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GUIDE

©2008 Metametrix, inc. All rights reserved · GI Effects Stool Profiles U.S. patent pending · 70040 rev 0708 v2

2


Introduction Predominant Bacteria

Introduction

Proper gastrointestinal (GI) function is critical to adequate


nutritional status and can impact all aspects of body function.


The GI EffectsSM Stool Profiles address key components

of proper GI health including measurement of beneficial


microbial flora, opportunistic bacteria, yeast, parasitic


infection, markers of inflammation, immune function,


and digestion and absorption. The microbial population is


measured using PCR amplification of the genetic material of


each organism, allowing for sensitive detection, and the ability


to detect and identify organisms that cannot be cultured or


are extremely difficult to grow under laboratory conditions.

Reference Range Interpretation

Standard microbiological results are reported as Colony


Forming Units per gram of feces (CFU/gram). One CFU


is equivalent to one microorganism. Metametrix detects


microorganisms by DNA analysis. Each genome detected


represents one cell, or one CFU. Because there are very large


numbers of microorganisms in stool, results are expressed


in standard scientific notation. For example, Bacteroides sp.

may be reported as 2.57 E7, or 2.5 x 107, or 25,000,000 CFU/


gram, which is read as 25 million CFU per gram of feces.


The exponent is kept constant within a section of the report


to facilitate direct comparisons between organisms. The


cutoff for clinical significance for predominant bacteria has


been set at 1E7 (1 x 107), for opportunistic bacteria 1E5 (1 x

105), and for pathogens at 1E3 (1 x 103). Rather than semiquantitative

results (+1 to +4), the new methodology provides


full quantitative analysis.

Abnormal Bacteria, Fungi and/or Parasites

Suspect:

1. Inadequate physical and immune barrier functions

Food sensitivities/leaky gut s yndrome (elevated IgG)

Low intestinal secretory IgA

Gluten intolerance/Celiac disease

Inflammatory bowel disease

Decreased colonic short-chain fatty acids

2. Medication history

Antibiotics

NSAIDs

Antacids, proton pump inhibitors, and acid-blockers

3. Inadequate digestive and absorptive function

Hypochlorhydria

Pancreatic insufficiency

Intestinal inflammation

Rapid transit time

Nutrient insufficiencies

Diet high in red meat, saturated fat, or refined

carbohydrates

4. Pathogenic invasion and gut flora imbalances (dysbiosis)

Exposure to pathogens (water/food contamination/

foreign travel/depressed immune system)

Inadequate predominant flora

Treatment Using Four “R” program for


intestinal health

Remove offending foods, medications, gluten (if sensitive) and

reduce poor quality fats, refined carbohydrates, sugars, and


fermented foods (if yeast is present). Consider antimicrobial,


antifungal, and/or antiparasitic therapies in the case of


opportunistic/pathogenic bacterial, yeast, and/or parasite


overgrowth (see below for specific recommendations).

Replace what is needed for normal digestion and absorption

such as betaine HCl, pancreatic enzymes, herbs that


aid in digestion such as deglycyrrhizinated licorice and


marshmallow root, dietary fiber, and water.

Reinoculate with favorable microbes (probiotics such as

Lactobacillus sp., Bifidobacter sp., and Saccharomyces boulardii).

To enhance the growth of the favorable bacteria, supplement


with prebiotics such as inulin, xylooligosaccharides, larch


arabinogalactans, beta glucan, and fiber.

Repair mucosal lining by giving support to healthy intestinal

mucosal cells, goblet cells, and to the immune system.


Consider L-glutamine, essential fatty acids, zinc, pantothenic


acid and vitamin C.

Predominant Bacteria

Microorganisms in the GI tract perform a host of useful


functions, such as fermenting unused energy substances,


communicating with the immune system, preventing growth


of harmful species, regulating the development of the gut,


producing vitamins for the host (such as biotin and vitamin


K), and producing hormones to direct the host to store fats.[1]

Intestinal microflora are also thought to have many beneficial


local and systemic roles such as improving lactose tolerance,


supplying short chain fatty acids (SCFA) as an energy


substrate for the host, anti-tumor properties, neutralizing


certain toxins, stimulating the intestinal immune system,


reducing blood lipid levels and preventing obesity and type


II diabetes.[2] Under normal homeostatic conditions, the

intestinal microflora are of central importance in preventing


colonization by pathogens, termed “colonization resistance.”[3]

Predominant organisms are considered to be beneficial when


they are in balance.

Predominant, Opportunistic, and Pathogenic Bacteria


3

Low Predominant Bacteria

Significance:

Dysbiosis: Predominant bacteria should be present at

normal levels in the healthy gut. Bacteroides sp. and

Bifidobacter sp. should be present in the greatest amounts.[4]

Low levels of beneficial fecal bacteria such as Bifidobacter

sp., Lactobacillus sp. and E. coli have been associated with

irritable bowel syndrome, characterized by alternating


diarrhea, cramps, and food intolerance.[5]

Low levels of predominant bacteria increase the

likelihood of acquiring opportunistic and pathogenic


organisms.[3]

Treatment Options:

Probiotics

Prebiotics such as psyllium, oat bran, oligofructose,

xylooligosaccharide, inulin, beta-glucan, and/or


arabinogalactan[6]

Increase intake of fresh vegetables and fibers

Address other GI Effects abnormalities

High Predominant Bacteria

Significance:

Dysbiosis: Predominant bacteria should be present

at normal levels in the healthy gut. Bacteroides sp.

and Bifidobacter sp. should be present in the greatest

amounts[4].

