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RESEARCH. TECHNOLOGY. RESULTS.

2025
INTERPRETIVE GUIDE
EDITION
GI-MAP ® – Unparalleled DNA-Based Stool Testing
Our mission: to deliver innovative, accurate and clinically relevant
diagnostic testing in a timely and cost-effective manner
 FIRST OF ALL

THANK YOU FOR CONSIDERING US!

“At Diagnostic Solutions Laboratory, we’re not content

with the range of clinical testing currently available to
practitioners. We believe that every patient should achieve
optimal health, and we’re driven to give clinicians the tools
to do so. Our mission, therefore, is to use our resources to
bring the most advanced, innovative, and clinically relevant
testing to healthcare providers worldwide.”

Tony Hoffman
President and CEO

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 GI-MAP® INTERPRETIVE GUIDE

CONTENTS
THANK YOU............................................................................................................2

INTRODUCTION......................................................................................................4

HOW TO READ THE REPORT..................................................................................5

PATHOGENS............................................................................................................6

H. PYLORI AND VIRULENCE FACTORS............................................................... 16

COMMENSAL/KEYSTONE BACTERIA.................................................................. 20

OPPORTUNISTIC BACTERIA................................................................................ 23

FUNGI/YEAST....................................................................................................... 27

VIRUSES................................................................................................................ 29

PARASITES............................................................................................................ 31

INTESTINAL HEALTH MARKERS......................................................................... 36

ADD-ON TESTS..................................................................................................... 40

ANTIBIOTIC RESISTANCE GENES........................................................................ 42

STOOLOMX™ ........................................................................................................ 44

GI-MAP PATTERNS .............................................................................................. 56

SUPPORT INFO.................................................................................................... 63

RESEARCH. TECHNOLOGY. RESULTS. 3

 GI-MAP®

INTRODUCTION
The Gastrointestinal Microbial Assay Plus (GI-MAP®) is an innovative
clinical tool that measures gastrointestinal microbiota DNA from a single
stool sample with state of the art, quantitative polymerase chain reaction
(qPCR or real-time PCR) technology.

The GI-MAP was designed to detect microbes that may be disturbing

normal microbial balance or contributing to illness as well as indicators
of digestion, absorption, inflammation, and immune function. The
following guide may be useful for understanding the nature of each of the
microorganisms found on the GI-MAP, as well as clinical implications and
treatment guidelines.

Please see the GI-MAP white paper for additional, fully referenced, information.
➠

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 GI-MAP® INTERPRETIVE GUIDE

HOW TO READ
THE REPORT
GI-MAP quantifies bacteria, fungi, viruses, and parasites using qPCR. This
is a leap forward from older methodologies that report only positive or
negative. Results are reported as colony forming units per gram of stool
(CFU/g). One CFU is roughly equivalent to one microorganism (or one cell).
Results are expressed in standard scientific notation. A reported result of
3.5e7 is equivalent to 3.5 x 107 CFU/g, which equals 35,000,000 CFU/g, or
35 million CFU per gram of stool.

Figure 1. The normal reference range for C. difficile, Toxin A is 0–1,000 CFU/g. The
patient’s result is very high at 1.21 x 105, or 121,000 CFU/g.

Reference ranges were developed using known positive, diseased samples to

construct cut off values that distinguish disease-causing amounts of pathogenic
and opportunistic microbes. Reference ranges for the pathogens were correlated
with an FDA cleared assay for GI pathogens. The GI-MAP is capable o​ f detecting as
low as 0.1 cell per gram of stool.

Table 1. Scientific notation; a basic reference table.

1.0e1 1 X 101 10 Ten

1.0e2 1 X 102
100 One hundred
1.0e3 1 X 103 1,000 One thousand
1.0e4 1 X 104
10,000 Ten thousand
1.0e5 1 X 105 100,000 One hundred thousand
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1.0e6 1 X 106
1,000,000 One million

RESEARCH. TECHNOLOGY. RESULTS. 5

 PATHOGENS
The GI-MAP includes pathogens (bacterial, parasitic, and viral) commonly known
to cause intestinal gastroenteritis. It’s important to note that not all individuals
with positive findings for pathogens will present with symptoms. Many factors,
including the health of the individual, the transient nature of some pathogens, and
the presence and expression of virulence factors all contribute to an individual’s
symptoms. Toxins are a type of virulence factor produced by certain pathogens.
Since GI-MAP is a DNA-based test, results reflect the levels of pathogenic strains
carrying the toxin genes, not the levels of any toxins that may be produced.

BACTERIAL PATHOGENS fever, malaise; lasting several

days to several weeks

Campylobacter » Vast majority of those with

symptoms of gastroenteritis
• Epidemiology
recover without treatment
» One of the most common causes
• Therapeutic Approaches
of foodborne illness in the U.S.
& Considerations
» Fecal contamination of
» See patient’s calprotectin level
poultry and water
to determine GI inflammation
• Clinical Implications » Consider high dose probiotics,
» May be infectious at very broad-spectrum antimicrobial herbs,
low exposures and 5R Protocol (see Table 2)
» Symptoms range from mild to » Heavy infections can be treated with
➠

severe abdominal pain, diarrhea, azithromycin and fluoroquinolones

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» In asymptomatic patients with positive

Clostridium difficile,
toxins A and/or B, the genes are likely
Toxin A and Toxin B
not “turned on,” and thus not causing
The GI-MAP tests only for the genes for disease. It is still prudent to avoid
toxin A and toxin B, which are carried by antibiotics in these patients to prevent
C. difficile. The GI-MAP does not measure CDAD. Consider antimicrobial herbal
toxins directly for any microbe. formulas, which can suppress C. diff
without activating toxin production.
• Epidemiology
» Additional testing for toxins A
» 2–10% of population are carriers,
and B may be warranted
most are asymptomatic
» Prolonged use of antibiotics
may be causative factor Enterohemorrhagic E. coli (EHEC)
• Clinical Implications • Epidemiology

» Symptoms include inflammation, » Fecal contamination of food

abdominal pain, cramping, (undercooked beef, raw milk, and
fever, and diarrhea unpasteurized juice) and water

» Symptoms often present during » Implicated in hemorrhagic colitis,

antibiotic use and often subside may progress to hemolytic
once antibiotics are discontinued uremic syndrome (HUS)

» Gastrointestinal (GI) infection • Clinical Implications

can cause reactive arthritis » Symptoms include fever,
• Therapeutic Approaches abdominal cramping, fatigue,
& Considerations nausea, and diarrhea
» See patient’s calprotectin and » Symptoms may last up to a week
secretory IgA (SIgA) levels to • Therapeutic Approaches
determine GI inflammation & Considerations
and immune response. » See patient’s calprotectin and SIgA
» Consider Saccharomyces boulardii, levels to determine GI inflammation
high dose probiotics, broad- and immune response.
spectrum antimicrobial herbs, » Antibiotics may be contraindicated;
and 5R Protocol (see Table 2) they can initiate hemolytic
» Mild infections can be treated uremic syndrome (HUS)
with metronidazole » Consider high-dose probiotics (300+
» Heavy infections can be treated billion CFU/g) such as: Lactobacillus
with vancomycin and fidaxomicin acidophilus‚ Bifidobacterium
» Asymptomatic patients may bifidum‚ Bifidobacterium longum‚
➠

not need treatment Lactobacillus rhamnosus‚

RESEARCH. TECHNOLOGY. RESULTS. 7

 PATHOGENS

Table 2. Clinical Approach — The Five “R” Treatment Protocol.

The 5R Protocol is a widely accepted clinical guideline to treating pathogens and imbalances in the
GI microbiota and restoring health to the gastrointestinal tract. Re-test patients with the GI-MAP in
3–6 months to monitor progress and make changes to the treatment protocol as needed.

Broad-spectrum antimicrobial herbs including:

Antimicrobial berberine, caprylic acid, garlic oil, oil of
oregano, uva ursi, olive leaf extract

REMOVE Research the recommended antibiotic for the

Antibiotics specific microbe present. Avoid medications to
Using a course of antimicrobial, which the microbe is thought to have resistance.
antiviral, antifungal, or
antiparasitic therapies in cases
Antifungal Caprylic acid, garlic oil, oil of oregano, olive leaf extract
where these organisms are
present. It may also be necessary
to remove offending foods, gluten, Black walnut, garlic oil, oil of oregano, Artemisia
or medication that may be acting Antiparasitic (wormwood), berberine, goldenseal, gentian root
as antagonists. extract, quassia bark extract, citrus seed extract

Olive leaf extract, purified silver, cat’s claw, monolaurin,

Antiviral osha root (Ligusticum porteri), vitamin A, vitamin C,
vitamin D, reishi mushrooms, Echinacea, zinc

REPLACE
In cases of maldigestion or Betaine hydrochloride, apple cider vinegar,
Digestive
malabsorption, it may be herbal bitters, ox bile, lactase, pancreatic
support
necessary to restore proper enzymes (amylase, lipase, protease), pepsin
digestion by supplementing
with digestive enzymes.

Lactobacillus acidophilus‚ Bifidobacterium

REINOCULATE
bifidum‚ Bifidobacterium longum‚ Lactobacillus
Probiotics
Recolonization with rhamnosus‚ Bifidobacterium breve‚ Lactobacillus
healthy, beneficial bacteria. casei‚ Saccharomyces boulardii
Supplementation with probiotics,
along with the use of prebiotics
helps re-establish the proper Beta-glucan, fiber, inulin, pectin, xylooligosaccharides,
Prebiotics
microbial balance. galactooligosaccharides, larch arabinogalactans

Immune
REPAIR Colostrum, immunoglobulins, S. boulardii
Support
Restore the integrity of the gut L-Glutamine, aloe vera extract, deglycyrrhizinated
mucosa by giving support to Intestinal licorice, marshmallow root, okra, N-acetyl glucosamine,
healthy mucosal cells, as well as Barrier Repair quercetin, S. boulardii, slippery elm, zinc carnosine,
immune support. vitamin A, essential fatty acids, B vitamins

REBALANCE
Support
Address whole body health and Sleep, diet, exercise, and stress management
Consideration
lifestyle factors so as to prevent
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future GI dysfunction.

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Bifidobacterium breve‚ Lactobacillus • Clinical Implications

casei‚ Streptococcus thermophilus » Symptoms may include severe
» Consider bacteriophages, broad- abdominal cramps and diarrhea
spectrum antimicrobial herbs, » Shiga toxins inhibit protein synthesis
and 5R Protocol (see Table 2) & elicit strong inflammatory response

• Therapeutic Approaches
E. coli O157 & Considerations
• Epidemiology » See patient’s calprotectin and SIgA
» Fecal contamination of food levels to determine GI inflammation
and liquids (dairy, undercooked and immune response.
beef, vegetables, juices) » Antibiotics may be contraindicated;
» Implicated in many outbreaks and they can initiate HUS
cases of bloody diarrhea and HUS » Consider high-dose probiotics
» High prevalence worldwide (300+ billion CFU/d)
» Consider bacteriophages, broad-
spectrum antimicrobial herbs,
and 5R Protocol (see Table 2)

SOURCES OF EXPOSURE AND RE-INFECTION

To effectively treat infections and prevent reinfection, exposure should be

identified and eliminated. Most exposure to pathogens occurs via fecal-
oral transmission, most often due to use of contaminated water sources
or improper hand hygiene. This may include drinking contaminated water,
eating raw foods washed in contaminated water or harvested (e.g. shellfish) in
contaminated water, or improper handwashing.

To remove microorganisms from food, the FDA recommends first washing

your hands, running cool water over fruits and vegetables, while rubbing or
scrubbing, and then letting them dry out before eating. During treatment,
consider all possible sources of fecal transmission: romantic partners, children
(especially if in diapers or not toilet-trained), sheets, towels, water source to
the home, etc...
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RESEARCH. TECHNOLOGY. RESULTS. 9

 PATHOGENS

Enteroinvasive E. coli / Shigella • Therapeutic Approaches

& Considerations
• Epidemiology
» See patient’s calprotectin and SIgA
» Fecal contamination of ingested foods
levels to determine GI inflammation
• Clinical Implications and immune response
» Symptoms include diarrhea (with blood » Antibiotics may be contraindicated;
and/or mucus), vomiting, fever, chills, they can initiate HUS
fatigue, and abdominal cramping » Consider high-dose probiotics
» Symptoms are generally self-limiting (300+ billion CFU/d)
» Gastrointestinal (GI) infection » Consider bacteriophages, broad-
can cause reactive arthritis spectrum antimicrobial herbs,
• Therapeutic Approaches and 5R Protocol (see Table 2)
& Considerations
Shiga-like Toxin E. coli stx1
» See patient’s calprotectin and SIgA
levels to determine GI inflammation • Epidemiology
and immune response. » Most common cause of
» Antibiotics may be contraindicated; traveler’s diarrhea
they can initiate HUS • Clinical Implications
» Consider high-dose probiotics » Diarrhea is the most
(300+ billion CFU/d) common symptom
» Consider bacteriophages, broad-
• Therapeutic Approaches
spectrum antimicrobial herbs, & Considerations
and 5R Protocol (see Table 2) » See patient’s calprotectin and SIgA
levels to determine GI inflammation
Enterotoxigenic E. coli LT/ST and immune response
• Epidemiology
» Antibiotics may be contraindicated;
» Fecal contamination of ingested
they can initiate HUS
foods (hamburger meat, unpasteurized
» Consider high-dose probiotics
milk, and contaminated water)
(300+ billion CFU/d)
• Clinical Implications
» Consider bacteriophages, broad-
» Symptoms include watery, spectrum antimicrobial herbs,
bloody diarrhea and 5R Protocol (see Table 2)
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Shiga-like Toxin E. coli stx2 » Symptoms include fever,

vomiting, and severe diarrhea
• Epidemiology
» Typically self limiting within seven days
» Fecal contamination of ingested
foods (undercooked meat, » GI infection can cause reactive
unpasteurized milk, juice, and water) arthritis and may be involved
in ankylosing spondylitis
• Clinical Implications
» Systemic infections may require
» Symptoms may include severe
treatment with antibiotics
abdominal cramps and diarrhea
• Therapeutic Approaches
» Toxins may elicit strong
& Considerations
inflammatory response
» See patient’s calprotectin and SIgA
• Therapeutic Approaches levels to determine GI inflammation
& Considerations
and immune response
» See patient’s calprotectin and SIgA
» Remove sources of infection
levels to determine GI inflammation
» Consider high-dose probiotics
and immune response
(300+ billion CFU/d)
» Antibiotics may be contraindicated;
» Consider broad-spectrum
they can initiate HUS
antimicrobial herbs and 5R
» Consider high-dose probiotics
Protocol (see Table 2) Antibiotics
(300+ billion CFU/d)
are contraindicated; they may
» Consider bacteriophages, broad-
cause relapse of infection
spectrum antimicrobial herbs,
and 5R Protocol (see Table 2)
» Antibiotics and antidiarrheal medicines Table 3.
are contraindicated; they may FOOD SOURCES OF SALMONELLA
increase the risk of developing HUS Poultry and poulty products

