comprehensive stool analysis / parasitology x3 images/csap3_ddi.pdf · expected /beneficial...

LAB #: F000000-0000-0PATIENT: Sample PatientID: PATIENT-S-00018SEX: FemaleAGE: 28

CLIENT #: 12345DOCTOR: Doctors Data, Inc.3755 Illinois Ave.St. Charles, IL 60174 USA

Comprehensive Stool Analysis / Parasitology x3

BACTERIOLOGY CULTURE

Expected/Beneficial flora Commensal (Imbalanced) flora Dysbiotic flora

4+ Bacteroides fragilis group 3+ Beta strep, group B 4+ Citrobacter freundii

4+ Bifidobacterium spp. 2+ Pseudomonas fluorescens 3+ Klebsiella pneumoniae ssp pneumoniae

4+ Escherichia coli 4+ Alpha hemolytic strep

4+ Lactobacillus spp. 1+ Gamma hemolytic strep

4+ Enterococcus spp.

3+ Clostridium spp.

NG = No Growth

BACTERIA INFORMATION

YEAST CULTURE

Normal flora Dysbiotic flora

1+ Saccharomyces cerevisiae/boulardii 3+ Candida glabrata

MICROSCOPIC YEAST YEAST INFORMATION

Result: Expected:

Many None - Rare

Comments: Date Collected: Date Received: 4/26/2010Date Completed: 4/27/2010

v5.09©DOCTOR’S DATA, INC. ADDRESS: 3755 Illinois Avenue, St. Charles, IL 60174-2420 CLIA ID NO: 14D0646470 MEDICARE PROVIDER NO: 148453

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Expected /Beneficial bacteria make up a significant portion of the total microflora in a healthy & balanced GI tract. These beneficial bacteria have manyhealth-protecting effects in the GI tract including manufacturing vitamins, fermenting fibers, digesting proteins and carbohydrates, and propagating anti-tumor and anti-inflammatory factors.Clostridia are prevalent flora in a healthy intestine. Clostridium spp. should be considered in the context of balance with other expected/beneficial flora.Absence of clostridia or over abundance relative to other expected/beneficial flora indicates bacterial imbalance. If C. difficile disease is suspected, toxinA&B testing is recommended.Commensal (Imbalanced) bacteria are usually neither pathogenic nor beneficial to the host GI tract. Imbalances can occur when there are insufficientlevels of beneficial bacteria and increased levels of commensal bacteria. Certain commensal bacteria are reported as dysbiotic at higher levels.Dysbiotic bacteria consist of known pathogenic bacteria and those that have the potential to cause disease in the GI tract. They can be present due to anumber of factors including: consumption of contaminated water or food, exposure to chemicals that are toxic to beneficial bacteria; the use of antibiotics,oral contraceptives or other medications; poor fiber intake and high stress levels.

Yeast normally can be found in small quantities in the skin, mouth, intestine and mucocutaneousjunctions. Overgrowth of yeast can infect virtually every organ system, leading to an extensive arrayof clinical manifestations. Fungal diarrhea is associated with broad-spectrum antibiotics oralterations of the patient’s immune status. Symptoms may include abdominal pain, cramping andirritation. When investigating the presence of yeast, disparity may exist between culturing andmicroscopic examination. Yeast are not uniformly dispersed throughout the stool, this may lead toundetectable or low levels of yeast identified by microscopy, despite a cultured amount of yeast.Conversely, microscopic examination may reveal a significant amount of yeast present, but no yeastcultured. Yeast does not always survive transit through the intestines rendering it unvialble.

The microscopic finding of yeast in the stool ishelpful in identifying whether there isproliferation of yeast. Rare yeast may benormal; however, yeast observed in higheramounts (few, moderate, or many) is abnormal.

* Aeromonas, Campylobacter, Plesiomonas, Salmonella, Shigella, Vibrio, Yersinia, &Edwardsiella tarda have been specifically tested for and found absent unless reported.