Blood infections of Mycoplasma have been linked to

chronic fatigue syndrome and fibromyalgia.[7]

Fusobacterium increases putrification in the colon.

Overgrowth of Lactobacillus sp. could produce D-lactic

aciduria in those with short bowel syndrome. Limit


intake of simple carbohydrates.[8]

Overgrowth of certain Clostridia sp. clusters may play a

role in certain cases of autism.[9, 10]

If Prevotella sp. is in the 5th quintile suspect possible oral/

throat infection.[11]

Treatment Options:

Reduce poor quality fats, refined carbohydrates and

sugars, and encourage intake of fresh vegetables. High


fiber foods might exacerbate patient symptoms.

For Lactobacillus sp. or Clostridia sp. overgrowth,

supplement with Bifidobacter sp. or Saccharomyces boulardii

probiotics, respectively.

May need to use anti-microbial agents

Address other GI Effects abnormalities

Balance flora using appropriate probiotics

Opportunistic Bacteria

Opportunistic Bacteria present

Significance:

Generally self-limiting and not normally considered

pathogenic

Often exacerbated by low predominant bacteria,

pathogen or parasite infection, poor diet, antibiotic use,


and lowered gut immunity.

Treatment Options:

Probiotics

Prebiotics: Do not use fructooligosaccharide (FOS) if

Klebsiella sp. or Citrobacter sp. are present.

May need to use anti-microbial agents followed by preand

probiotics

Herbal agents include goldenseal, citrus seed extract,

garlic, uva ursi, oregano oil, and olive leaf extract

Visit www.emedicine.com to search for the pathology

of the individual opportunistic bacteria and treatment


options.

Address other GI Effects abnormalities

Pathogenic Bacteria

Pathogenic Bacteria present

Helicobacter pylori

Helicobacter pylori (H. pylori) bacterium causes peptic ulcer

disease and has been associated with increased gastric cancer


risk. H. pylori is a Type I carcinogen. It is estimated that 50%

of the world’s population is infected with H. pylori.

Symptoms:

Acute gastritis with abdominal pain, nausea and

vomiting, usually within two weeks of infection.


Recurrent abdominal symptoms (non-ulcer dyspepsia)


without ulcer disease are common.

Treatment Options (Adult Dosages):

Standard treatment for H. pylori consists of a combination

of 3 or 4 drugs, antibiotics, and proton pump inhibitors,


for 7-14 days. Current recommendations can be found


at www.acg.gi.org. Eradication does not generally exceed

80%.

Supplementation with lactoferrin (200 mg/d), prebiotics,

and vitamin C (up to 5 grams), may improve treatment


efficacy, while reducing adverse reactions.[12][13]

Botanical combination treatments have also been shown

to be effective in eradicating H. pylori from the GI tract.

Botanicals* (see page 7)

Pathogenic Bacteria Yeast/Fungi

4

Clostridium difficile

Suspect recent antibiotic use, especially the cephalosporins,


ampicillin/amoxicillin, and clindamycin.

Symptoms:

Cramping, lower abdominal p ain, fever and diarrhea

usually decreases once antibiotics are stopped, though


can continue for up to 4 weeks

Treatment Options (Adult Dosages):

Do not treat if patient is asymptomatic. Stop use of

causative antibiotics.

In severe cases: Vancomycin 125 mg PO qid for 10-14d;

Metronidazole 500 mg PO tid or 250 mg PO qid for


10-14d

Herbal antibiotics such as berberine or oregano oil

Replete beneficial bacteria, esp. S. boulardii

Campylobacter sp.

Contaminated animal food sources are the primary cause,


especially poultry and red meat. Dogs may also become


infected from rodents and birds and infect humans. Suspect


hydrochloric acid insufficiency and/or secretory IgA


deficiency.

Symptoms:

Symptom onset is generally abrupt. Influenza-like

symptoms are common, including headache and malaise.


GI symptoms include abdominal pain, nausea, and


vomiting. The degree of diarrhea varies. Campylobacter sp.

has been associated with reactive arthritis.

Treatment Options (Adult Dosages):

Generally self-limiting infection not requiring treatment

Support rehydration if diarrhea is present

If infection persists treat with Erythromycin: 500 mg

erythromycin stearate, base, or estolate salts (or 400 mg


ethylsuccinate) every 6h PO.

Entero-hemorrhagic Escherichia coli


(EHEC)

Also referred to as Shiga toxin-producing E. Coli (STEC).


Suspect ingestion of contaminated food, especially


undercooked ground beef, raw milk, unpasteurized apple juice,


water, and lettuce.

Symptoms:

Typical symptoms include severe abdominal cramping,

watery or bloody diarrhea, and vomiting. In some cases


(up to 10%) it can cause hemorrhagic colitis or hemolytic


uremic syndrome.