Salmonella Meat

Dairy
• Epidemiology
» Fecal contamination of ingested foods Raw, fresh, ready-to-eat produce such as:
• Tomatoes
(eggs, poultry, meat, unpasteurized • Leafy greens
milk, raw fruits, and vegetables) • Sprouts
• Berries
» Exposure to pets (reptiles,
• Melons
amphibians, baby chicks)

• Clinical Implications
» May be asymptomatic
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RESEARCH. TECHNOLOGY. RESULTS. 11

 PATHOGENS

Vibrio cholerae Yersinia enterocolitica

• Epidemiology • Epidemiology
» Fecal contamination of ingested » Fecal contamination of ingested
foods (raw shellfish) and often picked foods and liquids (water, undercooked
up during international travel pork, meats, and dairy products)

• Clinical Implications • Clinical Implications

» May be asymptomatic or » Symptoms usually develop four
cause mild symptoms to seven days after exposure
» Severe infections present with and are self-limiting
profuse watery diarrhea (“rice-water » Symptoms include water
stools”), vomiting, rapid heart rate, or bloody diarrhea, fever,
loss of skin elasticity, thirst, dry vomiting, and abdominal pain
mucous membranes, low blood (may resemble appendicitis)
pressure, restlessness, or irritability » Symptoms may mimic Crohn’s disease
• Therapeutic Approaches » May trigger autoimmune thyroiditis
& Considerations or inflammatory arthritis in
» See patient’s calprotectin and SIgA susceptible individuals
levels to determine GI inflammation
• Therapeutic Approaches
and immune response. & Considerations
» Rehydration therapy » Consider probiotics, broad-
» Zinc, especially in children spectrum antimicrobial herbs
» Consider probiotics, broad- and 5R Protocol (see Table 2)
spectrum antimicrobial herbs » Heavy infections can be treated
and 5R Protocol (see Table 2) with doxycycline in combination
» Heavy infections may be with an aminoglycoside
treated with doxycycline » Trimethoprim-sulfamethoxasole,
chloramphenicol, and rifaximin
may also be useful treatments
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PARASITIC PATHOGENS

Cryptosporidium Entamoeba histolytica

Epidemiology • Epidemiology

» Fecal contamination of ingested » Fecal contamination of

foods and liquids (contaminated ingested foods or water
water and swimming pools, » Pets may be a source of exposure
undercooked meat, and raw milk) » Sexual contact may be a
» Common cause of traveler’s diarrhea source of exposure

• Clinical Implications • Clinical Implications

» Symptoms typically last 2­–3 » Symptoms include diarrhea,
weeks and are self-limiting fulminating colitis (resembling
» If symptoms persist, look for sources of ulcerative colitis), and dysentery
contamination, such as drinking water » Extreme cases may invade
» Can cause reactive arthritis liver and lung tissues

• Therapeutic Approaches • Therapeutic Approaches

& Considerations & Considerations

» May not require treatment » See patient’s calprotectin and SIgA

levels to determine GI inflammation
» See patient’s calprotectin and SIgA
and immune response
levels to determine GI inflammation
and immune response » Treatment may be indicated,
even in asymptomatic carriers
» If necessary, consider anti-parasitic
herbal treatments containing » Mild infections can be treated
ingredients such as black walnut, with Iodoquinol, paromomycin,
garlic oil, oil of oregano, Artemisia or diloxanide furoate*
(wormwood), berberine, goldenseal, » Moderate to heavy infections can
gentian root extract, quassia bark be treated with metronidazole
extract, citrus seed extract or tinidazole, followed by
» Consider probiotics and iodoquinol or paromomycin*
5R Protocol (see Table 2) » If appropriate, consider anti-parasitic
» Search for and remove sources herbal treatments (see Table 2)
of fecal contamination » Consider probiotics and
» Heavy infections can be 5R Protocol (see Table 2)
treated with nitazoxanide* » Avoid reinfection by fecal
➠

contamination

RESEARCH. TECHNOLOGY. RESULTS. 13

 PATHOGENS

Giardia » May cause malnutrition and

vitamin B12 deficiency
• Epidemiology
» Can cause reactive arthritis
» Most commonly isolated
protozoan worldwide • Therapeutic Approaches
» Found in outside water sources & Considerations
(lakes, streams, ponds) and can » See patient’s calprotectin and SIgA
get past filtration systems levels to determine GI inflammation
» Carried by animals and immune response

» Common in daycare workers » Infections can be treated

with tinidazole, nitazoxanide,
• Clinical Conditions
metronidazole, paramomycin,
» May be asymptomatic, especially furazolidone, or quinacrine*
in patients with adequate levels
» Consider probiotics and 5R
of normal bacteria and SIgA
Protocol (see Table 2) to repair
» Symptoms include acute diarrhea, and rebuild the gut mucosa
bloating, cramps, weight loss, intestinal
malabsorption, and steatorrhea
* Additional information (dosing, efficacy, etc.) on
» Can cause urticaria or neurologic
pharmaceutical treatment for parasites may be
symptoms such as irritability,
found at www.cdc.gov/parasites/index.html and in
sleep disorder, or depression
the Physician’s Desk Reference.

Giardia intestinalis protozoan

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VIRAL PATHOGENS

Adenovirus 40/41 Norovirus GI/GII

• Epidemiology • Epidemiology
» Common cause of diarrhea in infants » Fecal contamination of
and children but can also affect adults ingested foods and water
» Mainly transmitted by fecal » Common cause of stomach
contamination (fecal-oral route) flu on cruise ships

• Clinical Implications » Common cause of non-

bacterial gastroenteritis and
» Causative agents of gastrointestinal
outbreaks in the world
disease and gastroenteritis
» Symptoms include fever and watery • Clinical Implications
diarrhea, usually limited to 1–2 weeks » Symptoms include nausea and
» May also be present in the stool vomiting, diarrhea, abdominal
of asymptomatic carriers and cramps, low-grade fever, muscle
may not require treatment aches, fatigue, and headache
» Generally short-lived, lasting
• Treatment
about 24–72 hours
» Handwashing
» Hydration • Treatment

» Antiviral herbs such as cat’s claw, » Antivirals are not recommended

osha root, reishi mushrooms, » Supportive care for the gastric
vitamins A, C, and D, zinc, Echinacea mucosa, hydration, and immune-
» Address other imbalances on boosting agents may be warranted
the GI-MAP and use 5R Protocol – Handwashing
(see Table 2) to rebuild gut – Hydration
health and gut immunity – Antiviral herbs such as cat’s claw,
osha root, reishi mushrooms,
vitamins A, C, and D, zinc, Echinacea
– Address other imbalances on
the GI-MAP and use 5R Protocol
(see Table 2) to rebuild gut health
➠

RESEARCH. TECHNOLOGY. RESULTS. 15

 H. pylori
AND VIRULENCE FACTORS
Helicobacter pylori (H. pylori) Virulence Factors
Recent studies have shown that nearly Of the 50% of the population believed to
50% of the world’s population may harbor be infected with H. pylori, only 2% develop
H. pylori. And, although many carriers gastric cancer. Positive H. pylori virulence
are asymptomatic, H. pylori is known to factors on the GI-MAP represent the genetic
have a causative role in ulcers, chronic potential for an H. pylori strain to cause
gastritis, and stomach cancer. Additionally, pathology. For example, some clinicians
in early phases of colonization, patients may choose an aggressive treatment
may experience hypochlorhydria followed protocol for a patient with dyspepsia and
by a change to hyper aciduria. Over time, a family history of gastrointestinal cancer,
additional H. pylori strains may colonize, who shows elevated H. pylori and positive
including those with Virulence Factors and virulence factors. (See Table 4)
increased disease potential.
• Treatment
• Epidemiology » Asymptomatic patients may
» Fecal contamination, oral to oral, not require treatment
and family inter-infection are » Consider herbal formulas to eradicate
common modes of transmission or suppress H. pylori. Ingredients may
• Clinical Implications include: deglycyrrhizinated licorice,
mastic gum, methylmethionine
» Dyspepsia, abdominal pain,
sulfonium chloride, vitamin C,
nausea, vomiting and chronic
zinc carnosine, bismuth citrate,
gastrointestinal symptoms
berberine, goldenseal, oil of oregano,
» Peptic ulcers
grape extract, Chinese goldthread
» May induce mucosal atrophy
extract, yerba mansa extract
and metaplastic changes
» See pancreatic elastase-1 to
determine if maldigestion and/or
hypochlorhydria might be present
» Consider high-dose probiotics
➠

and 5R Protocol (see Table 2)

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» Rebuild healthy gastric mucosa

by reducing stress and giving
soothing and healing agents such as
glutamine, aloe, DGL, and vitamin A
» Address dental hygiene; the
mouth is a reservoir for H. pylori
» Consider sources of exposure,
especially romantic partners Figure 2. An example antibiotic resistance
or family members gene measured on the GI-MAP for H. pylori.
» Address other imbalances Number and letter combinations are single
on the GI-MAP nucleotide polymorphisms (SNPs), or gene
targets, that are involved in H. pylori drug
» For peptic ulcer disease, the first-
resistance. If any SNP is detected (present),
line triple therapy (prescription) then the H. pylori strain/s are resistant to
treatment includes a proton pump that class of antibiotics. In this example,
inhibitor, clarithromycin, and the patient’s H. pylori is resistant to the
amoxicillin or metronidazole clarithromycin class of antibiotics and it would
be prudent to use a different antibiotic when
» Fluoroquinolones and tetracycline
tailoring a treatment protocol.
are used in second-line
regimens against H. pylori
Note: In supporting individuals with H. pylori, consider
» See the GI-MAP Antibiotic Resistance
the patient history, clinical symptoms, virulence genes,
Genes results for Helicobacter when and the amount of H.pylori DNA detected in order to
designing an antibiotic protocol design a customized treatment plan.

Helicobacter pylori bacterium

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RESEARCH. TECHNOLOGY. RESULTS. 17

 H. PYLORI

Table 4. H. pylori virulence factors and disease associations.

Helicobacter pylori Virulence Factors

Quick Reference Guide

The virulence factor genes on GI-MAP® are found exclusively on the genome of H. pylori.
These genes code for proteins that will predispose one to more serious H. pylori infections.
The chart below provides details of each virulence factors tested on the GI-MAP.

Gene Acronym Gene Name Genetic Characteristics Associations with Disease

BabA Blood Group Antigen • Promotes DNA breakage in host cell May promote carcinogenesis
Binding Adhesion • Improves H. pylori adherence (“stickiness”)
to epithelial cells
• May promote other virulence factors,
especially CagA
CagA Cytotoxin Associated • Promotes H. pylori adhesion and Promotes carcinogenesis, strong
Gene A colonization association. Also associated with
• Affects barrier function of gastric epithelial peptic ulcer disease
tight junctions
• Promotes loss of cell polarity
• Antagonizes VacA
• Evades the immune system and affects the
activity of dendritic cells and B-cells.
Helicobacter pylori Virulence Factors
• Considered part of the “pathogenicity
island” which includes VirB and VirD
virulence factors. This is a closely-associated Quick Reference Guide
group of genes that work synergistically and
often transfer as a unit.
DupA Duodenal Ulcer- • Promotes inflammation Associated with duodenal ulcers,
Gene Acronym Gene NameGene A
Promoting • Genetic Characteristics Associations
specifically with Disease
IceA Induced by Contact with • Transcription of this gene is only initiated Associated with dyspepsia and
Epithelium A after adhesion to the gastric epithelium gastric & duodenal ulcers
• Promotes inflammation and associated with
elevated IL-8 NOT associated with gastric cancer
OipA Outer Inflammatory • Promotes inflammation Associated with carcinogenesis and
Diagnostic Solutions Laboratory
Protein A| RESEARCH. TECHNOLOGY. RESULTS. | www.diagnosticsolutionslab.com
peptic ulcer disease 1
• Drives IL-8 production
VacA Vacuolating Toxin A • Enters the host cell by endocytosis Associated with gastric
• Affects mitochondrial function inflammation, peptic ulcer disease,
• Disrupts tight junctions and gastric cancers
• Causes a programmed necrosis by inducing
the production of large vacuoles inside the
host cells; inducing cellular swelling;
disrupting cell barrier thus causing nutrient
leakage
• Facilitates nutrient acquisition (iron,
minerals, amino acids, etc.)
• Inhibits antigen presentation in vitro
• Antagonizes CagA
VirB & VirD • Part of the CagA “pathogenicity island” Evaluate next to CagA virulence
• Both genes can potentiate CagA virulence factors. VirB & VirD, if positive, can
factor by aiding in its transmission to host potentiate CagA virulence and
epithelial cels clinical associations
• In the absence of CagA, these virulence
factors are unlikely to change clinical
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outcome of H. pylori infections.

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 GI-MAP® INTERPRETIVE GUIDE

• How To Target Treatments in the VirB and VirD if they are found in
Presence of Virulence Factors: Helicobacter pylori
isolation (without CagA present).Virulence Fa
» Generally, when virulence factors are » Below is a chart of treatment
present, the treatment goal will be to considerations for each of the
Quick Referen
fully eradicate the H. pylori population. virulence factors. These would be
This can be confirmed by retesting used in addition to the standard
the full GI-MAP, the pathogen panel,
HoworTotheTarget Treatments
H. Pylori panel 4–6 weeks Presence of treatments
in theafter Virulence for H. pylori alone.
Factors:
completing
Generally, treatment.
when virulence The
factors aregoal is the treatment goal will be to fully eradicate the H. pylori population. This c
present,
be confirmed
to achieveby retesting
a resultthe
of <full
dl GI-MAP,
on the the pathogen panel, or the H. Pylori panel 4–6 weeks after completing treatm
The goal is to The
retest. achieve a result of
exception to <dl
thisonmay
the retest.
be The exception to this may be VirB and VirD if they are found in isolatio
(without CagA present).
Below is a chart of treatment considerations for each of the virulence factors. These would be used in addition to the sta
Table 4a.for
treatments H.H.
pylori
pylorivirulence
alone. factors and treatment considerations.
Virulence Factor Special Treatment Considerations
BabA More aggressive treatment may be warranted; consider the use of adhesion
inhibitions, particularly cranberry
CagA Target inflammatory support, promote T-cell activity, consider curcumin,
resveratrol/red wine, ginger, Nigella sativa, low salt diet
DupA Consider the use of demulcents for mucosal protection
IceA Inflammatory support, consider the use of adhesion inhibitors
OipA Inflammatory support
VacA Mitochondrial support, consider Nigella sativa, green tea, red wine/resveratrol,
Scutellaria baicalensis
VirB & VirD No additional treatments necessary

Please see the GI-MAP white paper for

Diagnostic Solutions Laboratory | RESEARCH. TECHNOLOGY.
additional, RESULTS.
fully referenced, | www.diagnosticsolutionslab.com
information.
➠

RESEARCH. TECHNOLOGY. RESULTS. 19

 COMMENSAL/
KEYSTONE
BACTERIA
Trillions of microorganisms inhabit the human intestine to make up
a complex ecosystem that plays an important role in human health.
Commensal bacteria extract nutrients and energy from our diets, maintain
gut barrier function, produce vitamins (biotin and vitamin K), and protect
against colonization by potential pathogens.