PARASITOLOGY/MICROSCOPY * PARASITOLOGY INFORMATION

Sample 1

Rare Trichuris trichiura eggsMod Giardia lamblia trophsMod YeastFew WBC

Sample 2

Few Giardia lamblia trophsMany YeastFew WBC

Sample 3

Rare Trichuris trichiura eggsFew Giardia lamblia trophsMany YeastMod WBC

GIARDIA/CRYPTOSPORIDIUM IMMUNOASSAY

Within Outside Reference Range

Giardia lamblia Pos Neg

Cryptosporidium Neg Neg

Comments: Date Collected: Date Received: 4/26/2010Date Completed: 4/27/2010


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Intestinal parasites are abnormal inhabitants of the gastrointestinal tract thathave the potential to cause damage to their host. The presence of any parasitewithin the intestine generally confirms that the patient has acquired theorganism through fecal-oral contamination. Factors such as contaminated foodand water supplies, day care centers, increased international travel, pets,carriers such as mosquitoes and fleas, and sexual transmission havecontributed to an increased prevalence of intestinal parasites. It is estimatedthat close to one billion people worldwide are infected. Damage to the hostincludes parasitic burden, migration, blockage and pressure. Immunologicinflammation, hypersensitivity reactions and cytotoxicity also play a large rolein the morbidity of these diseases. The infective dose often relates to severityof the disease and repeat encounters can be additive.

There are two main classes of intestinal parasites that can cause humanintestinal disease. They include protozoa and helminths. The protozoa typicallyhave two stages; the trophozoite stage that is the metabolically active, invasivestage and the cyst stage, which is the vegetative inactive form resistant tounfavorable environmental conditions outside the human host. Helminths arelarge, multicellular organisms that are generally visible to the naked eye in theiradult stages. Like protozoa, helminths can be either free-living or parasitic innature. In their adult form, helminths cannot multiply in humans.

In general, acute manifestations of parasitic infection may involve diarrhea withor without mucus and or blood, fever, nausea, or abdominal pain. Howeverthese symptoms do not always occur. Consequently, parasitic infections maynot be diagnosed or eradicated. If left untreated, chronic parasitic infectionscan cause damage to the intestinal lining and can be an unsuspected cause ofillness and fatigue. Chronic parasitic infections can also be associated withincreased intestinal permeability, irritable bowel syndrome, irregular bowelmovements, malabsorption, gastritis or indigestion, skin disorders, joint pain,allergic reactions, and decreased immune function.

In some instances, parasites may enter the circulation and travel to variousorgans causing severe organ diseases such as liver abscesses andcysticercosis. In addition, some larval migration can cause pneumonia and inrare cases hyper infection syndrome with large numbers of larvae beingproduced and found in every tissue of the body.

Giardia lamblia is flagellated protozoan thatinfects the small intestine and is passed in stooland spread by the fecal-oral route. Waterbornetransmission is the major source of giardiasis.Cryptosporidium is a coccidian protozoa thatcan be spread from direct person-to-personcontact or waterborne transmission.

*A trichrome stain and concentrated iodine wetmount slide is read for each sample submitted.




DIGESTION /ABSORPTION


Elastase > 500 > 200 µg/mL

Fat Stain None None - Mod

Muscle fibers None None - Rare

Vegetable fibers Rare None - Few

Carbohydrates Neg Neg

INFLAMMATION


Lysozyme* 1200 <= 600 ng/mL

Lactoferrin 188 < 7.3 µg/mL

White Blood Cells Mod None - Rare

Mucus Pos Neg

IMMUNOLOGY


Secretory IgA* 458 51 - 204 mg/dL

Comments: Date Collected: *For Research Use Only. Not for use in diagnostic procedures.

Date Received: 4/26/2010Date Completed: 4/27/2010


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Elastase findings can be used for the diagnosisor the exclusion of exocrine pancreaticinsufficiency. Correlations between low levelsand chronic pancreatitis and cancer have beenreported. Fat Stain: Microscopic determinationof fecal fat using Sudan IV staining is aqualitative procedure utilized to assess fatabsorption and to detect steatorrhea. Musclefibers in the stool are an indicator of incompletedigestion. Bloating, flatulence, feelings of“fullness” may be associated with increase inmuscle fibers. Vegetable fibers in the stool maybe indicative of inadequate chewing, or eating“on the run”. Carbohydrates: The presence ofreducing substances in stool specimens canindicate carbohydrate malabsorption.