Treatment Options:

The infection is generally self-limiting

Rehydrate if diarrhea is present

Antibiotic therapy hasn’t proven useful in EHEC infection

and can predispose to development of hemolytic uremia

Streptomycin, sulfonamides, and tetracycline have

demonstrated resistance to many EHEC strains

Probiotic/prebiotic therapy

Yeast/Fungi

Yeast/Fungi present

Commonly identified species: Candida, Rhodotorula,

Geotrichum, Sacchoromyces, Trichosporon, Candida are detailed

below. If other commonly identified species are reported,


consider patient symptoms and degree of infection to decide


if anti-fungal therapy is warranted. Saccharomyces sp. may be

reported if patient is supplementing with S. boulardii. Restore

proper predominant microflora populations and address all


other imbalances found on the GI Effects test report.

Candida sp.

Candida sp. is a normal inhabitant of the gastrointestinal

flora and is present in 40-65% of the human population


with no harmful effects. However, in conditions allowing for


overgrowth, Candida sp. is the most common causal agent of

opportunistic fungal infections. The esophagus is the most


commonly infected site, followed by the stomach then the


small and large bowel. Approximately 15% of people develop


systemic candidiasis.

Symptoms:

Gastric pain, nausea and vomiting, gas, bloating,

intestinal permeability, imbalance in gut microflora,


opportunistic bacterial infection

Treatment Options:

Reduce intake of refined carbohydrates and sugars

Prescriptive agents: fluconazole, intraconazole,

ketoconazole, nystatin

Herbal agents (use in combination for greater efficacy):

oregano oil, berberine, goldenseal, undecylenic acid,


caprylic acid, grapefruit seed extract, uva ursi, garlic (allicin)

S. boulardii aids in the growth of beneficial bacteria,

crowds out yeast, and helps with immune support

Avoid fructooligosaccharide (FOS) as it may feed the yeast

Yeast/Fungi Present: taxonomy unavailable

Uncommon yeast/fungi is present, and one that likely colonizes


other animals, or has not been identified as pathogenic to


humans. Infection with Candida, Rhodotorula, Geotrichum,

Saccharomyces, and Trichosporon species have been ruled out. If

present at +2 or below, it is likely that this yeast is transient due


to ingestion of molds or other yeasts, and is not problematic to


humans. Consider patient symptoms before treating.

Yeast/Fungi Parasites

5

Treatment Options:

Reduce intake of refined c arbohydrates and sugars

If presentation is consistent with a fungal infection, use

antifungals followed by prebiotics and probiotics

Avoid FOS powder as it may feed the yeast

Address other abnormal results on the GI Effects test

first, with the expectation that rare yeast/fungi will be


crowded out when healthy conditions are restored

Parasites

Parasite present

Pharmaceutical recommendations for each parasite are


from the 2007 publication in The Medical Letter, “Drugs for


Parasitic Infections.”[14]

Blastocystis sp.

Blastocystis sp. is transmitted via fecal-oral route or from

contaminated food or water. Seven subspecies have


been identified and Blastocystis sp. 4 infection has been

correlated with disease. Blastocystis sp. 2 is considered to be

asymptomatic.[15-17]

Symptoms:

May include diarrhea, cramps, nausea, fever, vomiting,

abdominal pain or fatigue. Blastocystis sp. has been

associated with irritable bowel syndrome, infective


arthritis and intestinal obstruction. In certain cases,


chronic fatigue may be the only complaint.

Treatment Options:

Blastocystis sp. can be prevented by personal hygiene and

sanitary conditions

Clinical significance of infection by these organisms is

controversial

Metronidazole 750 mg PO tid x 10d or iodoquinol 650

mg PO tid x 20d or trimethoprim/sulfamethoxazole 1 DS


tab PO bid x 7d have been reported to be effective

Infection is difficult to get rid of, botanicals may not

be strong enough. Use of broad spectrum antiparasitic


botanicals is most effective.*

Botanicals* (see page 7)

Clonorchis sinensis (Chinese Liver Fluke)

Clonorchis sinensis is found in pickled, smoked, salted,

imported, or undercooked freshwater fish.

Symptoms :

Frequently asymptomatic. Inflammation and intermittent

obstruction of the biliary ducts. Acute abdominal


pain, nausea, diarrhea and eosinophilia can occur. In


long-standing infections, cholangitis, cholelithiasis,


pancreatitis and cholangiocarcinoma can develop.

Treatment Options:

Praziquantel, 75 mg/kg/d PO in 3 doses x 2d

Albendazole 10 mg/kg/d PO x 7d

Botanicals* (see page 7)

Cryptosporidium

Water, including swimming pools, is a common source of


contamination as it is resistant to chlorine. Outbreaks are


associated with raw milk and meat, and Cryptosporidium is a

likely cause of traveler’s diarrhea.

Symptoms:

Watery diarrhea is the most frequent symptom, and can

be accompanied by dehydration, weight loss, abdominal


pain, fever, nausea and vomiting. May be very severe in


immunocompromised patients.

Treatment Options:

Usually self-limiting in an immunocompetent person,

with symptoms lasting 1-2 weeks

If symptoms persist look for possible water

contamination

Nitazoxanide, 500 mg PO bid x 3d for persistent

infections

Botanicals* (see page 7)

Dientamoeba fragilis

Fecal-oral transmission and water contamination are common


sources. Often accompanies pinworm.

Symptoms:

Diarrhea, fatigue and abdominal bloating, although

often asymptomatic. In chronic infections, abdominal


tenderness, nausea and weight loss may be present.