Bacteria Lactobacillus, lactic acid bacteria which are part of normal flora of human intestine
➠

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 GI-MAP® INTERPRETIVE GUIDE

THE FOLLOWING COMMENSAL/KEYSTONE BACTERIA

ARE REPORTED ON THE GI-MAP
Table 5.
COMMENSAL BACTERIA
Gram-negative species of the Bacteroidetes phylum. Immune-modulating normal
gut species. Believed to be involved in microbial balance, barrier integrity, and
Bacteroides fragilis neuroimmune health (Hsiao 2013). High levels may result from reduced digestive
capacity or constipation. Low levels may contribute to reduced anti-inflammatory
activity in the intestine.

Gram-positive genus in the Actinobacteria phylum. Present in breast milk. Colonizes

the human GI tract at birth. Common in probiotics. Thrives on a wide variety of
Bifidobacterium spp.
prebiotic fibers. Low levels may result from low fiber intake or reduced mucosal
health. High levels are more common in children than in adults.

Gram-positive genus of lactate-producing bacteria in the Firmicutes phylum. High levels

Enterococcus spp. may be due to reduced digestive capacity, constipation or small intestinal bacterial
overgrowth. Low levels may indicate insufficiency of beneficial bacteria.

Gram-negative genus in the Proteobacteria phylum. Normal gut flora. Escherichia coli
(E. coli) is the primary species in this genus. Most E. coli are nonpathogenic (pathogenic
Escherichia spp. E. coli strains are measured separately in “Pathogens” section of the GI-MAP). High levels
may be indicative of increased intestinal inflammatory activity. Low levels may
indicate reduced mucosal health and decreased protection against pathogenic E. coli.

Gram-positive genus of lactate-producing bacteria in the Firmicutes phylum. Many

strains used as probiotics. High levels may result from reduced digestive capacity or
Lactobacillus spp.
excessive intake of carbohydrates. Low levels may be due to low carbohydrate intake
or high salt intake, and may also indicate reduced mucosal health.

Gram-negative genus in the Proteobacteria phylum. Closely related to E. coli (in the
Enterobacter spp. same taxonomic family). High levels may indicate increased intestinal inflammatory
activity. Low levels may indicate reduced mucosal health.

Keystone species and primary mucus degrader. Generates mucus-derived sugars and
metabolic products that support the growth and energy needs of other gut microbes.
Akkermansia municiphila
Promotes mucosal health and mucus production. Low levels associated with obesity
and metabolic dysfunction. High levels linked to multiple sclerosis.

Widely recognized as an important keystone species in the Clostridia class, as well

Faecalibacterium as a major butyrate producer. Promotes anti-inflammatory processes and mucosal
prausnitzii homeostasis. Reduced levels have been associated with a wide range of chronic
inflammatory and autoimmune diseases.

A genus of Gram-positive anaerobic bacteria in the Clostridia class that inhabit the
human colon. The Roseburia genus has five well-characterized species, all of which
produce short chain fatty acids (SCFAs), such as acetate, propionate, and butyrate.
Roseburia can also produce butyrate from acetate promoting balance in energy
Roseburia spp.
homeostasis. The genus is widely recognized to influence colonic motility, support
immunity, and suppress inflammation. Low levels are associated with several disease
(including irritable bowel syndrome, obesity, Type 2 diabetes, nervous system
conditions and allergies).
➠

RESEARCH. TECHNOLOGY. RESULTS. 21

 COMMENSAL/KEYSTONE BACTERIA

• Therapeutic Options for Abnormally

Low Commensal Bacterial Findings
FIRMICUTES AND
» Use a broad-spectrum, diverse BACTEROIDETES PHYLA
probiotic formula, 50–450 billion
Gram-negative Bacteroidetes and gram-
CFUs/day depending on findings.
positive Firmicutes are bacterial phyla that
May contain: Lactobacillus acidophilus‚
dominate the entire human digestive tract,
Bifidobacterium bifidum‚ Bifidobacterium
including the mouth, nose, throat, and
longum‚ Lactobacillus rhamnosus‚
colon. An abnormal result in one or both of
Bifidobacterium breve‚ Lactobacillus
these phylum suggest imbalanced normal
casei‚ Streptococcus thermophilus.
microbes in the GI tract. Further, high
» Increase dietary intake of vegetables Firmicutes and low Bacteroidetes (resulting in
and fibers (psyllium, oat bran) a high F/B ratio) suggest microbial imbalance
» Remove dietary sugar and which may be related to increased caloric
refined carbohydrates extraction from food, fat deposition and
» Prebiotic supplementation (resistant lipogenesis, impaired insulin sensitivity, and
starch, xylooligosaccharide, inulin, increased inflammation.
beta-glucan, arabinogalactan)
» Fermented foods, if tolerated
High Firmicutes/Bacteroidetes Ratio
» Reduce inflammation and address
other imbalances on the GI-MAP • Causes:
» Poor diet
• Therapeutic Options for Abnormally
High Commensal Bacterial Findings » Dysbiosis
» Consider any additional findings » Maldigestion or hypochlorhydria
on GI-MAP and treat accordingly • Therapeutic Approaches
» Re-establish commensal bacteria & Considerations
using 5R protocol (see Table 2) » Balance commensal bacteria using
» Remove dietary sugar and the 5R Protocol (see Table 2)
refined carbohydrates » When Firmicutes phyla is high, consider
» In certain situations, overgrowth of using Bifidobacteria probiotics and
commensal bacteria may be treated Saccharomyces boulardii primarily.
judiciously with antimicrobial herbs » Lactobacillus spp.
when all other findings are normal. and Bacillus spp. (found in
probiotics) can elevate Firmicutes
» Optimize the diet; a lower fat diet
may help to normalize the F/B ratio
» Address all other imbalances
➠

on the GI-MAP

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OPPORTUNISTIC
BACTERIA
Many bacteria measured on the GI-MAP are considered opportunistic
pathogens, as they only cause disease and illness in some individuals,
particularly the immune-compromised. Many individuals come into contact
with opportunistic bacteria and experience no symptoms. Most sources
consider these microbes to be normal in the stool. However, they can cause
gastroenteritis and inflammation at high levels in vulnerable patients.
Symptoms may include diarrhea, loose stools, abdominal pain, or even
constipation. Overgrowth and excessive colonization by opportunistic bacteria
may occur when the commensal bacteria are impaired by poor diet, antibiotic
use, parasitic infection, or a weakened immune system. When intestinal
permeability is present (see zonulin), these microbes could escape the lumen
of the gut and infect extraintestinal sites.
➠

RESEARCH. TECHNOLOGY. RESULTS. 23

 OPPORTUNISTIC BACTERIA

OPPORTUNISTIC/OVERGROWTH MICROBES
Table 6.
DYSBIOTIC & OVERGROWTH BACTERIA
Common group of gram-positive bacteria in the Firmicutes phylum. Some strains are
Bacillus spp. used as probiotics. High levels may result from reduced digestive function, SIBO,
or constipation.

Gram-positive species in the Firmicutes phylum. High levels may result from reduced
Enterococcus faecalis
stomach acid, PPI use, compromised digestive function, SIBO or constipation. High
Enterococcus faecium natural resistance to some antibiotics, which may result in overgrowth.

Gram-negative group in the Proteobacteria phylum. May produce histamine. High levels
Morganella spp. may indicate increased intestinal inflammatory activity. High levels may cause diarrhea,
and may also be associated with SIBO.

Pseudomonas spp. Gram-negative bacteria in the Proteobacteria phylum. High levels may indicate increased
Pseudomonas intestinal inflammatory activity and may cause abdominal cramping and loose stools.
aeroginosa Some strains of P. aeroginosa may produce toxins that can damage cells.

Gram-positive bacteria in the Firmicutes phylum. High levels may result from reduced
Staphylococcus spp.
digestive capacity, and intestinal inflammatory activity. Some strains may produce
Staphylococcus aureus toxins and contribute to loose stools or diarrhea.

Gram-positive bacteria in the Firmicutes phylum. Streptococcus spp. colonize skin and
mucous membranes throughout the body; High levels in the intestine may result from
Streptococcus spp. low stomach acid, PPI use, reduced digestive capacity, SIBO or constipation; Elevated
levels may also be indicative of intestinal inflammatory activity, and may cause
loose stools.

COMMENSAL & OVERGROWTH MICROBES

A genus of Gram-negative sulfate reducing bacteria. The bacteria produce hydrogen
Desulfovibrio spp. sulfide (H2S), a metabolite which can influence cell signaling and reduce oxidative stress
at low concentrations and pose toxicity at higher concentrations.

Family of bacteria-like microbes that produce methane. Facilitates carbohydrate

fermentation and short-chain fatty acid production by beneficial bacteria. High levels
Methanobacteriaceae
linked to chronic constipation, as well as some types of SIBO and IBS. Low levels
(family) may indicate reduced production of short-chain fatty acids and may be associated
with inflammation.

INFLAMMATORY & AUTOIMMUNE-RELATED BACTERIA

Citrobacter spp. Gram-negative bacteria in the Proteobacteria phylum. High levels may indicate
Citrobacter freundii. increased intestinal inflammatory activity.

Gram-negative bacteria in the Proteobacteria phylum. Common residents of the oral

Klebsiella spp. cavity and respiratory tract. May cause diarrhea, gas, abdominal pain, and bloating;
Klebsiella pneumoniae Common after long-term antibiotic use; May release histamine in the gut; High levels
may indicate increased intestinal inflammatory activity.

Mycobacterium avium Bacterial species in the Actinobacteria phylum. Higher levels have been associated
subsp. paratuberculosis with Crohn’s disease and rheumatoid arthritis.

Gram-negative bacteria in the Proteobacteria phylum. High levels may indicate

Proteus spp.
increased intestinal inflammatory activity; May contribute to loose stools or diarrhea;
➠

Proteus mirabilis Pets or wild animals can be a source.

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 GI-MAP® INTERPRETIVE GUIDE

Table 6a.
COMMENSAL INFLAMMATORY & AUTOIMMUNE-RELATED BACTERIA
Gram-negative genus in the Proteobacteria phylum. Closely related to E. coli (in the
Enterobacter spp. same taxonomic family). High levels may indicate increased intestinal inflammatory
activity. Low levels may indicate reduced mucosal health.

Gram-negative genus in the Proteobacteria phylum. Normal gut flora. Escherichia coli
(E. coli) is the primary species in this genus. Most E. coli are nonpathogenic (pathogenic
Escherichia spp. E. coli strains are measured separately in “Pathogens” section of the GI-MAP). High levels
may be indicative of increased intestinal inflammatory activity. Low levels may
indicate reduced mucosal health and decreased protection against pathogenic E. coli.

Genus of gram-negative bacteria in the Fusobacteria phylum. Commonly found in the

Fusobacterium spp. oral cavity, and may also be found in the intestine. Associated with inflammatory
processes, as well as autoimmune conditions such as systemic sclerosis.

Gram-negative species in the Bacteroidetes phylum. Associated with rheumatoid

Prevotella spp.
arthritis. High levels may result from reduced digestive capacity, or a high-starch diet.

• Therapeutic Options and » If using antibiotics, see the

Considerations for Abnormally High Physician’s Desk Reference for
Levels of Opportunistic Bacteria
appropriate antibiotics for the specific
» Consider high-dose probiotics microorganisms that are overgrown
(300+ billion CFU/d)
» If using antibiotics, consider rifaxamin,
» Consider broad-spectrum which remains in the GI tract and
antimicrobial herbs including: is also used to treat small intestinal
berberine, caprylic acid, garlic oil, oil of bacterial overgrowth (SIBO)
oregano, uva ursi, or olive leaf extract
» Optimize diet (low sugar, low refined
carbs, high plant-based foods and fiber)
» See SIgA level to determine mucosal
immunity and if patient is protected
from overgrowth symptoms
» Use the 5R Protocol (see Table 2)
» Identify and remove potential sources
of contamination or re-infection
» Address all other imbalances
on the GI-MAP
Bacillus cereus
➠

RESEARCH. TECHNOLOGY. RESULTS. 25

 OPPORTUNISTIC BACTERIA

• Opportunistic Bacteria as a or sustain the autoimmune process.

Trigger for Autoimmunity Gastrointestinal symptoms are less
» Certain opportunistic bacteria may common when these bacteria are
initiate autoimmune thyroiditis elevated. When intestinal permeability
or inflammatory arthritis such as is present (see zonulin), these microbes
rheumatoid arthritis and ankylosing could escape the lumen of the gut
spondylitis. These bacteria may trigger and infect extraintestinal sites.

Table 7. Opportunistic Bacteria and Viruses Associated with Autoimmunity.

OPPORTUNISTIC BACTERIA AND AUTOIMMUNE ASSOCIATION

Citrobacter spp. Rheumatoid arthritis

Fusobacterium spp. Systemic sclerosis or inflammatory bowel disease

Crohn’s disease, ulcerative colitis, ankylosing spondylitis, and other

Klebsiella spp. spondyloarthropathies (which include ankylosing spondylitis, arthritis associated
with Crohn’s or ulcerative colitis, psoriatic arthritis, and reactive arthritis)

M. avium subsp.
Rheumatoid arthritis, Crohn’s disease, Type I diabetes, possibly psoriasis
paratuberculosis

Prevotella copri Rheumatoid arthritis

Proteus spp. Rheumatoid arthritis

Proteus mirabilis Rheumatoid arthritis and spondyloarthropathies (listed above)

VIRUSES AND AUTOIMMUNE ASSOCIATION

Systemic lupus erythematosus, systemic sclerosis, type 1 diabetes,

Cytomegalovirus (CMV)
rheumatoid arthritis

Rheumatoid arthritis, lupus, Sjogren’s, multiple sclerosis, autoimmune

Epstein Barr Virus (EBV)
thyroid disorders
➠

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 GI-MAP® INTERPRETIVE GUIDE

FUNGI/YEAST
Fungal organisms are commonly found in the human digestive tract, but fungal
overgrowth can cause illness in susceptible individuals. Fungal growth may
be localized in the body. For instance, Candida spp. may be high in the large
intestine but normal in the small intestine, and vice versa. In a patient with
suspected fungal overgrowth, additional tests may be necessary to understand
the complete picture of fungal overgrowth. Urinary D-arabinitol or antibodies to
Candida are sometimes used.

