The Gastrointestinal Microbial Assay Plus (GI-MAP)- Comprehensive panel of microbial targets, immune and digestive markers

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) 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. With a culture based test it is not possible to measure strict anaerobes, viruses or virulence factors. 

The GI-MAP's accuracy and reliability allows personalized protocols to address gut dysfunction based on which infections are urgent, which areas of the gut are already optimized, and which areas should be addressed after an infection is resolved. Additionally, the quantification of identified micro-organisms offers a remarkable ability to see how treatment modalities are working because a retest after treatment can show whether a parasite has resolved, dysbiosis has improved, and more.

Learn more about the GI-MAP in clinical practice by watching our webinar: https://www.youtube.com/watch?v=QL_ekGVOdaE

Indications

• Autoimmune molecular mimicry (if caused by pathogens)
• Diarrhea
• Digestion
• Foodborne illness
• Gastritis
• Gastroenteritis (if it has viral causes)
• Gut dysbiosis
• Immunity
• Inflammation
• Suspected bacterial, parasitic or viral pathogenesis (incl. detection of antibiotic resistant bacteria)

Overview

Overview

The Gastrointestinal Microbial Assay Plus (GI-MAP) was designed to assess a patient’s microbiome from a single stool sample, with particular attention to microbes that may be disturbing normal microbial balance and may contribute to perturbations in the gastrointestinal (GI) flora or illness. The panel is a comprehensive collection of microbial targets as well as immune and digestive markers. It screens for pathogenic bacteria, commensal bacteria, opportunistic pathogens, fungi, viruses, and parasites. It primarily uses multiplex, automated, DNA analysis to give integrative and functional medicine practitioners a better view into the gastrointestinal microbiome.

Methodology

Quantitative polymerase chain reaction (qPCR)

Analytes 

BACTERIAL PATHOGENS

• Campylobacter
• C. difficile Toxin A
• C. difficile Toxin B
• Enterohemorrhagic E. coli
• E. coli O157
• Enteroinvasive E. coli/Shigella
• Enterotoxigenic E. coli LT/ST
• Shiga-like Toxin E. coli stx1
• Shiga-like Toxin E. coli stx2
• Salmonella
• Vibro cholerae
• Yersinia enterocolitica
• H. pylori

  • Virulence Factor, babA

  • Virulence Factor, cagA

  • Virulence Factor, dupA

  • Virulence Factor, iceA

  • Virulence Factor, oipA

  • Virulence Factor, vacA

  • Virulence Factor, virB

  • Virulence Factor, virD

PARASITIC PATHOGENS

• Cryptosporidium
• Entamoeba histolytica
• Giardia

VIRAL PATHOGENS

• Adrenovirus 40/41
• Norovirus GI
• Norovirus GII

NORMAL/COMMENSAL BACTERIA

• Akkermansia Mucinophilia
• Bacteroides fragilis
• Bifidobacterium spp.
• Clostridia (class)
• Enterobacter spp.
• Enterococcus spp.
• Escherichia spp.
• Faecalbacterium prausnitzii
• Lactobacillus spp.

BACTERIAL PHYLA

• Bacteroidetes
• Firmicutes
• Firmicutes/Bacteroidetes Ratio

ADDITIONAL DYSBIOTIC/OVERGROWTH BACTERIA

• Bacillus spp.
• Enterococcus faecalis
• Enterococus faecium
• Morganella spp.
• Pseudomonas spp.
• Pseudomonas aeruginosa
• Staphylococcus spp.
• Staphylococcus aeureus
• Streptococcus spp.
• Methanobacteriaceae (family)

POTENTIAL AUTOIMMUNE TRIGGERS

• Citrobacter spp.
• Citrobacter freundii
• Fusobacterium spp.
• Klebsiella spp.
• Klebsiella pneumoniae
• Mycobacterium avium subsp. paratuberculosis
• Prevotella spp
• Proteus spp.
• Proteus mirabilis

FUNGI/YEAST

• Candida albicans
• Candida spp.
• Geotricum spp.
• Microsporidia spp.
• Rhodoturula spp.

OPPORTUNISTIC VIRUSES

• CMV- Cytomegalovirus
• EBV- Epstein Bar Virus

PARASITES & WORMS:

PROTOZOA

• Blastocystis hominis
• Chilomastix mesnelli
• Cyclospora spp.
• Dientamoeba fragilis
• Endolimax nana
• Entamoeba coli
• Pentatrichomonas hominis

WORMS

• Ancyclostroma duodenale
• Ascaris lumbricoides
• Necator americanis
• Trichuris trichiura
• Taenia spp

INTESTINAL HEALTH MARKERS:

DIGESTION

• Elastase-1
• Steatocrit

IMMUNE RESPONSE

• SIgA
• Anti-gliadin SIgA

INFLAMMATION

• Calprotectin

GI MARKERS

• ß-Glucuronidase
• Occult Blood - FIT

ANTIBIOTIC RESISTANCE GENES (Optional add-on):

Phenotypes | HELICOBACTER

• Amoxicillen
• Clarithromycin
• Fluroquinolines
• Tetracycline

Practical

Specimen

Stool sample 

Container

• 1x orange-capped stool vial

Patient preparation

• Please refrain from taking aspirin for two days prior to collecting your sample.
• Never discontinue prescription medication without first consulting your physician.