Treatment Options:

Iodoquinol, 650 mg PO tid x 20d; Paromomycin, 25-35

mg/kg/d PO in 3 doses x 7d; Tetracycline, 500 mg PO qid


x 10d or Metronidazole, 500-750 mg PO tid x 10d

Botanicals* (see page 7)

Endolimax nana or Entamoeba hartmanni

Endolimax nana and Entamoeba hartmanni are considered to

be non-pathogenic amoeba. Detection is significant in that it


means the patient has ingested something contaminated with


fecal material. Increased personal hygiene is recommended.

Parasites


6

Entamoeba histolytica

Entamoeba histolytica is the only amoeba considered

pathogenic. Contaminated food or water, pets, sexual contact,


and fecal-oral route are possible sources of transmission. Cysts


are sensitive to chlorinated water.

Symptoms:

Range from asymptomatic t o fulminating colitis

(resembling ulcerative colitis), dysentery, and


extraintestinal lesions on the liver, lung, brain, skin and


other tissues

Treatment Options:

Asymptomatic carriers should be treated in order to

avoid spread

For asymptomatic patients: Iodoquinol, 650 mg PO tid x

20d; Paromomycin, 25-35 mg/kg/d PO in 3 doses x 7d or


Diloxanide furoate, 500 mg PO tid x 10d

For mild to moderate intestinal disease: Metronidazole,

500-750 mg PO tid x 7-10d or Tinidazole, 2 g once PO


daily x 3d followed by either Iodoquinol, 650 mg PO tid


x 20d or Paromomycin, 25-35 mg/kg/d PO in 3 doses x


7d

For severe intestinal and extraintestinal disease:

Metronidazole, 750 mg PO tid x 7-10d or Tinidazole, 2


g once PO daily x 5d followed by either Iodoquinol, 650


mg PO tid x 20d or Paromomycin, 25-35 mg/kg/d PO in


3 doses x 7d

Botanicals* (see page 7)

Enterobius vermicularis (pinworm)

Enterobius vermicularis is transmitted from fecal-oral route.

Females emerge from the anus and lay eggs on the perianal


surface. Eggs can survive on bed linens and fabrics for 2-3


weeks.

Symptoms:

Nocturnal perianal pruritus which can lead to skin

bacterial infection, abdominal pain and anorexia. It may


enter the vagina and has been associated with some cases


of cystitis.

Treatment Options:

Mebendazole, 100 mg PO once, repeat in 2 weeks;

Pyrantel pamoate, 11 mg/kg base PO once (max. 1 g),


repeat in 2wks

Albendazole, 400 mg PO once; repeat in 2wks

Botanicals* (see page 7)

Giardia lamblia

Giardia lamblia is a flagellate considered to be a pathogen

and the most common cause of diarrheal disease worldwide.


Transmitted via contaminated water, food or the fecal-oral


route.

Symptoms:

Often asymptomatic. Incubation period is 1-3 weeks and

symptoms range from acute diarrhea, to chronic diarrhea


with bloating, intestinal malabsorption, steatorrhea


(possibly due to bile salt deconjugation) and weight


loss. Generally self-limiting, however 30-60% develop


chronic giardiasis. Unusual presentations include allergic


manifestations such as urticaria, reactive arthritis, and


biliary tract disease. May induce lactose intolerance, B12


deficiency and reduced sIgA.

Treatment Options:

Metronidazole 250 mg PO tid x 5-7d

Avoid fatty foods as giardia feeds on bile salts

Paromomycin, 25-35 mg/kg/d PO in 3 doses x 5-10d; or

Furazolidone, 100 mg PO qid x 7-10d; or Quinacrine,


100 mg PO tid x 5d

Botanicals* (see page 7)

Necator americanus and


Ancylostoma duodenale (hookworm)

Necator americanus and Ancylostoma duodenale are transmitted

via skin contact with contaminated soil, or oral ingestion


of the larvae. Worms can travel to the lungs or attach to the


mucosa of the GI and suck blood.

Symptoms:

Itching and a rash at the site of penetration. While a light

infection may cause no symptoms, heavy infection can


cause anemia, abdominal pain, diarrhea, loss of appetite


and weight loss. Has been associated with reactive


arthritis.

Treatment Options:

Albendazole, 400 mg PO once; Mebendazole, 100 mg PO

bid x 3d or 500 mg once, or Pyrantel pamoate, 11 mg/kg


(max. 1g) PO x 3d

Botanicals* (see page 7)

Schistosoma mansoni

Schistosoma mansoni is transmitted through skin contact with

contaminated water or oral ingestion. Larvae can migrate to


the lungs and liver and can live for 25-30 years. Eggs secrete


an enzymatic substance that destroys surrounding tissues.

Symptoms:

Infection is generally asymptomatic unless there is

repeated exposure leading to heavy worm burden. Severe


infection can lead to myalgias, abdominal pain, diarrhea,


cough, tender liver, ulceration of the intestinal mucosal


layer. It has been linked with reactive arthritis and


sacroilitis.

Parasites Botanical Treatments

7

Treatment Options:

Praziquantel 4 0 mg/kg/d in 2 doses x 1d, or

Oxamniquine 15 mg/kg once

Botanicals* (see below)

Strongyloides sp.