• Common Causes of Yeast Has been suggested to cause a

Overgrowth Include: cluster of symptoms including GI
» Antibiotic use complaints, fatigue, and muscle or
» High intake of sugar, starches, joint pain but evidence is weak.
and dietary fungi (beer, » Geotrichum spp.
bread, nuts, cheese, corn) – May cause disease in
» Hypochlorhydria immunosuppressed patients.
» Impaired immune function Low levels may be a dietary
» Dysbiosis artefact; certain strains are
used to make soft cheeses.
• Fungi/Yeast Targeted on the GI-MAP
» Microsporidia spp.
» Candida albicans and Candida spp.
– The GI-MAP specifically detects
– Commensal fungi that
Encephalitozoon intestinalis, which
can be pathogenic to
affects the GI. May cause diarrhea
immunocompromised patients.
and wasting. Can disseminate
Causes vaginal yeast infections
to ocular, genitourinary,
➠

and can be fatal in systemic

and respiratory tracts.
infections. May cause diarrhea.
RESEARCH. TECHNOLOGY. RESULTS. 27
 FUNGI/YEAST

Candida albicans

» Rhodotorula spp. • Therapeutic Options and

Considerations for Abnormally
– Common in soil, plants,
High Levels of Fungi/Yeast
bathrooms, and in beverages like
» Reduce intake of sugars,
milk, juice, and water. May be a
starches, and fungi
commensal. Can cause disease
in immunosuppressed patients. » See SIgA levels and consider
immune support
• Common Symptoms of
» Consider high-dose probiotics,
Fungal Dysbiosis
Saccharomyces boulardii, and
» GI symptoms: Gas, bloating,
the 5R Protocol (see Table 2)
constipation, nausea,
» Consider antifungal herbs such
vomiting, and diarrhea.
as caprylic acid, undecylenic acid,
» Other symptoms: Eczema,
oregano oil, berberine, and/or garlic
athlete’s foot, vaginal yeast
» Consider pharmaceutical antifungals
infections, thrush, and jock itch.
in severe cases. Nystatin is preferred
because it stays in the GI tract.
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VIRUSES
Cytomegalovirus
• Epidemiology
» Herpes virus that has infected
60% of the US population
» One in three children have
contracted CMV by five years old
» Passed around in child daycare centers

• Clinical Implications
» Positive CMV on the GI-MAP
indicates active infection of Cytomegalovirus is a viral genus of the viral family
known as Herpesviridae
the GI, NOT past infection
» Active infection may be asymptomatic
or cause mild flu-like symptoms • Therapeutic Options and
» CMV can also cause viral pneumonia, Considerations
transaminitis, splenomegaly, » No treatment is needed
colitis, fever, and encephalitis if asymptomatic
» Common in inflammatory bowel » Prevent spreading CMV with
disease, immunocompromised regular handwashing
patients » Antiviral herbs such as cat’s claw,
» CMV colitis has a similar presentation osha root, reishi mushrooms,
to Clostridium difficile infection vitamins A, C, and D, zinc, Echinacea
» CMV has been implicated in » Address other imbalances on
autoimmune diseases: lupus, the GI-MAP and use 5R Protocol
systemic sclerosis, type 1 diabetes, (see Table 2) to rebuild gut
and rheumatoid arthritis health and gut immunity
➠

RESEARCH. TECHNOLOGY. RESULTS. 29

 VIRUSES

Epstein Barr Virus arthritis, lupus, Sjogren’s,

multiple sclerosis, autoimmune
• Epidemiology
thyroid disorders
» One of the most common
» EBV may increase the risk of gastric
viruses worldwide; infects
cancer; especially if H. pylori present
90–95% of the population
» May cause colitis
» Commonly contracted in childhood
and causes mild symptoms » Found in 30–64% of IBD patients

• Clinical Implications • Therapeutic Options and

Considerations
» Positive finding on the GI-MAP
» Rest and hydration
indicates active EBV infection of
the GI, not past infections » Antiviral herbs such as cat’s claw,
osha root; antiviral fungi such as
» Can cause infectious
reishi and/or Cordyceps mushrooms
mononucleosis (mono)
» Vitamins A, C, and D, zinc, Echinacea
» Symptoms include fatigue, fever,
swollen lymph nodes, inflamed » Address other imbalances on
throat, enlarged spleen, and more the GI-MAP and use 5R Protocol
(see Table 2) to rebuild gut
» May last two to four weeks in
health and gut immunity
adolescents and adults
» Follow-up blood testing may be
» May cause fatigue for weeks or months
indicated, including an EBV Early
» Associated with autoimmune
Antigen and EBV PCR test
conditions such as rheumatoid
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PARASITES
A parasite is an organism that lives and feeds on a host organism at the
expense of the host. The GI-MAP tests for pathogenic parasites and protozoa
(some of which are non-pathogenic) most commonly occurring in the GI tract.
Sources of exposure should be identified and eliminated to prevent reinfection.

PROTOZOA

Blastocystis hominis » Consider nitazoxanide or tinidazole,

oregano oil, and S. boulardii
• Epidemiology
» Herbal treatments may
» Fecal contamination of food
not be as effective
or water is common
» Consider Artemisia, Coptis, or
» Found worldwide
other broad-spectrum anti-
• Clinical Implications parasitic herbal formulas
» Symptoms include diarrhea, » Infection can be treated with
abdominal pain, nausea and metronidazole, iodoquinol or
vomiting, fever, fatigue, irritable trimethoprim/sulfamethoxazole*
bowel syndrome, infective arthritis
» Consider probiotics and
• Therapeutic options and considerations 5R Protocol (see Table 2)
» Difficult to eradicate
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RESEARCH. TECHNOLOGY. RESULTS. 31

 PARASITES

Chilomastix mesnili
• Epidemiology
» Fecal contamination of food or water

• Clinical Implications
» Considered non-pathogenic and
may not cause symptoms
» May indicate dysbiosis or
Cyclospora
suppressed immunity

• Therapeutic Options
and Considerations » Can cause bloating,
flatulence, and burping
» Look for and address sources
of fecal-oral contamination » Flu-like symptoms such as fatigue,
headaches, and low fever may be
» Consider probiotics and
present in some individuals
5R Protocol (see Table 2)
» Infection is usually self-limiting, with
» Address other imbalances
symptoms usually lasting about seven
on the GI-MAP
days, but can last weeks or months
in immunosuppressed patients

Cyclospora spp. • Therapeutic Options

(Cyclospora cayetanensis) and Considerations
» In cases lasting more than seven
• Epidemiology
days, treatment with an antibiotic
» Fecal contamination of food and water combination of trimethoprim and
» Associated with water- and sulfamethoxazole may be necessary*
food-borne outbreaks » Consider probiotics, broad-spectrum
» Common cause of traveller’s diarrhea anti-parasitic herbal formula, and
» May be found on imported fresh the 5R Protocol (see Table 2)
produce from tropical regions » Look for and address
• Clinical Implications sources of reinfection
» Symptoms include prolonged
watery diarrhea, abdominal
cramping, loss of appetite, weight
Dientamoeba fragilis
loss, nausea, and vomiting • Epidemiology
» May cause alternating » Not well understood; probably fecal
diarrhea and constipation contamination of food or water
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• Clinical Implications » Look for and address sources

» May be asymptomatic of fecal contamination
» May cause diarrhea, abdominal » Address other imbalances
pain, nausea, fever, fatigue, weight on the GI-MAP
loss, appetite loss, and/or fatigue

• Therapeutic Options Entameoba coli

and Considerations
• Epidemiology
» “Moderate” amounts of DNA, that
are not above the laboratory » Fecal contamination of food or water
reference range, may cause » Found in the large intestine,
symptoms and warrant treatment considered to be non-pathogenic
» Infection can be treated with • Clinical Implications
iodoquinol, paromomycin, » May be indicative of dysbiosis,
or metronidazole* conservative treatment may be
» Consider probiotics, broad-spectrum indicated if clinical presentation is
anti-parasitic herbal formula, and consistent with enteroparasitosis
the 5R Protocol (see Table 2)
• Therapeutic Options
» Look for and address and Considerations
sources of reinfection
» Consider probiotics and the
» Address other imbalances 5R Protocol (see Table 2)
on the GI-MAP
» Look for and address sources
of fecal contamination
Endolimax nana » Address other imbalances
on the GI-MAP
• Epidemiology
» Fecal contamination of food or water

• Clinical Implications
Pentatrichomonas hominis
» Considered non-pathogenic; • Epidemiology
individuals may be asymptomatic » Fecal contamination of food or water
» May be indicative of dysbiosis, • Clinical Implications
conservative treatment may be
» Considered harmless, a non-pathogen
indicated if clinical presentation is
» Infected individuals are
consistent with enteroparasitosis
usually asymptomatic
• Therapeutic Options » May contribute to dysbiosis
and Considerations
» Also colonizes dogs, cats,
» Consider probiotics and the
➠

and other animals

5R Protocol (see Table 2)
RESEARCH. TECHNOLOGY. RESULTS. 33
 PARASITES

• Therapeutic Options • Clinical Implications

and Considerations » Early symptoms are itching and rash
» May be asymptomatic where the larvae penetrated the skin
» In women with vaginosis, consider » Symptoms of heavy infestations
treatment to reduce chances include: abdominal pain,
of vaginal contamination or diarrhea, fatigue, weight loss,
reinfection (find treatments for iron deficiency anemia (IDA),
Trichomonas vaginalis elsewhere) coughing, and loss of appetite
» If treatment is needed, consider » Infected individuals may
a broad-spectrum anti- also be asymptomatic
parasitic herbal formula
• Therapeutic Options
» Consider probiotics and the and Considerations
5R Protocol (see Table 2)
» Heavy infections can be treated with
» Look for and address sources albendazole or mebendazole*
of fecal contamination
» Individuals presenting with IDA
» Address other imbalances may need iron supplementation
on the GI-MAP
» Consider anti-parasitic herbal
treatments, gut immunity support,
and the 5R Protocol (see Table 2)
WORMS » Look for and remove
sources of reinfection

Ancylostoma duodenale and

Necatur americanus (Hookworms) Ascaris lumbricoides (Roundworm)
• Epidemiology • Epidemiology
» Infection occurs via skin contact » Fecal contamination of food or water
with soil contaminated with » Common in international
larvae or ingestion of larvae travellers and recent immigrants
» Infected cats and dogs are from Latin America and Asia
a source of exposure
• Clinical Implications
» Prevalent in southern Europe,
» Early symptoms include fever,
Northern Africa, India, Asia, Caribbean
coughing, wheezing, and dyspnea
islands, South America, and small
» Late symptoms include abdominal
areas of the United States
pain, nausea, vomiting, frequent
» Associated with poor sanitation,
throat clearing, dry cough,
inadequate housing construction,
➠

“tingling throat,” appendicitis,

and lack of access to medications
pancreatitis, and obstruction
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 GI-MAP® INTERPRETIVE GUIDE

» Can cause reactive arthritis » Consider anti-parasitic herbal

treatments, gut immunity support,
• Therapeutic Options
and Considerations and the 5R Protocol (see Table 2)

» Infections may be treated with » Look for and remove

albendazole, mebendazole, sources of reinfection
or ivermectin*
» Consider anti-parasitic herbal
Taenia spp. (Tapeworm)
treatments, gut immunity support,
and the 5R Protocol (see Table 2) • Epidemiology
» Look for and remove » Fecal contamination of undercooked
sources of reinfection pork (T. solium) or beef (T. saginata)
» T. solium is found worldwide,
but prevalent in communities
Trichuris trichiura (Whipworm) who raise and eat pigs
• Epidemiology » T. saginata is prevalent in Africa, parts
» Fecal contamination of produce of Eastern Europe, the Philippines,
or person-to-person contact and Latin America where people
» Prevalent in Asia, Africa, raise cattle and eat raw beef
South America, and rural • Clinical Implications
southeastern United States
» May be asymptomatic or
• Clinical Implications present with mild symptoms
» Most individuals are asymptomatic, » Symptoms include abdominal
however diarrhea with mucus pain, nausea, weakness,
and blood may occur in some increased appetite, loss of
infected individuals appetite, headache, constipation,
dizziness, diarrhea, pruritus ani,
• Therapeutic Options
and Considerations hyperexcitability, and anemia
» Infections may be treated with • Therapeutic Options
albendazole, mebendazole, and Considerations
or ivermectin* » Infections may be treated with
» Individuals presenting with IDA albendazole or praziquantel*
may need iron supplementation » Consider anti-parasitic herbal
treatments, gut immunity support,
and the 5R Protocol (see Table 2)
» Look for and remove
sources of reinfection
➠

Microscopic cross section of a whipworm

(Thichuris trichiura)
RESEARCH. TECHNOLOGY. RESULTS. 35
 INTESTINAL
HEALTH
MARKERS
DIGESTION » Chew thoroughly and
relax at meal time
» Pepsin
Pancreatic Elastase 1 » Plant or pancreatic enzyme
supplements
Elastase 1 is a digestive enzyme secreted
exclusively by the pancreas, giving a » Digestive herbs
direct indication of pancreatic function. » Bile salts
Elastase 1 is unaffected by pancreatic » Taurine
enzyme replacement therapy. » Consider underlying causes
• Causes of Low Elastase 1:
» Suppressed pancreatic function
» Gallstones Table 8. Staging of pancreatic
» Hypochlorhydria, especially insufficiency based on fecal elastase-1.
if H. pylori present Fecal Elastase-1
Clinical Significance
» Cystic fibrosis Result

» Low levels may be found < 200 ug/g Pancreatic insufficiency

in vegetarians/vegans
200–500 ug/g Decreased pancreatic output
• Common Approaches for Addressing
> 500 ug/g Normal pancreatic output
Low Pancreatic Digestive Enzyme Levels:
» Digestive support with betaine HCL
➠

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Steatocrit • Major Producers of β-glucuronidase are:

» Bacteroides fragilis
Fecal fats are normally emulsified by bile » Bacteroides vulgatus
salts and absorbed in the small intestines.
» Bacteroides uniformis
High levels of fat in the stool may be an
» Clostridium paraputrificum
indication of maldigestion, malabsorption,
or steatorrhea. » Clostridium clostridioforme
» Clostridium perfringens
• Causes of Elevated Steatocrit:
» Escherichia coli
» Hypochlorhydria
» Eubacterium
» Maldigestion
» Peptostreptococcus
» Malabsorption
» Ruminococcus
» Pancreatic insufficiency (see elastase-1)
» Staphylococcus
» Bile salt insufficiency
» Improper mastication • Clinical Indications of High
β-glucuronidase:
» Celiac disease
» Dysbiosis in the colon or small
• Therapeutic Approaches and intestinal bacterial overgrowth (SIBO)
Considerations for High Fecal Fats:
» Extremely elevated cases associated
» Support digestion with betaine HCL with colon cancer risk
» Pepsin » Problems with detoxification, especially
» Digestive herbs or “bitters” estrogen (via glucuronidation pathway)
» Bile salts » Overexposure to toxins or drugs
» Taurine
• Therapeutic Approaches and
» Consider underlying causes of Considerations for Elevated
malabsorption, such as celiac disease, β-glucuronidase:
dysbiosis, or food sensitivities » Address dysbiosis, if present
» Promote bacterial diversity with
probiotics, fiber, prebiotics,
and fermented foods
ADDITIONAL GI MARKERS » Consider liver support such
as milk thistle and calcium
Beta-Glucuronidase D-glucarate, especially if patient
is taking hormone replacement
High levels of fecal beta-glucuronidase can or has increased cancer risk
indicate unfavorable metabolic changes in » If there are no signs of dysbiosis on the
the colon. Beta-glucuronidase may indicate GI-MAP, consider a SIBO breath test
➠

dysbiosis and interference with Phase II

detoxification involving glucuronidation.
RESEARCH. TECHNOLOGY. RESULTS. 37
 INTESTINAL HEALTH MARKERS

Occult Blood Fecal IMMUNE RESPONSE

Immunochemical Testing (FIT)
FIT is quantitative and directly measures
Secretory IgA (SIgA)
the concentration of hemoglobin present
in stool, rather than just the qualitative Immunoglobulin A is the primary
presence of hemoglobin. This test uses immunoglobulin in the intestinal mucosa.
antibodies specific for human hemoglobin It represents a “first line of defense” in
and therefore does not require dietary response to antigens and pathogens in
restrictions or multiple samples, the GI and respiratory tracts. In addition to
significantly reducing the appearance protecting against pathogens, SIgA plays a
of false positives. This method has major role in helping to maintain balance
better detection of lower hemoglobin in the microbiome and protecting against
concentrations than qualitative tests, exposure to food-derived antigens.
eliminating potential false negatives as well.
Low Fecal SIgA – The gut immune system
Literature suggests a result of 10 ug/g may
is suppressed. Investigate underlying
be indicative of potentially more serious
causes, such as chronic dysbiosis,
conditions such as polyps or colorectal
antigen exposure, chronic stress,
cancer. A variety of ailments can cause
immunocompromised patient, or even
lower counts of blood in stool, such as
protein malnutrition.
hemorrhoids, anal fissures, pathogenic
infection such as giardia, liver disease, and • Therapeutic Approaches
upper GI infections. for Low SIgA Levels:
» Address any chronic GI
• Possible Causes of
Positive Occult Blood: infections, if appropriate

» Bleeding ulcer » Address microbiome imbalances

» Inflammatory bowel disease » Address chronic stress and

adrenal health, if needed
» Cancer
» Colostrum or immunoglobulins
» Intestinal polyps
» Supplement with S. Boulardii
» Upper GI bleeds that cause
iron deficiency anemia » GI mucosal support with glutamine
» Lactobacillus and
• Common Approaches for
Bifidobacteria probiotics
Addressing Fecal Occult Blood
» General immune support
» Identify source
» Essential fatty acids
» Follow-up testing recommended
» Zinc
» Address other imbalances
➠

on the GI-MAP

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 GI-MAP® INTERPRETIVE GUIDE

High Fecal SIgA – Elevated immune Eosinophil Activation Protein

response to antigens in the GI tract. (EDN/EPX)
Investigate underlying causes, such as
chronic dysbiosis, acute infections, acute EDN/EPX is a protein released by activated
stress, or food sensitivities. eosinophils which has strong cytotoxic
characteristics. The protein plays a
• Therapeutic Approaches significant role in a variety of inflammatory
for High SIgA Levels:
and mast-cell mediated pathologies in
» Address GI infections addition to fighting pathogens, particularly
» Address any food allergies viral infections.
and sensitivities
» General immune support High Eosinophil Activation Protein –
The accumulation of eosinophil activation
Anti-gliadin SIgA – Gliadin is a component protein in the intestine is associated with
of gluten, the protein found in wheat and inflammation and tissue damage, and the
other field grass grains such as barley, level of EPA in the stool can serve as an
malt, and rye. The presence of fecal anti- objective measure for chronic inflammation
gliadin antibodies can indicate an immune in the GI tract. In the case of inflammatory
response (in the gut) to gluten in the bowel disease, the marker can be used
diet. Fecal anti-gliadin antibodies do not to evaluate disease activity and predict
necessarily correlate with blood levels. relapse. The EPA marker can also be used
to determine the effectiveness of a food
High Anti-gliadin SIgA – Elevated immune
elimination diet to control symptoms or
response to gliadin in the lumen of the gut.
disease progression.
• Treatment:
• Possible Causes of Elevated
» Consider gluten elimination Eosinophil Activation Protein:
for a trial period » Respiratory allergies
» If patients have been gluten-free, » Asthma
consider hidden sources of gluten and
» Food allergies and sensitivities
gliadin cross-reactive food such as
» IBD
dairy, corn, oats, millet, rice and yeast
» IBS
» Consider intestinal barrier
support, including supplements » Eosinophilic esophagitis (EE)
such as L-glutamine, zinc » Functional dyspepsia
carnosine, and colostrum » Acid reflux
» Intestinal barrier damage/dysfunction
» Anxiety (IBS-related anxiety)
» Intestinal parasites
➠

RESEARCH. TECHNOLOGY. RESULTS. 39

 INTESTINAL HEALTH MARKERS

INFLAMMATION ADD-ON
Calprotectin
Fecal calprotectin is the most studied
TESTS
The following optional add-on tests
marker of gastrointestinal inflammation.
can be ordered with the GI-MAP.
High calprotectin indicates neutrophil
infiltration to the gut mucosa. Calprotectin
is the gold standard marker for the Zonulin
diagnosis and monitoring of inflammatory
bowel disease. It is used to differentiate Zonulin is a protein that opens intercellular
IBD from irritable bowel syndrome. tight junctions in the gut lining (the
connections between epithelial cells that
• Possible Causes of
make up the gastrointestinal lining). Zonulin
Elevated Calprotectin
increases intestinal permeability in the
» Intestinal infections and pro-
jejunum and ileum and is considered a
inflammatory dysbiosis
biomarker for barrier permeability.
» Food allergens, toxins and certain
drugs (e.g., non-steroidal anti- • Therapeutic Approach for
Elevated Intestinal Permeability:
inflammatory drugs [NSAIDs])
» Address dysbiosis (pathogens and
» Inflammatory bowel disease
opportunistic microbe overgrowth,
» Polyps
lack of beneficial microbes)
» Diverticulitis
» Eliminate gluten, address
» Colorectal cancer
potential food sensitivities
• Therapeutic Approaches » Promote a healthy intestinal barrier
and Considerations with L-glutamine, butyrate, essential
» Address possible causes of fatty acids, aloe vera, probiotics, zinc
elevated calprotectin carnosine, slippery elm, marshmallow,
» Persistently elevated calprotectin may deglycyrrhizinated licorice
indicate chronic inflammatory disease;
Zonulin is available as an optional add-on to
further evaluation by a qualified
the GI-MAP, or as a stand-alone test.
medical professional is advised
» Consider anti-inflammatory
support (e.g., anti-inflammatory
diet, curcumin, omega-3 fatty
acids, aloe, and resveratrol)
➠

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 GI-MAP® INTERPRETIVE GUIDE

Gluten Peptide Universal Antibiotic Resistance

(AR) Genes Panel
The Gluten Peptide test detects the
presence of gluten in stool. Gluten is The Universal Antibiotic Resistance Genes
broken into gliadin and glutenin subunits Panel detects the presence of 55 genetic
during the digestive process. A specific elements associated with resistance to
section of the gliadin protein, referred 10 different classes of antibiotics. Useful
to as the 33-mer peptide,* is resistant to for patients who have been hospitalized,
digestion in the human gastrointestinal treated with antibiotics, or who have
(GI) tract but can be accurately detected in stubborn, chronic infections, the Universal
stool several days after the consumption Antibotic Resistance Genes panel can
of gluten. inform practitioners if antibiotic resistance
is a potential stumbling block for patients.
The Gluten Peptide test can help
practitioners monitor a patient’s gluten-free The Universal Antibiotic Resistance (AR)
(GF) diet compliance. Any detected level of Gene Panel is available as an optional
the fecal gluten protein indicates dietary add-on only to the GI-MAP, or Pathogens
exposure to gluten within the previous Panel. See page 42 for more information
2–4 days.† regarding AR Genes testing on the GI-MAP
and antibiotic stewardship.
• Clinical Implications:
» For patients following a GF diet,
detected levels of the gluten StoolOMX™
peptide can indicate accidental
exposure from hidden sources StoolOMX measures gut microbial
or food cross-contamination metabolites that evaluate 25 bile acids
» For patients regularly consuming and 9 short chain fatty acids, providing
gluten, detected levels are actionable insights into conditions like IBS,
expected findings IBD, and bile acid diarrhea.

The Gluten Peptide marker is available as an StoolOMX is available as an optional add-

optional add-on to the GI-MAP, or as a stand- on to the GI-MAP. Please see StoolOMX on
alone test. page 44 for a detailed interpretive overview.

* Because of structural homology (the structural similarity)

of gluten proteins, detected 33-mer gliadin protein may
indicate the consumption of wheat, rye, barley, corn, or
oat grain.
† Speed of digestion (motility and transit time) can
influence the transience of gluten peptide in stool.
➠

RESEARCH. TECHNOLOGY. RESULTS. 41

 ANTIBIOTIC
RESISTANCE
GENES
In an effort to promote antibiotic stewardship, the GI-MAP includes results
of H. pylori Antibiotic Resistance Genes in the microbiome as part of the test.
Additionally, the Universal Antibiotic (AR) Resistance Genes panel can be ordered as
an add-on to the GI-MAP or to the GI-Pathogens panel.

Antibiotic Stewardship Universal Antibiotic Resistance Genes

Antibiotic stewardship is the effort to measure The Universal Antibiotic resistance genes
and improve how antibiotics are prescribed apply to all of the microorganisms within the
by clinicians and used by patients. If an fecal sample. Since microbes can rapidly share
antibiotic resistance gene is present, then that DNA under stress, the presence of antibiotic
class of antibiotics is designated POSITIVE resistance in any organism is reason enough
for antibiotic resistance. A positive result for to avoid that drug class.
the presence of resistance genes for a given
antibiotic indicates that the antibiotic is not an
ideal choice for an antibiotic protocol.

H. pylori Antibiotic Resistance Genes

The H. pylori Antibiotic Resistance Genes are
specific to the H. pylori genome detected
on an individuals’ GI-MAP. These results
will only be reported if the H. pylori result is
➠

5.0e2 or greater.

42 diagnosticsolutionslab.com
 GI-MAP® INTERPRETIVE GUIDE

Figure 4. Sample H. pylori Antibiotic Resistance Genes Section. See additional

details in the “Helicobacter pylori” section of this guide (Page 17, Figure 2).

Patient: Ima Test Accession:

UNIVERSAL ANTIBIOTIC RESISTANCE GENES

Result Reference Result Reference Result Reference

b-Lactams Negative Negative Macrolides Negative Negative Trimethoprim Negative Negative

blaNDM-1 Absent acrA Absent dfrA1 Absent

CTX-M 1 Absent acrB Absent dfrA12 Absent

CTX-M 2 Absent emrE Absent dfrA14 Absent

CTX-M 8/25 Absent ermA Absent dfrA15 Absent

CTX-M 9 Absent ermB Absent dfrA17 Absent

GES Absent ermC Absent dfrA5 Absent

OXA-1 Absent macA Absent dfrA7 Absent

PER-1 Absent macB Absent dfrB1 Absent

PER-2 Absent mefA Absent dfrB2 Absent

SHV Absent mphA Absent dfrB3 Absent

TEM Absent msrA Absent

VEB Absent tolc Absent

Fluoroquinolones Positive Negative Ciprofloxacin Negative Negative Sulfonamides Positive Negative

qnrA Present emea Absent sul1 Present

qnrB Absent pmra Absent sul2 Present

qnrS1 Absent sul3 Present

Vancomycin Negative Negative Nitroimidazoles Negative Negative Methacillin Negative Negative

vanA Absent nimA Absent mecA Absent

vanA2 Absent nimB Absent Chloramphenicol Negative Negative

vanB Absent nimC Absent
cata13 Absent
vanC1 Absent nimD Absent

vanC2-1 Absent nimE Absent

vanC2-2 Absent

Figure 5. Sample Universal Antibiotic Resistance Genes Panel. Available as

➠

Detection of resistance-associated genes may not confer phenotypic drug resistance. Detected genes cannot be associated with specific microbes.
an optional add-on only to the GI-MAP, or Pathogens Panel.

RESEARCH. TECHNOLOGY. RESULTS. 43

 StoolOMX ™

StoolOMX measures gut microbial metabolites—a comprehensive set of bile acids

(BA) and short chain fatty acids (SCFA) via LC-MS/MS. This data offers an in-depth
understanding of the stool metabolome and its clinical applications. The StoolOMX
profile can be ordered as an add-on to the GI-MAP.

Under normal physiological conditions,

BILE ACIDS most bile acids are reabsorbed, and
Primary bile acids are natural products very few bile acids are excreted in stool.
produced in the liver from cholesterol Under abnormal physiological conditions,
synthesis. These primary bile acids are excess bile acids enter the colon and can
conjugated with either taurine or glycine promote inflammation and diarrheal
to increase solubility and are stored in symptoms while exerting negative effects on
the gallbladder as bile. commensal bacteria.

