parasites, direct smears, concentration and identification 
  87209  Smear, primary source with interpretation; complex special stain (eg, trichrome, iron hemotoxylin) for ova and parasites 
  87328  Infectious agent antigen detection by immunoassay technique (eg, enzyme immunoassay (EIA), enzyme-linked immunosorbent assay (ELISA), immunochemiluminometric assay (IMCA)), qualitative or semiquantitative, multiple-step method; cryptosporidium 
  87329  Infectious agent antigen detection by immunoassay technique (eg, enzyme immunoassay (EIA), enzyme-linked immunosorbent assay (ELISA), immunochemiluminometric assay (IMCA)), qualitative or semiquantitative, multiple-step method; giardia
  87336  Infectious agent antigen detection by immunoassay technique (eg, enzyme immunoassay (EIA), enzyme-linked immunosorbent assay (ELISA), immunochemiluminometric assay (IMCA)), qualitative or semiquantitative, multiple-step method; Entamoeba histolytica dispar group
  87500  Infectious agent detection by nucleic acid (DNA or RNA); vancomycin resistance (eg, enterococcus species van A, van B), amplified probe technique 
  87641  Infectious agent detection by nucleic acid (DNA or RNA); Staphylococcus aureus, methicillin resistant, amplified probe technique 
  87798  Infectious agent detection by nucleic acid (DNA or RNA), not otherwise specified; amplified probe technique, each organism 
  89160  Meat fibers, feces 
ICD-10-CM (effective 10/01/15)  K58.0  Irritable bowel syndrome with diarrhea 
  K58.1  Irritable bowel syndrome with constipation 
  K58.2  Mixed irritable bowel syndrome 
  K58.8  Other irritable bowel syndrome 
  K58.9 Irritable bowel syndrome without diarrhea, Irritable bowel syndrome NOS 
  Z11.0  Encounter for screening for intestinal infectious diseases 
  Z11.2  Encounter for screening for respiratory tuberculosis 
  Z11.8  Encounter for screening for other infectious and parasitic diseases 
  Z11.9  Encounter for screening for infectious and parasitic diseases, unspecified 
ICD-10-PCS (effective 10/01/15)    Not applicable. ICD-10-PCS codes are only used for inpatient services. There are no ICD procedure codes for laboratory tests. 
Type of Service Pathology/ Laboratory  
Place of Service    

Procedure and diagnosis codes on Medical Policy documents are included only as a general reference tool for each policy. They may not be all-inclusive.

This medical policy was developed through consideration of peer-reviewed medical literature generally recognized by the relevant medical community, U.S. FDA approval status, nationally accepted standards of medical practice and accepted standards of medical practice in this community, Blue Cross and Blue Shield Association technology assessment program (TEC) and other non-affiliated technology evaluation centers, reference to federal regulations, other plan medical policies and accredited national guidelines.

"Current Procedural Terminology© American Medical Association.  All Rights Reserved" 

History From 2014 Forward     


Annual review, adding medical necessity statement for testing prior to fecal microbiota transplant for specific organisms. Policy being reformatted for clarity. 


Interim review to remove reference to CAM 20469, as this policy has been retired. No changes to policy intent. 


Interim review to update coding. No change to policy intent.  


Annual review, no change to policy intent. Removing codes 83993 and 82656 from code list. 


Annual review, no change to policy intent. Updating rationale and references. 


Updated category to Laboratory. No other changes 


Annual review, no change to policy intent. Updating background, description, guidelines, rationale and references. 


Interim update to remove coding related to fecal calprotectin testing. 


Removed verbiage related to a fecal calprotectin policy, as we have archived that policy. No other changes made.


Annual review, no change to policy intent. Updated background, description, related policies, rationale and references. Added coding.


Annual review. Updated description, background & references. Added related policies and policy guidelines. No change to policy intent.

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