Lysozyme* is an enzyme secreted at the site ofinflammation in the GI tract and elevated levelshave been identified in IBD patients. Lactoferrinis a quantitative GI specific marker ofinflammation used to diagnose and differentiateIBD from IBS and to monitor patient inflammationlevels during active and remission phases of IBD.White Blood Cells (WBC): in the stool are anindication of an inflammatory process resulting inthe infiltration of leukocytes within the intestinallumen. WBCs are often accompanied by mucusand blood in the stool. Mucus in the stool mayresult from prolonged mucosal irritation or in aresponse to parasympathetic excitability such asspastic constipation or mucous colitis.

Secretory IgA* (sIgA) is secreted by mucosaltissue and represents the first line of defense ofthe GI mucosa and is central to the normalfunction of the GI tract as an immune barrier.Elevated levels of sIgA have been associatedwith an upregulated immune response.




SHORT CHAIN FATTY ACIDS


% Acetate 60 36 - 74 %

% Propionate 29 9 - 32 %

% Butyrate 11 9 - 39 %

% Valerate 0.4 1 - 8 %

Butyrate 0.15 0.8 - 3.8 mg/mL

Total SCFA’s 1.4 4 - 14 mg/mL

INTESTINAL HEALTH MARKERS


Red Blood Cells None None - Rare

pH 6.7 6 - 7.8

Occult Blood Neg Neg

MACROSCOPIC APPEARANCE

Appearance Expected

Color Brown Brown

Consistency Formed/Soft Formed/Soft

©DOCTOR’S DATA, INC. ADDRESS: 3755 Illinois Avenue, St. Charles, IL 60174-2420 CLIA ID NO: 14D0646470 MEDICARE PROVIDER NO: 1484530001422

Short chain fatty acids (SCFAs): SCFAs arethe end product of the bacterial fermentationprocess of dietary fiber by beneficial flora in thegut and play an important role in the health of theGI as well as protecting against intestinaldysbiosis. Lactobacilli and bifidobacteria producelarge amounts of short chain fatty acids, whichdecrease the pH of the intestines and thereforemake the environment unsuitable for pathogens,including bacteria and yeast. Studies have shownthat SCFAs have numerous implications inmaintaining gut physiology. SCFAs decreaseinflammation, stimulate healing, and contribute tonormal cell metabolism and differentiation. Levelsof Butyrate and Total SCFA in mg/mL areimportant for assessing overall SCFA production,and are reflective of beneficial flora levels and/oradequate fiber intake.

Red Blood Cells (RBC) in the stool may beassociated with a parasitic or bacterial infection,or an inflammatory bowel condition such asulcerative colitis. Colorectal cancer, anal fistulas,and hemorrhoids should also be ruled out.pH: Fecal pH is largely dependent on thefermentation of fiber by the beneficial flora of thegut.Occult blood: A positive occult blood indicatesthe presence of free hemoglobin found in thestool, which is released when red blood cells arelysed.

Color: Stool is normally brown because ofpigments formed by bacteria acting on bileintroduced into the digestive system from theliver. While certain conditions can causechanges in stool color, many changes areharmless and are caused by pigments in foodsor dietary supplements. Consistency: Stoolnormally contains about 75% water and ideallyshould be formed and soft. Stool consistencycan vary based upon transit time and waterabsorption.



Citrobacter freundii

NATURAL ANTIBACTERIALS

Disk Content Low Activity High Activity

1mg Berberine

33mg Black Walnut

46mg Caprylic Acid

11mg Oregano

10mg Uva Ursi

25mg Citrus Seed Extract

0.17mg Silver

PRESCRIPTIVE AGENTS

Resistant Intermediate Susceptible

Amoxacillin-Clavulanic Acid R

Ampicillin R

Cefazolin R

Ceftazadime S

Ciprofloxacin S

Trimeth-sulfa S

Comments: Date Collected: Natural antibacterial agent susceptibility testing is intended for research use only.Date Received: 4/26/2010 Not for use in diagnostic procedures.Date Completed: 4/27/2010


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Natural antibacterial agents may beuseful for treatment of patients whenorganisms display in-vitro sensitivity tothese agents. The test is performed byusing standardized techniques and filterpaper disks impregnated with the listedagent. Relative activity is reported for eachnatural agent based upon the diameter ofthe zone of inhibition or no growth zonesurrounding the disk. Data based on over5000 individual observations were used torelate the zone size to the activity level ofthe agent. A scale of relative activity isdefined for the natural agents tested.