Strongyloides sp. is transmitted via skin contact with contaminated

soil, or oral ingestion of the larvae. Larvae are


carried to the lungs or are swallowed and mature in the small


intestine.

Symptoms:

Itching and a rash at the site of penetration. While a

light infection may cause no symptoms, heavy infection


can cause epigastric pain, nausea and vomiting, gas,


and alternating constipation and diarrhea. Has been


associated with reactive arthritis.

Treatment Options:

Thiabendazole 50 mg/kg/d in two doses x 2d; Ivermectin

200 mcg/kg/d x 1-2d, or Albendazole 400 mg/d x 3d

Eradication is difficult, recheck stool in 3 months

Botanicals* (see below)

Taenia sp. (tapeworm)

Taenia sp. is transmitted by undercooked, infected beef.

Maturation from cyst to worm takes 2 months. Taenia sp. can

grow 4-8 meters long and can live 25 years.

Symptoms:

Often asymptomatic. Symptoms include GI complaints

such as abdominal pain, anorexia, weight loss or malaise.


Vitamin B12 deficiency may result.

Treatment Options:

Praziquantel, 5-10 mg/kg PO once, Niclosamide, 2 g PO once

Botanicals* (see below)

Trichuris trichiura (whipworm)

Trichuris trichiura is transmitted from ingested feces

contaminated soil, or underwashed vegetables. It is the


most common helminth infection. T. trichiura can become

embedded in the intestinal villi, feeds on tissue secretions and


can cause eosinophilin. Larvae hatch in the small intestine


and take up residence in the large intestine. Adult female lay


eggs for up to five years.

Symptoms:

Often asymptomatic and self-limiting. Symptoms

depend on the amount of worms present and the degree


of mucosal involvement. Severe infection can result


in bloody diarrhea, abdominal pain, nausea and irondeficiency


anemia.

Treatment Options:

Mebendazole, 100 mg PO bid x 3d or 500 mg once;

Albendazole, 400 mg PO x 3d, or Ivermectin, 200 mcg/


kg PO daily x 3d

Botanicals* (see below)

Parasite Present: taxonomy unavailable

The DNA probe identified kingdom protozoan, but genus and


species probes for known human pathogens were negative.


Suspect that the protozoan identified is likely NOT a human


pathogen, and probably a transient, non-colonizer of the


human GI. Evaluate patient symptoms and inflammatory


markers on the GI Effects test. If symptoms are consistent


with a parasite infection, consider treatment.

Treatment Options:

Address other abnormal results in the GI Effects test first,


with the expectation that a rare parasite will be crowded out


when healthy conditions are restored.

Consider exposures such as pets, sushi, camping, or

foreign travel

If presentation is consistent with parasite infestation, use

a broad spectrum antiparasitic treatment followed by preand


probiotics

Botanicals* (see below)

*Botanical Treatment

Individualized pharmaceutical interventions are listed below each parasite. Common botanical anti-parasitic herbs for each parasite listed


include black walnut, quassia, garlic, berberine, grapefruit seed extract, oil of oregano, barberry, and artemesia. When treating parasites


with botanicals, it is recommended to use a blend of several, to lengthen treatment duration, and to rotate antiparasitic agents

Adiposity Index • Drug Resistance Genes • Short Chain Fatty Acids (SCFA)

8

Adiposity Index

Adiposity Index imbalanced: high firmicutes


and low bacteroidetes

Research has indicated that obesity has a microbial component


that alters caloric yield from ingested food.[18] Altering the

gut microbiota may also improve insulin sensitivity and oral


glucose tolerance.[19] Treatments for obesity that result in

lowering the percentage of Firmicutes may assist in weight


control.

Cause:

Bacteria classes known to increase c aloric extraction

from food are present

Dysbiosis

The Firmicutes class consist of Clostridia sp., Streptomyces

sp., Lactobacillus sp., Mycoplasma sp., Bacillus sp. (see

results under “Predominant Bacteria”)

The Bacteroidetes class consist of Bacteroides sp. and

Prevotella sp. (see results under “Predominant Bacteria”)

Treatment Options:

Balance predominant bacteria using 4R protocol

Remove opportunistic bacteria, especially Bacillus sp.

Supplement with Bifidobacter sp. and S. boulardii

Reduce refined carbohydrates

Address all GI Effects imbalances

Drug Resistance Genes

Cause:

Bacterial resistance to antibiotic class

Treatment Options:

Avoid using class of antibiotics for which patient has

drug resistance gene

Drug resistance names and antibiotics

aacA/aphD

Antibiotic:

Gentamicin, Kanamycin, Tobramycin (aminoglycosides)

Target Organism:

Gram-positive bacteria (cocci), namely Enterococci

mecA

Antibiotic:

Methicillin (Beta-Lactam)

Target Organism:

Aerobic, Gram-negative

vanA, vanB, vanC

Antibiotic:

Vancomycin and Teicoplanin (glycopeptides)

Target Organism:

Gram-positive bacteria, particularly beta-lactamase-producing


organisms such as Staphylococcus

gyrB, ParE

Antibiotic

Ciprofloxacin and later generation quinolones

Target Organism

Gram-positive and Gram-negative bacteria

PBP1a, PBP2B

Antibiotic:

Penicillin (Beta-Lactam)

Target Organism:

Broad spectrum

Short Chain Fatty Acids (SCFA)

Depressed total SCFA or N-Butyrate

Beneficial SCFA come from dietary carbohydrates that have


escaped digestion or absorption in the small bowel, or from


prebiotics that have undergone fermentation in the colon.