Age requirements

Can be used on all ages. However, often the microbiome of infants will appear very “dysbiotic”, as the microbiome and the infant’s immune system is very immature.

Available add-ons:

• Zonulin

Medications

We recommend continuing all prescription medications prior to testing. Please carefully document any relevant recent or current medication use. Medications that may alter the composition of the microbiome include:

• Antibiotics -(after finishing Antibiotics, wait 4-6 weeksbefore collecting sample)
• Immune Suppressants/ Oral steroids- will likely cause a lower Secretory IgA, Anti-gliadin, and calprotectin result (after finishing these meds, wait 4-6 weeks before collecting sample)

Supplements:
It is not necessary to discontinue most supplements before testing.  It is the provider’s discretion to recommend discontinuing supplements.  Many providers will want to understand the impact of supplements on the gut ecosystem and will want their patients to continue supplements during testing.  If a provider wants more of a “baseline” assessment using the GI-MAP, they may recommend discontinuing supplements prior to testing. There are a few categories of supplements that deserve consideration:

Non-prescription anti-microbial agents:
While we don’t require that people discontinue antibiotics or antimicrobial substances before collection their stool sample, doing the test while taking these substances can influence the test results.  If possible, we recommend discontinuing anti-microbial agents 4-6 weeks before testing.

Enzymes:
Oral enzyme use will not change the elastase-1 finding. If the enzyme contains lipase or ox bile, it may decrease the value for steatocrit.

Ox Bile/Lipase:
Ox bile/lipase intake will affect the steatocrit level but will not affect Elastase-1. If you would like to see your patient’s baseline without supplementation, discontinue at least 3 days before testing. If you would like to see how well-managed your patient is on their supplement, do not discontinue.

Probiotics:
Probiotic supplements can influence the normal and opportunistic bacteria flora. If you would like to assess your patient’s baseline microbial balance without supplementation, discontinue for ~2 weeks prior to testing. If you would like to see the influence of the current probiotic supplement, do not discontinue prior to testing.  

Biofilm disruptors:
There is no published evidence to suggest that a biofilm disruptor will improve detection of organisms. However, some clinicians choose to use a biofilm disruptor with their patients up to 14 days before testing. This is an option but not a requirement for testing.

Research

1. Abubakar I, Irvine L, Aldus CF, et al. A systematic review of the clinical, public health and costeffectiveness of rapid diagnostic tests for the detection and identification of bacterial intestinal pathogens in faeces and food. Health Technol Assess. 2007;11(36):1-216.
2. Amar CF, East CL, Gray J, Iturriza-Gomara M, Maclure EA, McLauchlin J. Detection by PCR of Eight groups of enteric pathogens in 4,627 faecal samples: re-examination of the English casecontrol Infectious Intestinal Disease Study (1993-1996). Eur J Clin Microbiol Infect Dis. 2007;26(5):311-323.
3. Bischoff SC, Barbara G, Buurman W, et al. Intestinal permeability — a new target for disease prevention and therapy. BMC gastroenterology. 2014;14:189.
4. Canny GO, McCormick BA. Bacteria in the intestine, helpful residents or enemies from within? Infection and immunity. 2008;76(8):3360-3373.
5. Fasano A, Shea-Donohue T. Mechanisms of disease: the role of intestinal barrier function in the pathogenesis of gastrointestinal autoimmune diseases. Nature clinical practice. 2005;2(9):416-422.
6. Iijima Y, Asako NT, Aihara M, Hayashi K. Improvement in the detection rate of diarrhoeagenic Bacteria in human stool specimens by a rapid real-time PCR assay. Journal of medical microbiology. 2004;53(Pt 7):617-622.
7.  Kahlau P, Malecki M, Schildgen V, et al. Utility of two novel multiplexing assays for the detection of gastrointestinal pathogens - a first experience. SpringerPlus. 2013;2(1):106.
8. Kamada N, Seo SU, Chen GY, Nunez G. Role of the gut microbiota in immunity and inflammatory disease. Nature reviews. Immunology. 2013;13(5):321-335.
9. Khanna S, Tosh PK. A clinician's primer on the role of the microbiome in human health and disease. Mayo Clinic proceedings. 2014;89(1):107-114.
10. Othman M, Aguero R, Lin HC. Alterations in intestinal microbial flora and human disease. Current opinion in gastroenterology. 2008;24(1):11-16.
11.  Rashid T, Ebringer A. Autoimmunity in Rheumatic Diseases Is Induced by Microbial Infections via Crossreactivity or Molecular Mimicry. Autoimmune diseases. 2012;2012:539282. 
12. Schabereiter-Gurtner C, Hirschl AM, Dragosics B, et al. Novel real-time PCR assay for detection of Helicobacter pylori infection and simultaneous clarithromycin susceptibility testing of stool and biopsy specimens. Journal of clinical microbiology. 2004;42(10):4512-4518.
13. Stecher B, Hardt WD. The role of microbiota in infectious disease.Trends in microbiology. 2008;16(3):107-114.
14.  Tiwana H, Wilson C, Walmsley RS, et al. Antibody responses to gut bacteria in ankylosing spondylitis, rheumatoid arthritis, Crohn's disease and ulcerative colitis. Rheumatology international. 1997;17(1):11-16.

See also Brochure under ‘Downloadable files’ for even more research.