Susceptible results imply that an infectiondue to the bacteria may be appropriatelytreated when the recommended dosage ofthe tested antimicrobial agent is used.Intermediate results imply that responserates may be lower than for susceptiblebacteria when the tested antimicrobialagent is used.Resistant results imply that the bacteria willnot be inhibited by normal dosage levels ofthe tested antimicrobial agent.



Klebsiella pneumoniae ssp pneumoniae

NATURAL ANTIBACTERIALS


1mg Berberine

33mg Black Walnut

46mg Caprylic Acid

11mg Oregano

10mg Uva Ursi


0.17mg Silver

PRESCRIPTIVE AGENTS

Resistant Intermediate Susceptible

Amoxacillin-Clavulanic Acid S

Ampicillin R

Cefazolin R

Ceftazadime S

Ciprofloxacin S

Trimeth-sulfa S

Comments: Date Collected: Natural antibacterial agent susceptibility testing is intended for research use only.Date Received: 4/26/2010 Not for use in diagnostic procedures.Date Completed: 4/27/2010


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Susceptible results imply that an infectiondue to the bacteria may be appropriatelytreated when the recommended dosage ofthe tested antimicrobial agent is used.Intermediate results imply that responserates may be lower than for susceptiblebacteria when the tested antimicrobialagent is used.Resistant results imply that the bacteria willnot be inhibited by normal dosage levels ofthe tested antimicrobial agent.



Saccharomyces cerevisiae/boulardii

NATURAL ANTIFUNGALS


1mg Berberine

46mg Caprylic Acid

10mg Uva Ursi

2.5mg Tannic Acid

11mg Oregano

45mg Undecylenic Acid


NON-ABSORBED ANTIFUNGALS

Low Activity High Activity

Nystatin

Comments: Date Collected: Yeast antifungal susceptibility testing is intended for research use only.Date Received: 4/26/2010 Not for use in diagnostic procedures.

Date Completed: 4/27/2010v5.09

©DOCTOR’S DATA, INC. ADDRESS: 3755 Illinois Avenue, St. Charles, IL 60174-2420 CLIA ID NO: 14D0646470 MEDICARE PROVIDER NO: 148453

0001424

Natural antifungal agents may be usefulfor treatment of patients when organismsdisplay in-vitro sensitivity to these agents.The test is performed by using standardizedtechniques and filter paper disksimpregnated with the listed agent. Relativeactivity is reported for each natural agentbased upon the diameter of the zone ofinhibition or no growth zone surrounding thedisk. Data based on over 5000 individualobservations were used to relate the zonesize to the activity level of the agent. Ascale of relative activity is defined for thenatural agents tested.

Non-absorbed antifungals may be usefulfor treatment of patients when organismsdisplay in-vitro sensitivity to these agents.The test is performed using standardizedcommercially prepared disks impregnatedwith Nystatin. Relative activity is reportedbased upon the diameter of the zone ofinhibition or no growth zone surrounding thedisk.



Candida glabrata

NATURAL ANTIFUNGALS


1mg Berberine

46mg Caprylic Acid

10mg Uva Ursi

2.5mg Tannic Acid

11mg Oregano

45mg Undecylenic Acid


NON-ABSORBED ANTIFUNGALS

Low Activity High Activity

Nystatin

AZOLE ANTIFUNGALS

Resistant S-DD Susceptible

Fluconazole R

Itraconazole R

Voriconazole R

Standardized test interpretive categories established for Candida spp. are used for all yeast isolates.