Primary, conjugated bile acids are the main Measuring concentrations and ratios of bile
component in bile. At mealtime, they aid in acids in stool can offer root-cause insights
the emulsification and absorption of dietary into digestive symptoms, malabsorptive
fats in the small intestine. After contributing disorders, immune system regulation, and
to fat absorption, the majority (~95%) of even metabolic impacts. Furthermore,
primary bile acids are reabsorbed in the altered patterns of bile acid metabolites have
distal ileum and returned to the liver via the emerging disease state associations and can
portal vein — a process called enterohepatic be used as part of diagnostic workup and
circulation. A small portion (~5%) of primary treatment management in conditions such as
bile acids will reach the colon, where bile acid diarrhea (BAD), inflammatory bowel
they are metabolized by gut bacteria and disease (IBD), and irritable bowel syndrome
deconjugated (glycine and taurine removed) (IBS) (-C, -D, -M).
to produce unconjugated secondary bile
StoolOMX measures 25 bile acid metabolites
acids. Deconjugation is generally favorable.
in total concentrations, percents, and ratios.
Commensal gut bacteria deconjugate bile This data offers an in-depth understanding
acids to facilitate their reabsorption and of the stool metabolome and impactful
➠

recycling while also preparing them for clinical considerations.

further bacterial modification.
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 GI-MAP® INTERPRETIVE GUIDE

BILE ACIDS – SUMMARY Total Primary Bile Acids Percent

• Percent concentration of
primary bile acids in stool
Total Bile Acids Concentration
» Primary bile acids should be present
• An absolute concentration of total
in very low concentrations in stool
bile acids in stool measured in ng/g
» Primary bile acids in the colon can be
» Reflects the amount of bile acids
damaging to the gut lining and can have
reaching the colon and not reabsorbed
antimicrobial action on the microbiome
in the distal ileum after digestion
» Higher levels of primary bile acids in a
• Elevated Total Bile Acids: stool sample are indicative of excess
» Excess/elevated bile acids in production or BAM and are associated
stool is an indication of bile acid with an array of GI symptoms and
malabsorption (BAM) and often disease states, including IBD
results in symptoms such as » See individual primary bile acid
diarrhea (bile acid diarrhea – BAD) concentrations on page 2 of the
» Quantification of bile acids may be part StoolOMX report for further analysis
of a comprehensive workup for irritable and associations
bowel syndrome with diarrhea (IBS-D),
as it is currently estimated that up to Total Secondary Bile Acids Percent
1/3 of IBS-D patients present with BAD
• Inverse of total primary bile acids in stool
» Elevated stool bile acids may suggest
» Listed as percent concentration
altered bile acid production or
of secondary bile acids in stool
reabsorption, which could be due to
» Secondary bile acids should be present
liver disease, gallbladder dysfunction,
in high concentrations in stool
intestinal issues, or diet composition
» Secondary bile acids play diverse
• Low Total Bile Acids:
roles in regulating intestinal
» Low total bile acid concentrations motility, gut barrier function,
in stool are generally favorable but metabolism, and immune balance
may be indicative of slow transit
» In general, a higher number of
or constipation
secondary bile acids relate to a
healthier, more diverse microbiome
and normal physiological GI function
» See individual secondary bile acid
concentrations on page 2 of the
StoolOMX report for further analysis
and associations
➠

RESEARCH. TECHNOLOGY. RESULTS. 45

 STOOLOMX™

Table 9. This section represents the most abundant bile acids.

PERCENTAGE BREAKDOWN OF MOST ABUNDANT BILE ACIDS

SECONDARY BILE ACIDS FUNCTION AVERAGE PERCENTAGE†

DCA is a major secondary bile acid that is formed from the

bacterial metabolism of CA. Low levels observed in ulcerative
colitis (UC). Elevated levels are associated with liver and colon
Deoxycholic Acid (DCA) cancer and metabolic imbalance. Implicated in modulating the 48%
immune response by inhibiting pro-inflammatory cytokine
production. Can inhibit Lactobacillus spp., Bifidobacterium spp., and
Bacteroides fragilis.

LCA is a major secondary bile acid that is formed from the

bacterial metabolism of CDCA. Low levels observed in UC.
Lithocholic Acid (LCA)* Elevated levels are associated with liver and colon cancer and 27%
may contribute to blood sugar dysregulation. Modulates immune
responses at normal levels.

Prevalent secondary bile acid in stool that has positive associations

with longevity. Influences metabolic health, interacts with cellular
Isolithocholic Acid receptors, and modulates immune responses at normal levels.
8%
(Iso-LCA) Influences the differentiation and function of T cells, particularly
T helper 17 (Th17) cells, which play a critical role in the
inflammatory response.

The remaining primary and secondary bile acid metabolites

Other 17%
measured on StoolOMX.

* On StoolOMX, the LCA value is a summation of LCA + Allo-LCA.; † Reference set at 50th percentile.

LCA/DCA Ratio Bile Acids: Therapeutic Applications

LCA and DCA are secondary bile acids formed Bile acids and the microbiome have a
from CDCA and CA in the colon. CDCA is bidirectional relationship and impact. It is
converted to LCA, and CA is converted to DCA. important to first evaluate patient symptoms,
This ratio can be useful in determining the such as stool frequency and Bristol stool type.
risk of certain disease states and conditions.
Always analyze StoolOMX results with
LCA is thought to be more toxic than DCA GI-MAP findings and support accordingly. It
due to its inhibitory effects on antioxidant is important to assess liver function, as bile
pathways. An elevated ratio can be seen acids are originally produced in the liver.
in patients with gallstones and after
If there are significant imbalances in the bile
cholecystectomy. A higher ratio is also
acids summary, review the list of individual
associated with an increased risk for colon
bile acids on page 2 of the StoolOMX report.
cancers, while a lower ratio may indicate a
reduced cancer risk.
➠

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 GI-MAP® INTERPRETIVE GUIDE

• A healthy microbiome is • Medication/Supplement

typically associated with: Considerations for BAM
» Total bile acid concentration » Bile acid sequestrants
in normal range – ex: cholestyramine, colesevelam
» High secondary bile acid percent » Tauroursodeoxycholic acid (TUDCA)
• An unhealthy microbiome is » Digestive support as needed
typically associated with: – Digestive enzymes, betaine HCL,
» Elevated total bile acid concentration digestive bitters, ox bile, etc.
» High primary bile acid percent, » Activated charcoal
as the microbiome is responsible » Pectin fibers
for converting primary bile acids » Probiotics
to secondary bile acids
» Polyphenols such as resveratrol
• Common GI-MAP patterns
that may be associated with
abnormal StoolOMX results: Table 10. GI-MAP microbes involved in
» Presence of pathogens deconjugation of primary bile acids to
secondary bile acids.
» Insufficiency dysbiosis
» Increased Firmicutes:Bacteroidetes ratio GI-MAP MICROBES
» Overgrowth of GI-MAP (report Firmicutes phyla
page 3) inflammatory opportunists
Bacteroidetes phyla
» Elevated Steatocrit
Escherichia spp.
» Decreased Elastase-1
Bacteroides spp.
» Elevated Calprotectin
Bifidobacterium spp.
• Lifestyle Considerations
Enterococcus spp.
» Evaluate macronutrient composition of
Lactobacillus spp.
diet with respect to calories from fat.
Methanobacteriaceae family
Patients may need to adopt a lower fat
diet if StoolOMX results are abnormal.
» Evaluate and ensure
adequate dietary fibers
» Anti-inflammatory dietary practices
» Support liver and gallbladder
» Incorporate regular exercise
➠

RESEARCH. TECHNOLOGY. RESULTS. 47

 STOOLOMX™

Cholesterol

Taurine or
Primary Bile Acids
Glycine Secondary Bile Acids
Short Chain Fatty Acids (SCFA)

Primary Bile Acids

Biliary
Duct

Diet
Lifestyle
Environment
Genetics

Secondary Bile
Acids

Portal
Vein
SCFAs Dietary Fiber
or Protein

Figure 6. Bile Acids and Fatty Acids Overview.

Primary bile acids are synthesized from cholesterol in the liver and conjugated with either taurine
or glycine. They are stored in the gallbladder and released during digestion to assist with the
absorption of fat and fat-soluble vitamins. Normally, ~95% of primary bile acids are reabsorbed via
the portal vein, while ~5% are metabolized by gut bacteria to produce secondary bile acids.

Saccharolytic short chain fatty acids (SCFAs) are primarily metabolites of dietary fiber fermentation
in the gut while proteolytic branched chain fatty acids (BCFAs) are metabolites of protein
fermentation. Acetate, propionate, and butyrate are three major SCFAs, which account for ~90% of
the SCFAs produced by gut microbiota. SCFAs are known to have numerous health effects and can
enhance fecal excretion of bile acids.
➠

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 GI-MAP® INTERPRETIVE GUIDE

SHORT CHAIN FATTY Major SCFAs

ACIDS – SUMMARY Acetate, butyrate, propionate, and valerate
are the major primary straight chain
Short chain fatty acids (SCFAs) are small metabolites. As preferred fuel for intestinal
(0-6 carbon) saturated fatty acids that cells, these metabolites provide a variety of
are produced from the microbiome (gut beneficial effects for intestinal health.
bacteria) by fermentation of food substrates.
Fermentation of carbohydrate—called SCFAs serve as an energy source for colon
saccharolytic fermentation—produces cells, strengthen the gut barrier and provide
straight chain fatty acids (SCFA). Fermentation metabolic and immune system signaling.
of protein—called proteolytic fermentation— They have a profound anti-inflammatory
produces branched chain fatty acids (BCFA). effect by inducing and selectively expanding
T-regulatory cells (T regs) in the large
StoolOMX measures 9 short chain fatty intestine, which, in turn, suppresses the pro-
acid metabolites in percentages, total inflammatory action of Th17. As metabolites
concentrations, and ratios. The test also of bacterial fermentation, their levels can
includes the ratio of straight chain fatty reflect gut microbiota composition.
acids to branched chain fatty acids. Ratios
can provide insight into dietary composition Low levels of SCFAs are linked to various
and digestive impacts such as saccharolytic conditions, including irritable bowel
and proteolytic (putrefactive) fermentation syndrome, obesity, and inflammatory bowel
and digestive insufficiency. Assessing SCFA disease. Low levels may also be related to
levels in stool offers a deeper look into slow motility.
digestive health and the overall balance of the
gut microbiome.

Table 11.
PERCENT BREAKDOWN OF MAJOR SHORT CHAIN FATTY ACIDS REPRESENTED ON STOOLOMX

MAJOR SCFA FUNCTION AVERAGE PERCENTAGE†

Most abundant SCFA. Involved in lipid synthesis and appetite

Acetate regulation, maintains energy balance and metabolic 52%
homeostasis. Resists oxidation and mitochondrial stress.

Primary energy source for colonic cells. Supports intestinal

barrier integrity, reduces intestinal inflammation, promotes
Butyrate 20%
motility, enhances fatty acid oxidation, inhibits tumor cell
progression, and fosters a balanced microbiome.

Supports intestinal barrier integrity, impacts energy balance,

Propionate gluconeogenesis, and lipid metabolism. Involved in appetite 25%
regulation. Proposed as a biomarker for IBS.

Stimulates intestinal epithelium growth, inhibits colon cancer

Valerate cell production, modulates glucose and lipid metabolism. 3%
➠

Antimicrobial effects against C. difficile.

† Reference set at 50th percentile.

RESEARCH. TECHNOLOGY. RESULTS. 49
 STOOLOMX™

SCFA/BCFA Ratio Short Chain Fatty Acids:

Therapeutic Applications
Saccharolytic straight chain fatty acids
(SCFAs) are primary metabolites of • Causes for Low SCFA Levels:
dietary fiber fermentation in the gut » Diarrhea (rapid transit leading to
while proteolytic branched chain fatty decreased SCFA production)
acids (BCFAs) are metabolites of protein » Constipation (slow transit leading
fermentation. to increased SCFA absorption)
» Inflammation (high calprotectin)
Ideally, saccharolytic SCFAs should make
» Chronic antibiotic use
up ~95% of total SCFAs, while BCFAs should
make up ~5% of total SCFAs. » Low complex carbohydrate
and fiber intake
The production of branched chain fatty acids » Insufficiency dysbiosis
leads to other fermentation products that
» Inflammatory bowel disease
can be harmful to the colon epithelium, such
as ammonia, phenol, p-cresol, or biogenic • Cause for High SCFA Levels:
amines. BCFAs are mainly produced during » Increased transit time (diarrhea)
fermentation of branched chain amino • Causes for High BCFA Levels:
acids (valine, leucine, and isoleucine) by the
» High protein intake and low fiber
intestinal microbiota.
and/or polyphenol intake (Western diet)
High levels of BCFAs compared to » Low total SCFAs
saccharolytic SCFAs can indicate » Weak digestion/hypochlorhydria
weak digestion, poor transit, and » Increased age
inflammatory dysbiosis. There may also » Metabolic imbalance
be associations between elevated BCFA
• Therapeutic Options and Considerations
concentrations in stool and obesity, IBD,
to Increase Levels of SCFAs:
hypercholesterolemia, and metabolic-
» Ensure diet is high and diverse in
associated fatty liver disease (MAFLD).
plant-based fibers, polyphenols,
The SCFA/BCFA ratio may decline with age, and fermented foods
primarily due to a significant decrease in » Avoid antibiotics
SCFA levels in stool. » Consider probiotics to support
butyrate-producing organisms
» Consider support with butyrate salts
» Intestinal barrier support
» Support digestion if indicated
» Maintain a healthy weight
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Table 12. The bacteria involved in the production of saccharolytic straight chain fatty acids and
proteolytic branched chain fatty acids. Acetate, propionate, and butyrate make up ~90–95% of
fecal SCFAs, with valerate and caproate comprising a smaller percentage. Isobutyrate,
isovalerate, 2-methylbutyrate, and isocaproate make up ~5–10% of fecal SCFAs. Microbiota
listed below each metabolite are involved in the production of that respective fatty acid.