They are also produced by fermentation of fiber by anaerobic


bacteria in the large bowel. Production of SCFA in the


intestinal lumen plays an important role in the maintenance of


the intestinal barrier. Short chain fatty acids and specifically


n-butyrate serve as the fuel for the colonocytes.[20] Butyrate has

been shown to be protective against colon cancer.

Cause:

Low anaerobic bacteria (see “Predominant Bacteria”)

Antibiotic treatment

Insufficient fiber intake/poor diet

Slow transit time (more time for SCFA absorption)

Treatment Options:

Consider pre- and probiotic supplementation if the

predominant bacteria are low

Psyllium, oat bran, oligofructose, inulin

xylooligosaccharide, beta-glucan, or arabinogalactan

Increase dietary intake of fruits and vegetables

In ulcerative colitis, Crohn’s or those at risk for colon

cancer, consider butyrate enemas or enteric-coated


butyrate supplements

Enemas are contraindicated for those with GI bleeds

SCFA • Inflammation Immunology

9

Elevated total SCFA or N-Butyrate

Presence of short chain fatty acids and n-butyrate are essential


for the health of the colon. In general, high-normal levels of


these in the stool could mean that there is optimal fiber intake


and a balanced bacterial population. However, extremely


elevated SCFAs and n-butyrate in the stool could indicate


underlying GI abnormalities and need to be evaluated in


conjuction with the other GI Effects markers. Values of 184


mM/g or greater are above the 95% confidence interval.

Cause:

Bacterial overgrowth[21]

Rapid transit time (less time for SCFA absorption)[22]

Malabsorption[23]

Pancreatic insuffiency resulting in carbohydrate

maldigestion and increased bacterial fermentation

Bacterial fermentation of blood[24]

Treatment Options:

Address all GI imbalances including bacterial

overgrowth, parasite infection, gluten intolerance, food


allergy, vitamin, mineral, or essential fatty acid (EFA)


deficiency, or chronic NSAID usage.

Normalize transit time

Pancreatic enzymes, betaine HCl, or digestive herbs.

Inflammation

Elevated Lactoferrin, WBCs, or Mucus present

Lactoferrin is an iron-binding glycoprotein released from


neutrophils during inflammation. It is a marker of leukocyte


activity and is a primary component of the host’s first line


immune defense against infection.

Cause:

Mucosal inflammation

Bacterial or yeast overgrowth

Parasite infection

Inflammatory bowel disease, e.g. Crohn’s, ulcerative

colitis

Treatment Options:

Due to infection:

Remove pathogens

Probiotics and prebiotics to replenish beneficial bacteria

and establish proper balance

Enhance the endogenous immune (sIgA) defense by

supplementing with L-glutamine, S. boulardii and/or

colostrum

Due to non-infectious inflammation, e.g. Inflammatory


Bowel Disease:

Balance the intestinal flora, if indicated

Anti-inflammatory herbs and nutrients, e.g. turmeric,

ginger, EPA/DHA, quercetin, antioxidants

Mucosa support, e.g. vitamin A, zinc, folic acid, aloe

vera, licorice, L-glutamine, butyrate (for UC), N-acetyl


glucosamine, slippery elm

Rule out food sensitivities

Test Interferences:

Colostrum has a high concentration of lactoferrin, so

those breast feeding or supplementing with colostrum


could show false positives

False negatives can be seen in those with severe immune

compromise

Immunology

Depressed Fecal sIgA

Cause:

Chronic stress

Immunocompromise

Dysbiosis

Immuno-suppressing medication

Treatment Options:

Support gut mucosa, e.g. glutamine, probiotics (S.

boulardii, Bifidobacteria), colostrum, immunoglobulins,

essential fatty acids, zinc, and stress reduction

Support immune function

Elevated Fecal sIgA

Cause:

Immune response to eliminate pathogenic organisms in

GI tract

Sensitivities to foods

Treatment Options:

Support immune function

Remove pathogens, parasites, opportunistic bacteria,

virus

Rule out food sensitivities

Elimination diet

Elevated Anti-Gliadin Antibody

Cause:

Gluten enteropathy or sensitivity in colon

Treatment Options:

Remove gluten on trial basis

Consider Celiac Profile

Consider nutrients and herbs for mucosal healing

Additional Tests

Additional Tests • Digestion

10

Additional Tests

Depressed pH

Cause:

Bacterial overgrowth

Carbohydrate maldigestion (increases bacterial

proliferation and the production of SCFAs)

Lipid malabsorption

Rapid transit time (less time for SCFA absorption)

Treatment Options:

Support digestion and absorption

Supplementary plant or pancreatic enzymes, betaine

HCl, disaccharidases (if needed)

Normalize transit time

Address all GI Effects imbalances

Elevated pH

Cause:

Decreased bacterial production of SCFAs

Insufficient flora, dietary fiber, or water

Inadequate acid-producing organisms such as

Lactobacillus sp.