Comments: Date Collected: Yeast antifungal susceptibility testing is intended for research use only.Date Received: 4/26/2010 Not for use in diagnostic procedures.Date Completed: 4/27/2010


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Non-absorbed antifungals may be usefulfor treatment of patients when organismsdisplay in-vitro sensitivity to these agents.The test is performed using standardizedcommercially prepared disks impregnatedwith Nystatin. Relative activity is reportedbased upon the diameter of the zone ofinhibition or no growth zone surrounding thedisk.

Susceptible results imply that an infectiondue to the fungus may be appropriatelytreated when the recommended dosage ofthe tested antifungal agent is used.Susceptible - Dose Dependent (S-DD)results imply that response rates may belower than for susceptible fungi when thetested antifungal agent is used.Resistant results imply that the fungus willnot be inhibited by normal dosage levels ofthe tested antifungal agent.

Lab number: F000000-0000-0 CSAPx3 Page: 1Patient: Sample Patient Client: 12345

INTRODUCTION

This analysis of the stool specimen provides fundamental information about the overall gastrointestinal health of the patient. When abnormal microflora or significant aberrationsin intestinal health markers are detected, specific interpretive paragraphs are presented. If no significant abnormalities are found, interpretive paragraphs are not presented.

Clostridium spp

Clostridia are expected inhabitants of the human intestine. Although most clostridia in the intestine are not virulent, certain species have been associated with disease. Clostridium perfringens is a major cause of food poisoning and is also one cause of antibiotic-associated diarrhea. Clostridium difficile is a causative agent in antibiotic-associated diarrhea and pseudomembranous colitis. Other species reported to be prevalent in high amounts in patients with Autistic Spectrum Disorder include Clostridium histolyticum group, Clostridium cluster I, Clostridium bolteae, and Clostridium tetani.

If these disease associations are a concern further testing may be necessary.

Washington W, Allen S, Janda W, Koneman E, Procop G, Schreckenberger P, Woods, G. Koneman’s Color Atlas and Textbook of Diagnostic Microbiology, 6th edition. Lippincott Williams and Wilkins; 2006. pg 931-939

Song Y, Liu C, Finegold SM. Real-Time PCR Quantitation of Clostridia in Feces of Autistic Children. Applied and Environmental Microbiology. Nov. 2004, 6459-6465.

Parracho H, Bingham MO, Gibson GR, McCartney AL. Differences Between the Gut Microflora of Children with Autistic Spectrum Disorders and That of Healthy Children. Journal of Medical Microbiology. 2005;54, 987-991.

Imbalanced flora

Imbalanced flora are those bacteria that reside in the host gastrointestinal tract and neither injure nor benefit the host. Certain dysbiotic bacteria may appear under the imbalances category if found at low levels because they are not likely pathogenic at the levels detected. When imbalanced flora appear, it is not uncommon to find inadequate levels of one or more of the beneficial bacteria and/or a fecal pH which is more towards the alkaline end of the reference range (6.5 - 7.2). It is also not uncommon to find hemolytic or mucoid E. coli with a concomitant deficiency of beneficial E. coli and alkaline pH, secondary to a mutation of beneficial E. coli in alkaline conditions (DDI observations). Treatment with antimicrobial agents is unnecessary unless bacteria appear under the dysbiotic category.

1999-2010 Doctor’s Data, Inc.

Lab number: F000000-0000-0 CSAPx3 Page 2Patient: Sample Patient Client: 12345

Mackowiak PA. The normal microbial flora. N Engl J Med. 1982;307(2):83-93.

Dysbiotic Flora

In a healthy balanced state of intestinal flora, the beneficial bacteria make up a significant proportion of the total microflora. However, in many individuals there is an imbalance or deficiency of beneficial flora and an overgrowth of non-beneficial (imbalance) or even pathogenic microorganisms (dysbiosis). This can be due to a number of factors including: consumption of contaminated water or food; daily exposure of chemicals that are toxic to beneficial bacteria; the use of antibiotics, oral contraceptives or other medications; poor fiber intake and high stress levels.