BACTERIA INVOLVED IN SHORT CHAIN FATTY ACID PRODUCTION

SACCHAROLYTIC STRAIGHT CHAIN FATTY ACIDS (SCFA) PROTEOLYTIC BRANCHED CHAIN FATTY ACIDS (BCFA)

Acetate
• Blautia hydrogenotrophica
Isobutyrate
• Bifidobacterium spp.
• Bacteroides spp.
• Lactobacillus spp.
• Clostridium spp.
• Clostridium spp.
• Streptococcus spp.
~90–95 Percent of Fecal SCFAs

Propionate

~5–10 Percent of Fecal SCFAs

• Bacteroidetes
• Negativicutes Isovalerate
• Megasphaera elsdenii • Bacteroides spp.
• Lachnospiraceae • Clostridium spp.
• Coprococcus catus
• Akermansia municiphilia

Butyrate
• Firmicutes phyla
2-Methylbutyrate (from leucine)
• Faecalibacterium prausnitzii
• Bacteroides spp.
• Roseburia spp.
• Clostridium spp.
• Eubacterium spp.
• Clostridium coccoides

Valerate (potentially toxic)

• Clostridia

Isocaproate (associated with disease)

Caproate (potentially toxic – from lactate)
• Megasphaera elsdenii
• Clostridium spp. BS-1

• Therapeutic Options and • Therapeutic Options and

Considerations to Decrease Considerations to Decrease
Levels of SCFAs: Levels of BCFAs:
» Low-FODMAP diet » Increase fiber intake (particularly
» Maintain a healthy weight insoluble fibers) and/or decrease
» Support digestion if indicated protein intake
» Consider multi-strain probiotics to » Consider underlying associations such
decrease acetate concentrations as inflammatory bowel disease, chronic
kidney disease, obesity, type 2 diabetes
➠

mellitus, MAFLD, or impaired digestion

RESEARCH. TECHNOLOGY. RESULTS. 51

 STOOLOMX™

INDIVIDUAL BILE ACID RESULTS

Research is more widely available on the clinical implications of certain primary and
secondary bile acids compared to others.

Table 13.
PRIMARY BILE ACIDS

MARKER ABBR GUIDE

Major primary bile acid. May be increased in IBS-D patients.

CA levels in stool may serve as a biomarker for IBS and
Cholic Acid CA
UC. During a UC flare, deconjugation of CA to DCA may be
impaired. Can inhibit Roseburia spp. and Lactobacillus spp.

Major primary bile acid. May be increased in IBS-D patients

Chenodeoxycholic Acid CDCA and may contribute to visceral hypersensitivity. Elevated
levels may be associated with metabolic imbalance.

Taurochenodeoxycholic Acid TCDCA Minor primary bile acid.

Taurocholic Acid TCA A whole grain diet may increase levels of TCA.

Glycochenodeoxycholic Acid GCDCA May be increased in IBS-D patients.

Glycocholic Acid GCA A whole grain diet may increase levels of GCA.

Lower levels are associated with pre-diabetes. HCA levels

Hyocholic Acid HCA
may serve as an indication of metabolic health.

Table 14.
SECONDARY BILE ACIDS

MARKER ABBR GUIDE

LCA is a major secondary bile acid that is formed from

the bacterial metabolism of CDCA. Low levels observed
Lithocholic Acid* LCA in UC. Elevated levels are associated with liver and colon
cancer and may contribute to blood sugar dysregulation.
Modulates immune responses at normal levels.

DCA is a major secondary bile acid that is formed from the

bacterial metabolism of CA. Low levels observed in ulcerative
colitis (UC). Elevated levels are associated with liver and colon
Deoxycholic Acid DCA cancer and metabolic imbalance. Implicated in modulating
the immune response by inhibiting pro-inflammatory cytokine
production. Can inhibit Lactobacillus spp., Bifidobacterium spp.,
Bacteroides fragilis, and Clostridium difficile.

Prevalent secondary bile acid in stool that has positive

associations with longevity. Influences metabolic health,
interacts with cellular receptors, and modulates immune
Isolithocholic Acid Iso-LCA
responses at normal levels. Influences the differentiation
➠

and function of T cells, particularly T helper 17 (Th17) cells,

which play a critical role in the inflammatory response.

52 diagnosticsolutionslab.com
 GI-MAP® INTERPRETIVE GUIDE

Table 14. Continued.

SECONDARY BILE ACIDS

MARKER ABBR GUIDE

Prevalent secondary bile acid in stool. May provide

12-Ketolithocholic Acid 12-KLCA anti-inflammatory effects in IBD, modulate cholesterol
metabolism, and improve glucose homeostasis.

Prevalent secondary bile acid in stool that has positive

3-oxoDeoxycholic Acid 3-oxoDCA
associations with longevity.

Enhances bile flow, hepatoprotective, and has

immunomodulatory properties. Levels in stool may
Ursodeoxycholic Acid UDCA serve as a biomarker of IBS and UC. Elevated levels
may be associated with metabolic imbalance.

May be negatively correlated with fecal calprotectin levels

in UC. Influences metabolic signaling pathways, modulates
Glycolithocholic Acid GLCA
gut microbiome, involved in lipid absorption, and aids in the
detoxification of potentially harmful bile acids.

Modulates the gut microbiome, cytoprotective, and influences

Glycoursodeoxycholic Acid GUDCA
lipid and glucose metabolism. May be elevated in IBS-D.

Modulates the gut microbiome. Involved in lipid absorption and

Glycodeoxycholic Acid GDCA
metabolic regulation. May be reduced in UC.

Involved in lipid absorption and metabolic regulation.

Taurolithocholic Acid TLCA Modulates inflammation and may exert cholestatic effects when
dysregulated. A whole grain diet may increase levels of TLCA.

Often used synthetically as a supplement. Used clinically for

cholestatic liver diseases. Cytoprotective, particularly in the
Tauroursodeoxycholic Acid TUDCA
liver. Involved in the regulation of bile acid metabolism and lipid
metabolism. Neuroprotective and modulates inflammation.

Involved in bile acid metabolism and lipid metabolism. Modulates

Taurodeoxycholic Acid TDCA
the gut microbiome and has anti-inflammatory properties.

Involved in bile acid metabolism and cholesterol metabolism.

7-Ketolithocholic Acid 7-KLCA
Modulates the gut microbiome.

Involved in bile acid metabolism and modulation of the gut

Dehydrolithocholic Acid DHLCA
microbiome. Exerts anti-inflammatory properties.

May be negatively correlated with fecal calprotectin levels in UC.

Hyodeoxycholic Acid HDCA May have anti-atherosclerotic effects. Involved in lipid absorption
and cholesterol metabolism. Modulates the gut microbiome.

Positive associations with longevity and exerts antibacterial

Alloisolithocholic Acid AlloIso-LCA
effects against gram-positive pathogens.

Involved in bile acid metabolism and exerts

3-Dehydrocholic Acid 3-DHCA
anti-inflammatory properties.
➠

* On StoolOMX, the LCA value is a summation of LCA + Allo-LCA.

RESEARCH. TECHNOLOGY. RESULTS. 53

 STOOLOMX™

INDIVIDUAL SHORT CHAIN FATTY ACIDS RESULTS

Table 15.
SACCHAROLYTIC STRAIGHT CHAIN FATTY ACIDS (SCFA)
MARKER GUIDE

Most abundant SCFA. Involved in lipid synthesis and appetite regulation, maintains
Acetate
energy balance and metabolic homeostasis. Resists oxidation and mitochondrial stress.

Primary energy source for colonic cells. Supports intestinal barrier integrity, reduces
Butyrate intestinal inflammation, promotes motility, enhances fatty acid oxidation, inhibits
tumor cell progression, and fosters a balanced microbiome.

Supports intestinal barrier integrity, impacts energy balance, gluconeogenesis, and lipid
Propionate
metabolism. Involved in appetite regulation. Proposed as a biomarker for IBS.

Stimulates intestinal epithelium growth, inhibits colon cancer cell production,

Valerate
modulates glucose and lipid metabolism. Antimicrobial effects against C. difficile.

Caproate Antimicrobial effects against C. difficile.

PROTEOLYTIC BRANCHED CHAIN FATTY ACIDS (BCFA)

MARKER GUIDE

Stimulates colonic sodium absorption. Elevated levels in stool

Isobutyrate
may be associated with cortisol levels and depression.

Elevated levels in stool may be associated with depression by its influence

on the gut flora, metabolic pathways, and inflammatory pathways. It
Isovalerate
can also interfere with neurotransmitter release. There is an association
between elevated levels of isovalerate and increased cortisol levels.

2-Methylbutyrate Branched chain fatty acid.

Produced primarily through the fermentation of branched chain

Isocaproate amino acids (BCAAs), particularly leucine. Energy source for many
tissues, especially during fasting or low carbohydrate intake.

SCFAs are known to have numerous health effects

and can enhance fecal excretion of bile acids.

Low levels of SCFAs are linked to various conditions,

including irritable bowel syndrome, obesity, and
inflammatory bowel disease.
➠

54 diagnosticsolutionslab.com
 GI-MAP® INTERPRETIVE GUIDE

Advanced Bile Acid Testing and

Short‑Chain Fatty Acid Evaluation in
One GI-MAP Add-on Panel
➠

RESEARCH. TECHNOLOGY. RESULTS. 55

 GI-MAP
PATTERNS
UNDERSTANDING COMMON
DYSBIOSIS PATTERNS
Understanding Common Dysbiosis Patterns With GI-MAP
WITH GI-MAP®

INSUFFICIENCY DYSBIOSIS
Insufficiency dysbiosis is characterized by low levels of beneficial bacteria that provide
critical support for healthy intestinal and immune function. Insufficient levels of beneficial
bacteria may result in an elevated risk of intestinal infections, increased intestinal
barrier permeability, decreased protective factors such as secretory IgA, and increased
inflammation. Lack of keystone bacteria is common in autoimmune, allergic, and chronic
inflammatory conditions.
Table 16.

Markers Characterizing Insufficiency Dysbiosis

Bacteroides fragilis
Bifidobacterium spp.
Enterococcus spp.
Commensal/Keystone Bacteria:
Escherichia spp.
(low levels)
Lactobacillus spp.
Akkermansia muciniphilia
Faecalbacterium prausnitzii
Roseburia spp.
Phyla Microbiota: Bacteroidetes
(low levels) Firmicutes
Secretory IgA (often low to very low levels)
Associated Intestinal Health Markers:
Zonulin (sometimes elevated)
➠

56 diagnosticsolutionslab.com
 GI-MAP® INTERPRETIVE GUIDE

INFLAMMATORY DYSBIOSIS
INFLAMMATORY DYSBIOSIS
Inflammatory dysbiosis is characterized by moderate to high levels of certain pathogens,
normal microbiota,
Inflammatory and is
dysbiosis opportunistic
characterizedmicrobes that promote
by moderate inflammation
to high levels of certainand increased
pathogens,
intestinal
normal permeability.
microbiota, andMany pro-inflammatory
opportunistic microbes microbes are gram-negative
that promote inflammation andbacteria that
increased
belong to permeability.
intestinal the Proteobacteria
Many phylum and produce
pro-inflammatory a form are
microbes of lipopolysaccharide (LPS) that
gram-negative bacteria that is
a potenttoactivator
belong of inflammatory
the Proteobacteria phylumresponses. Thisapattern
and produce form ofislipopolysaccharide
common in chronic immune
(LPS) that is
and
a inflammatory
potent conditions.
activator of inflammatory responses. This pattern is common in chronic immune
and inflammatory conditions.
Table 17. Markers Characterizing Inflammatory Dysbiosis
Markers Characterizing Inflammatory Dysbiosis
Campylobacter
C. difficile
Campylobacter
Pathogenic
C. difficile E. coli
Pathogens
Salmonella
Pathogenic E. coli
(low to high levels)
Pathogens Vibrio cholerae
Salmonella
(low to high levels) Yersinia enterocolitica
Vibrio cholerae
Giardia
Yersinia enterocolitica
Commensal/Keystone Bacteria Escherichia
Giardia spp.
(high levels) Enterobacter spp.
Commensal/Keystone Bacteria Escherichia spp.
(high levels) Morganella spp.
Enterobacter spp.
Pseudomonas
Morganella spp. spp.
Pseudomonas
Pseudomonas spp.aeroginosa
Desulfovibrio
Pseudomonasspp. aeroginosa
Citrobacter spp.
Desulfovibrio spp.
Citrobacter
Citrobacter freundii
spp.
Opportunistic Bacteria, Yeast, and Protozoa Klebsiella
Citrobacterspp.
freundii
(moderate to high levels)
Opportunistic Bacteria, Yeast, and Protozoa Klebsiella
Klebsiella pneumoniae
spp.
(moderate to high levels) Proteus spp.
Klebsiella pneumoniae
Proteus
Proteus mirabilis
spp.
Fusobacterium
Proteus mirabilisspp.
Candida spp.
Fusobacterium spp.
Candida
Candida albicans
spp.
Parasitic protozoa (specifically Giardia and Blastocystis hominis)
Candida albicans
Parasitic protozoa(may
β-Glucuronidase be elevated)
(specifically Giardia and Blastocystis hominis)
Occult Blood-FIT (may be elevated)
β-Glucuronidase (may be elevated)
Secretory IgA (often
Occult Blood-FIT low
(may belevels, but sometimes elevated)
elevated)
Associated Intestinal Health Markers:
Secretory IgA(often
Calprotectin (oftenelevated, but
low levels, sometimes
but sometimesvery low levels)
elevated)
Associated Intestinal Health Markers: Eosinophil Activation Protein (EDN/EPX) (may be elevated)
Calprotectin (often elevated, but sometimes very low levels)
Zonulin (may be elevated in some cases)
Eosinophil Activation Protein (EDN/EPX) (may be elevated)
Zonulin (may be elevated in some cases)
➠

Continued…
Continued…
RESEARCH. TECHNOLOGY. RESULTS. 57

www.diagnosticsolutionslab.com 2
 GI-MAP PATTERNS

DIGESTIVE
DIGESTIVE DYSFUNCTION
DYSFUNCTION DYSBIOSIS
DYSBIOSIS
Dysbiosis
Dysbiosis associated
associated with
with digestive
digestive dysfunction
dysfunction is is very
very common,
common, andand is
is often
often due
due to
to
low stomach acid (hypochlorhydria), insufficient bile acids, poor digestion (pancreatic
low stomach acid (hypochlorhydria), insufficient bile acids, poor digestion (pancreatic
insufficiency
insufficiency or
or brush
brush border
border enzyme
enzyme deficiency),
deficiency), reduced
reduced absorption,
absorption, and
and altered
altered
gastrointestinal
gastrointestinal motility. Altered digestion and motility can result in imbalances in
motility. Altered digestion and motility can result in imbalances in the
the
microbiome,
microbiome, characterized by overgrowth of certain species. Symptoms associated with
characterized by overgrowth of certain species. Symptoms associated with
digestive dysfunction include but are not limited to: excessive gas and bloating,
digestive dysfunction include but are not limited to: excessive gas and bloating, abdominalabdominal
discomfort,
discomfort, dyspepsia,
dyspepsia, heart
heart burn,
burn, gastroesophageal
gastroesophageal refluxreflux (GERD),
(GERD), constipation
constipation or
or
diarrhea, food sensitivities and intolerances.
diarrhea, food sensitivities and intolerances.
Table 18.
Markers
Markers Associated
Associated with
with Digestive
Digestive Dysfunction
Dysfunction
Pathogens
Pathogens Most types, especially if multiple pathogens are present
(low to high levels) Most types, especially if multiple pathogens are present
(low to high levels)
H. pylori Helicobacter pylori
H. pylori Helicobacter pylori
(moderate to high levels) (with or without virulence factors)
(moderate to high levels) (with or without virulence factors)
Commensal/Keystone Bacteria Enterococcus
Commensal/Keystone Bacteria Enterococcus
(high levels) Lactobacillus
(high levels) Lactobacillus