Hypochlorhydria

A high meat diet can stimulate ammonia production in

the bowel

Slow transit time (more time for SCFA absorption)

Elevated pH increases risk for colon cancer

Treatment Options:

Supplement with probiotics

Increase dietary fiber (esp. soluble) and water to increase

SCFA production and normalize transit time

Support digestion

Supplementation with betaine HCl or herbs to stimulate

gastric acid production, including ginger, peppermint, etc.

Address all GI Effects imbalances

Positive Occult Blood

Cause:

Bleeding in upper GI tract due to peptic ulcer,

inflammatory bowel disease, parasite infection, colon


cancer, hemorrhoids [25, 26]

Rule out false positive from red meat

Treatment Options:

Repeat occult blood test on two more occasions

Address all GI Effects imbalances

Rule out iron deficiency anemia

Consider sigmoidoscopy or colonoscopy to identify

source, treat accordingly

Anti-inflammatory medical food

Anti-inflammatory diet

Food allergens

Positive RBCs

Cause:

Bleeding in lower GI from hemorrhoids, intestinal

polyps, or tears around the anus due to constipation

Those with compromised liver function are more likely to

develop hemorrhoids

Treatment Options:

Treat constipation if present

Consider colonoscopy to identify source, treat

accordingly

Assess liver function

Soothe and repair gut mucosa

RBCs, occult blood

Digestion

Depressed Elastase 1

Elastase 1 is a digestive enzyme excreted by the pancreas,


exclusively, and has a direct correlation with pancreatic


function. Elastase 1 results are not affected by pancreatic


enzyme replacement therapy.[27,28] Optimal levels are > 500.

Cause:

Suppressed pancreatic function

Gallstones or post-cholecystectomy

Chronic pancreatitis

Diabetes

Hypochlorhydria

Cystic fibrosis

Treatment Options:

Support digestion with betaine HCl with pepsin, or plant

or pancreatic enzymes or digestive herbs

Bile salts, taurine, or cholagogues (esp. if high

triglycerides and constipation)

Relax while eating and chew thoroughly

Support diabetes regulation

Elevated Vegetable Fibers, Triglycerides

Cause:

Maldigestion

Hypochlorhydria

Pancreatic insufficiency

Bile salt insufficiency (if elevated triglycerides)

Inadequate chewing (if elevated vegetable fibers)

Treatment Options:

Support digestion with betaine HCl with pepsin, plant or

pancreatic enzymes or digestive herbs

Bile salts, taurine, or cholagogues (esp. if high

triglycerides and constipation)

Relax while eating and chew thoroughly

11

Digestion • Absorption

Elevated Putrefactive SCFA

Cause:

Protein maldigestion

Hypochlorhydria

Pancreatic insufficiency

Malabsorption, esp. if elevated long chain fatty acids or

cholesterol

Bacterial overgrowth of the small intestine

Treatment Options:

Support digestion with betaine HCl with pepsin, plant or

pancreatic enzymes or digestive herbs

Treat any underlying pancreatitis

Consider nutrients and herbs for mucosal support:

L-glutamine, Zn, EFAs, Vitamins A, E, and C,


pantothenic acid, N-acetyl glucosamine, glycyrrhiza, aloe


vera, slippery elm, etc.

Eliminate infection, address gluten intolerance, and food

sensitivities

Absorption

Elevated LCFA, Total Fat, or Cholesterol

Cause:

Malabsorption due to diarrhea, intestinal dysbiosis,

parasites, colitis, gluten intolerance, food allergy,


essential fatty acid deficiency, pancreatic or bile salt


insufficiency and/or chronic NSAID usage [29]

High dietary fat intake

Medications designed to bind and eliminate fats

If elevated cholesterol, suspect malabsorption, high

dietary intake or increased mucosal cell turnover


resulting from inflammation [30, 31]

Bacterial overgrowth of the small intestine (esp. if

elevated SCFAs)

Bacterial enzymes can also impair micelle formation,

resulting in lipid malabsorption

Treatment Options:

Support digestion with supplementary plant or

pancreatic enzymes, betaine HCl, digestive herbs, bile


salts or cholagogues, taurine or glycine, if indicated

Address food sensitivities or gluten intolerance

Check vitamin (esp. fat-soluble), mineral, and EFA status

Support mucosal health with nutrients such as

L-glutamine, Zn, EFAs, Vitamins A, E, and C,


pantothenic acid, N-acetyl glucosamine, glycyrrhiza, aloe


vera, slippery elm, etc.

Address all GI Effects imbalances

Botanical Sensitivities References

12

References

1. Guarner, F. and J.R. Malagelada, Gut flora in health and disease. Lancet, 2003.

361(9356): p. 512-9.


2. C., S., A dynamic partnership: Celebrating our gut flora. Anaerobe, 2005. 11(5): p.

247-251.


3. Lorian, V., Colonization resistance. Antimicrob Agents Chemother, 1994. 38(7): p.

1693.


4. Wang, M., et al., Comparison of bacterial diversity along the human intestinal


tract by direct cloning and sequencing of 16S rRNA genes. FEMS Microbiol Ecol,

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5. Camilleri, M., Probiotics and irritable bowel syndrome: rationale, putative


mechanisms, and evidence of clinical efficacy. J Clin Gastroenterol, 2006. 40(3): p.

264-9.