Phyla Microbiota Bacteroidetes and/or

Phyla Microbiota Bacteroidetes and/or
(high levels) Firmicutes
(high levels) Firmicutes
Bacillus spp.
Bacillus spp.
Enterococcus faecalis
Enterococcus faecalis
Enterococcus faecium
Enterococcus faecium
Morganella spp.
Morganella spp.
Staphylococcus spp.
Opportunistic Bacteria, Yeast, and Protozoa Staphylococcus spp.
Opportunistic Bacteria, Yeast, and Protozoa Staphylococcus aureus
Staphylococcus aureus
(moderate to high levels)
(moderate to high levels) Streptococcus spp.
Streptococcus spp.
Methanobacteriaceae (family)
Methanobacteriaceae (family)
Desulfovibrio spp.
Desulfovibrio spp.
Klebsiella pneumoniae
Klebsiella pneumoniae
Prevotella
Prevotella
Candida spp.
Candida spp.
Candida albicans
Candida albicans
Parasitic protozoa
Parasitic protozoa
Elastase-1 (often low to moderately low levels)
Intestinal Health Markers: Elastase-1 (often low to moderately low levels)
Intestinal Health Markers: Steatocrit (sometimes elevated)
Steatocrit (sometimes elevated)
➠

58 diagnosticsolutionslab.com

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 GI-MAP® INTERPRETIVE GUIDE

GI-MAP® PATTERNS ASSOCIATED

WITH
GI-MAP® IMMUNE-MEDIATED
PATTERNS ASSOCIATED
PATTERNS ASSOCIATED WITH
WITHFOOD REACTIONS
IMMUNE-MEDIATED
IMMUNE-MEDIATED FOOD REACTIONS
FOOD REACTIONS
The GI-MAP® (Microbial Assay Plus) can be used in conjunction with IgG Food Explorer™
and GI-MAP
The IgE Allergy
®
(Microbial to digPlus)
Explorer™Assay deeper
can into the root
be used cause of adverse
in conjunction food
with IgG reactions.
Food ExplorerIf™ the
gut barrier
and is permeable
IgE Allergy Explorer™ and/or digestion
to dig deeper is the
into suboptimal,
root causemaldigested
of adverse food
food proteins can
reactions. If the
trigger immune system responses.
gut barrier is permeable and/or digestion is suboptimal, maldigested food proteins can
trigger
These areimmune system
the key responses.
patterns to look for on the GI-MAP that are connected food sensitivities
and
Theseallergies.
are the key patterns to look for on the GI-MAP that are connected food sensitivities
and allergies.
Food
Table 19.Intolerance, Allergy, and Adverse Food Reactions Pattern
Morganella spp.
Food Intolerance, Allergy, and Adverse Food Reactions Pattern
Pseudomonas spp.
Morganella spp.
Pseudomonas aeroginosa
Pseudomonas spp.
Citrobacter freundii
Pseudomonas aeroginosa
Histamine Producing Klebsiella spp. High Opportunists (page 3)
Citrobacter freundii
Bacteria Klebsiella pneumoniae
Histamine Producing Klebsiella spp. High Opportunists (page 3)
Bacteria Proteus spp.
Klebsiella pneumoniae
Proteus mirabilis
Proteus spp.
Enterobacter spp.
Proteus mirabilis
Escherichia spp.
Enterobacter spp.
Fusobacterium spp.
Escherichia spp.
H. pylori High H. pylori Panel (page 2)
Fusobacterium spp.
Enterococcus faecalis
H. pylori High H. pylori Panel (page 2)
Pseudomonas aeruginosa Opportunists (page 3)
Enterococcus faecalis High
Mast Cell-Activating Staphylococcus aureus
Bacteria Pseudomonas aeruginosa Opportunists (page 3)
Streptococcus spp. High
Mast Cell-Activating Staphylococcus aureus
Bacteria Candida spp.
Streptococcus spp. High Fungi/Yeast (page 3)
Candida albicans
Candida spp.
Lipopolysaccharide producers High
High Fungi/Yeast (page 3)
Throughout report
Candida albicans
Commensal/Keystone Commensal/Keystone
Lactobacillus spp. producers
Lipopolysaccharide Low
High Throughout report
Bacteria Bacteria (page 2)
Commensal/Keystone Commensal/Keystone
Lactobacillus spp.
Eosinophil Activation Protein Low
Bacteria Bacteria (page 2)
(EDN/EPX)
Eosinophil Activation Protein Intestinal Health Markers
Intestinal Health Markers SIgA High (page 4)
(EDN/EPX)
Anti-gliadin IgA Intestinal Health Markers
Intestinal Health Markers SIgA High (page 4)
Zonulin
Anti-gliadin IgA
Zonulin Continued…
Continued…
➠

RESEARCH. TECHNOLOGY. RESULTS. 59

 GI-MAP PATTERNS

Table 19a.
Gut Barrier Permeability (“Leaky Gut”) Pattern
Gut Barrier Permeability (“Leaky
Any Pathogen
Gut”) Pattern
High Pathogens (page 1)
Any Pathogen High Pathogens (page 1)
Lactobacillus spp. Low Commensal/Keystone
Lactobacillus spp. Low Commensal/Keystone
Bacteria (page 2)
Akkermansia muciniphila Low; <dl
Intestinal Permeability Akkermansia muciniphila Low; <dl Bacteria (page 2)
Intestinal Permeability Candida albicans High Fungi/Yeast (page 3)
Candida albicans High Fungi/Yeast (page 3)
Anti-gliadin IgA Intestinal Health Markers
Anti-gliadin IgA High Intestinal
Zonulin High (page 4) Health Markers
Zonulin (page 4)
Faecalibacterium prausnitzii Low; <dl
Low Butyrate/SCFA Faecalibacterium prausnitzii Low; <dl Commensal/Keystone
LowProduction
Butyrate/SCFA Roseburia spp. Commensal/Keystone
Roseburia spp. Low Bacteria (page 2)
Production Firmicutes phylum Low Bacteria (page 2)
Firmicutes phylum
Bifidobacterium spp. Low; <dl
Bifidobacterium spp. Low; <dl
Escherichia spp.
Escherichia spp. Low Commensal/Keystone
Poor Mucosal Health Lactobacillus spp. Low Commensal/Keystone
Poor Mucosal Health Bacteria (page 2)
Lactobacillus spp. Bacteria (page 2)
Akkermansia muciniphila Low; dl
Akkermansia muciniphila Low; dl
Bacteroidetes phylum Low
Bacteroidetes phylum Low

Table 19b.
Digestive Insufficiency Pattern
Digestive Insufficiency Pattern
Firmicutes phylum
Firmicutes phylum
Bacteroidetes phylum
Bacteroidetes phylum Commensal/Keystone
Enterococcus spp. High
High Commensal/Keystone
Bacteria (page 2)
Enterococcus spp.
Lactobacillus spp. Bacteria (page 2)
Lactobacillus spp.
Akkermansia muciniphila
Akkermansia muciniphila
Bacillus spp.
Bacillus spp.
Enterococcus faecalis
Enterococcus faecalis
Enterococcus faecium
Digestive Insufficiency Enterococcus faecium
Digestive Insufficiency Staphylococcus spp.
Staphylococcus spp.
Staphylococcus aureus High Opportunists (page 3)
Staphylococcus aureus High Opportunists (page 3)
Streptococcus spp.
Streptococcus spp.
Desulfovibrio spp.
Desulfovibrio spp.
Methanobacteriaceae (family)
Methanobacteriaceae (family)
Fusobacterium spp.
Fusobacterium spp.
Steatocrit Detected; High Intestinal Health Markers
Steatocrit Detected; High Intestinal
(page 4) Health Markers
Pancreatic Elastase-1 Low
Pancreatic Elastase-1 Low (page 4)
➠

60 diagnosticsolutionslab.com
 Gas & Histamine GI-MAP® INTERPRETIVE GUIDE

RESEARCH. TECHNOLOGY. RESULTS. Producers on GI-MAP ®

GAS & HISTAMINE PRODUCERS ON GI-MAP

Faecalibacterium prausnitzii
Table 20.
Roseburia spp.
Primary Hydrogen Producers
Bacteroidetes phyla
Firmicutes phyla

Primary Methane Producers Methanobacteriaceae (family)

Bacteroides fragilis
Escherichia spp.
Enterobacter spp.
Desulfovibrio spp.
Morganella spp.
Pseudomonas aeruginosa
Primary Staphylococcus aureus
Hydrogen Sulfide Producers
Citrobacter spp.
Citrobacter freundii
Klebsiella spp.
Klebsiella pneumoniae
Proteus spp.
Proteus mirabilis
Fusobacterium spp.

Lactobacillus spp.
Morganella spp.
Pseudomonas
Pseudomonas aeruginosa
Citrobacter freundii
Klebsiella
Histamine Producing Bacteria
Klebsiella pneumoniae
Proteus
Proteus mirabilis
Enterobacter spp.
Escherichia spp.
➠

Fusobacterium spp.

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 GI-MAP PATTERNS

Microbe Categories and GI-MAP®

Patterns Associated with IBS & SIBO
MICROBE CATEGORIES
RESEARCH. TECHNOLOGY. RESULTS.

Table 21.
Primary Hydrogen Producers Mast Cell-Activating Microbes
Faecalibacterium prausnitzii H. pylori
Roseburia spp. Enterococcus faecalis
Bacteroidetes phyla Pseudomonas aeruginosa
Firmicutes phyla Staphylococcus aureus
Streptococcus spp.
Primary Methane Producers Candida spp.
Methanobacteriaceae (family) Candida albicans
Lipopolysaccharide producers (see LPS list)
Primary Hydrogen Sulfide Producers
Bacteroides fragilis Lipopolysaccharide (LPS)
Escherichia spp. Producing Bacteria
Enterobacter spp. Escherichia spp.
Desulfovibrio spp. Enterobacter spp.
Morganella spp. Morganella spp.
Pseudomonas aeruginosa Pseudomonas spp.
Staphylococcus aureus Pseudomonas aeruginosa
Citrobacter spp. Citrobacter spp.
Citrobacter freundii Citrobacter freundii
Klebsiella spp. Klebsiella spp.
Klebsiella pneumoniae Klebsiella pneumoniae
Proteus spp. Proteus
Proteus mirabilis Proteus mirabilis
Fusobacterium spp.

Histamine Producing Bacteria

Lactobacillus spp.
Morganella spp.
Pseudomonas
Pseudomonas aeruginosa
Citrobacter freundii
Klebsiella
Klebsiella pneumoniae
Proteus
Proteus mirabilis
Enterobacter spp.
Escherichia spp.
➠

Fusobacterium spp.
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• GI-MAP® + Zonunlin
provides you with true quantitative values.
It helps differentiate trace levels of an • GI Pathogens Profile
organism from frank elevations indicative of • H. pylori Profile
active infection.
• Zonulin Profile (Stool)

• Calprotectin (Stand-alone)

SPECIMEN • Gluten Peptide (Add-on or stand-alone)

REQUIREMENTS • Universal Antibiotic Resistance

Genes Panel (Add-on only)
Single Stool Sample — at ambient room
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RESEARCH. TECHNOLOGY. RESULTS. 63

 Diagnostic Solutions laboratory

Phone: 877-485-5336
Email: [email protected]
Web: diagnosticsolutionslab.com

Patient: Ima Sample

Accession: 00000000-0001
Collected: 08/02/2022
Received: 08/3/2022
DOB: 07/11/1981
Completed: 8/17/2022
5894 Shiloh Rd, Ste 101
Gender: M
877.485.5336
| Alpharetta GA 30005 Ordered by: Diane Farhi,
MD

DNA STOOL ANALYS

IS BY QUANTITATIV
YOUR PERSONALIZ E PCR
ED REPORT

PATHOGENS

The GI-MAP® include

s pathogens (bacterial,
not all individuals with parasitic and viral) commo
positive findings will presen nly known to cause gastroe
t with symptoms. Many nteritis. Note that
(such as immune health, factors, including the health
digestive function, and of the individual
presence and expression microbiome balance),
of virulence factors, all the transient nature of
contribute to pathogen most pathogens, and
virulence and individu the
BACTERIAL PATHOG al symptoms.
ENS
Campylobacter Result
Reference
C. difficile Toxin A < dl
< 1.00e3
1.21e5 High ↑
C. difficile Toxin B < 1.00e3

SAMPLE REPORT
2.27e5 High ↑
Enterohemorrhagic E. < 1.00e3
coli
E. coli O157 < dl
< 1.00e3
Enteroinvasive E. coli/Sh < dl
igella < 1.00e3
Enterotoxigenic E. coli < dl
LT/ST < 1.00e2
Shiga-like Toxin E. coli < dl
stx1 < 1.00e3
Shiga-like Toxin E. coli < dl
stx2 < 1.00e3
Salmonella < dl
< 1.00e3
Vibrio cholerae < dl
< 1.00e4
Yersinia enterocolitica < dl
< 1.00e5
4.46e3
PARASITIC PATHOG < 1.00e5
ENS
Cryptosporidium
Entamoeba histolytica < dl
< 1.00e6
Giardia < dl
< 1.00e4
< dl
VIRAL PATHOGENS < 5.00e3
Adenovirus 40/41
< dl
Scan with Your Camera
Norovirus GI/II < 1.00e10
< dl
< 1.00e7
KEY: Results are reported as
genome equivalents per
microbes measured per gram of stool, which is
gram of stool, based on a standard method for
qPCR analysis of DNA estimating the numbe
samples. r of
Results are expressed

Download a GI-MAP ®
in standard scientific notation
microbes per gram, which . For example, a reporte
equals 35,000,000 (35
million) microbes per gram d result of 3.5e7 is equivalent to 3.5 x 10 7
< dl represents results of stool.
below detectable limit.

Sample Report
The assays were develop
ed and/or the perform
determined by Diagnos ance characteristics
tic Solutions Laborato
ry.
CLIA# 11D-2097795
Medical Director - Diane
Farhi, MD
1

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