6. Gibson, G.R., Dietary modulation of the human gut microflora using the


prebiotics oligofructose and inulin. J Nutr, 1999. 129(7 Suppl): p. 1438S-41S.


7. Endresen, G.K., Mycoplasma blood infection in chronic fatigue and fibromyalgia


syndromes. Rheumatol Int, 2003. 23(5): p. 211-5.

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acidosis. Ann Intern Med, 1995. 122(11): p. 839-42.

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autistic spectrum disorders and that of healthy children. J Med Microbiol, 2005.


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10. Finegold, S.M., Therapy and epidemiology of autism--clostridial spores as key


elements. Med Hypotheses, 2008. 70(3): p. 508-11.

11. Tomazinho, L.F. and M.J. Avila-Campos, Detection of Porphyromonas gingivalis,


Porphyromonas endodontalis, Prevotella intermedia, and Prevotella nigrescens


in chronic endodontic infection. Oral Surg Oral Med Oral Pathol Oral Radiol Endod,

2007. 103(2): p. 285-8.


12. de Bortoli, N., et al., Helicobacter pylori eradication: a randomized prospective


study of triple therapy versus triple therapy plus lactoferrin and probiotics. Am J

Gastroenterol, 2007. 102(5): p. 951-6.

13. Jarosz, M., et al., Effects of high dose vitamin C treatment on Helicobacter pylori


infection and total vitamin C concentration in gastric juice. Eur J Cancer Prev,

1998. 7(6): p. 449-54.


14. Drugs for Parasite Infections. In: Treatments Guidelines from the Medical Letter,

2007. Vol 5 (suppl).


15. Noel, C., et al., Molecular phylogenies of Blastocystis isolates from different


hosts: implications for genetic diversity, identification of species, and zoonosis.

J Clin Microbiol, 2005. 43(1): p. 348-55.

16 Puthia, M.K., et al., Blastocystis ratti induces contact-independent apoptosis,


F-actin rearrangement, and barrier function disruption in IEC-6 cells. Infect

Immun, 2006. 74(7): p. 4114-23.

17. Kaneda, Y., et al., Ribodemes of Blastocystis hominis isolated in Japan. Am J Trop

Med Hyg, 2001. 65(4): p. 393-6.

18. Ley, R.E., et al., Microbial ecology: human gut microbes associated with obesity.

Nature, 2006. 444(7122): p. 1022-3.

19. Membrez, M., et al., Gut microbiota modulation with norfloxacin and ampicillin


enhances glucose tolerance in mice. Faseb J, 2008.


20. Royall, D., T.M. Wolever, and K.N. Jeejeebhoy, Clinical significance of colonic


fermentation. Am J Gastroenterol, 1990. 85(10): p. 1307-12.

21. Hoverstad, T., et al., Short-chain fatty acids in the small-bowel bacterial


overgrowth syndrome. Scand J Gastroenterol, 1985. 20(4): p. 492-9.

22. Oufir, L.E., et al., Relationships between transit time in man and in vitro


fermentation of dietary fiber by fecal bacteria. Eur J Clin Nutr, 2000. 54(8): p.

603-9.


23. Scheppach, W., et al., The effect of starch malabsorption on fecal short-chain


fatty acid excretion in man. Scand J Gastroenterol, 1988. 23(6): p. 755-9.


24. Holtug, K., H.S. Rasmussen, and P.B. Mortensen, Short chain fatty acids in


inflammatory bowel disease. The effect of bacterial fermentation of blood. Scand J

Clin Lab Invest, 1988. 48(7): p. 667-71.

25. Howarth, G.F., et al., High prevalence of undetected ulcerative colitis: data from


the Nottingham fecal occult blood screening trial. Am J Gastroenterol, 2002. 97(3):

p. 690-4.


26. Kronborg, O., Diverticulitis: a new high-risk group for colorectal cancer? Scand J

Gastroenterol, 2004. 39(8): p. 707-8.

27. Löser Chr, Möllgard A, Fölsch UR. Faecal elastase1: a novel, highly sensitive, and


specific tubeless pancreatic function test. Gut. 1996; 39: 580-586.

28. Stein J, Jung M, Sziegoleit A, Zeuzem S, Caspary WF, Lembcke B.


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pancreatic function. Clin Chem. 1996; 42:222-226.

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1006 p.


30. Thomson, A.B.R., First Principles of Gastroenterology: The Basis of Disease and an

Approach to Management. 2000: Gastroenterology Resource Centre.

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disease. Gastroenterology, 1985. 88(1 Pt 1): p. 134-42.

Botanical Sensitivities

When treating with botanicals, it is recommended to use a broad spectrum product. Treatment with botanicals might also require


a longer duration than treatment with pharmaceuticals. Antimicrobial botanicals may be rotated and/or administered in a pulsatile


fashion to improve efficacy. Listed below are the active ingredients tested for each botanical used in antimicrobial blends.

Botanical Active ingredient

Wormwood (Artemesia) Artemisinin


Olive leaf Oleuropein


Uva Ursi (Bearberry) Arbutin


Garlic Alliin


Undecylenic acid (from castor bean) Undecylenic acid


Oil of thyme Thymol


Oil of oregano Carvacrol


Goldenseal Berberine


Cat’s Claw Quinic acid
Black Walnut 5-hydroxy-1,4-naphthoquinone