A number of toxic substances can be produced by the dysbiotic bacteria including amines, ammonia, hydrogen sulfide, phenols, and secondary bile acids which may cause inflammation or damage to the brush border of the intestinal lining. If left unchecked, long-term damage to the intestinal lining may result in leaky gut syndrome, allergies, autoimmune disease (e.g. rheumatoid arthritis), irritable bowel syndrome, fatigue, chronic headaches, and sensitivities to a variety of foods. In addition, pathogenic bacteria can cause acute symptoms such as abdominal pain, nausea, diarrhea, vomiting, and fever in cases of food poisoning.

Bacterial sensitivities to a variety of prescriptive and natural agents have been provided for the pathogenic bacteria that were cultured from this patient’s specimen. This provides the practitioner with useful information to help plan an appropriate treatment regimen. Supplementation with probiotics or consumption of foods (yogurt, kefir, miso, tofu, tamari sauce) containing strains of lactobacilli, bifidobacteria, and enterococci can help restore healthy flora levels. Polyphenols in green and ginseng tea have been found to increase the numbers of beneficial bacteria. Hypochlorhydria may also predispose an individual to bacterial overgrowth, particularly in the small intestine. Nutritional anti-inflammatories can aid in reversing irritation to the GI lining. These include quercetin, vitamin C, curcumin, gamma-linoleic acid, omega-3 fatty acids (EPA, DHA), and aloe vera. Other nutrients such as zinc, beta-carotene, pantothenic acid, and L-glutamine provide support for regeneration of the GI mucosa. A comprehensive program may be helpful in individuals in whom a dysbiotic condition has caused extensive GI damage.

Lispki E. Digestive Wellness. New Canaan,CT: Keats Publishing;1996.

Mitsuoka T. Intestinal Flora and Aging. Nutr Rev 1992;50(12):438-446.

Weisburger JH. Tea and Health: The Underlying Mechanisms. Proc Soc Exp Biol Med 1999;220(4):271-275.4.

Pereira SP, Gainsborough N, Dowling RH. Drug-induced Hypochlorhydria Causes High Duodenal Bacterial Counts in the Elderly. Ailment Pharmacol Ther 1998;12(1)99-104.

Murray MT. Stomach Ailments and Digestive Disturbances. Rocklin, CA: Prima Publishing; 1997.



Citrobacter species

Citrobacter species, a gram-negative bacterium and member of the Enterobacteriaceae family, is considered dysbiotic at 3+ - 4+.

Citrobacter freundii complex, including Citrobacter freundii, Citrobacter youngae, Citrobacter braakii, Citrobacter sedlakii, Citrobacter werkmaniii, and less commonly Citrobacter koseri and Citrobacter farmeri, can cause diarrheal disease. Symptoms due to Citrobacter freundii complex seem to be a result of the elaboration of an E. coli-like heat-stable enterotoxin and hydrogen sulfide. Citrobacter freundii complex has been implicated as a cause of gastrointestinal infection and inflammation, acute dysentery, and dyspepsia. Acute symptoms can include profuse, watery diarrhea which is often unaccompanied by abdominal pain, fecal blood, or white blood cells.

Citrobacter species thrive on Fructooligosaccharides (FOS), a common ingredient in artificial or alternative sweetener.

Antibiotics may be indicated if symptoms are prolonged and in systemic infections. Refer to the bacterial sensitivities to identify the most appropriate pharmaceutical or natural agent.

Guarino, A, et al. Production of Eschericia coli Sta-Like Heat-Stable Enterotoxin by Citrobacter freundii Isolated from Humans. Journal of Clinical Microbiology. January 1987;110-114.

Washington W, Allen S, Janda W, Koneman E, Procop G, Schreckenberger P, Woods, G. Koneman’s Color Atlas and Textbook of Diagnostic Microbiology, 6th edition. Lippincott Williams and Wilkins; 2006. pg 686-689.

Murray PR, Baron EJ, Jorgensen JH, Pfaller MA, Yolken RH. Manual of Clinical Microbiology, 8th edition. Washington, DC: ASM Press; 2003. pg 701-704.

Klebsiella species

Klebsiella belongs to the Enterobacteriaceae family and is closely related to the genera Enterobacter and Serratia. This gram-negative bacterium is considered dysbiotic in the amount of 3 - 4+.

Klebsiellae are widely distributed in nature and in the gastrointestinal tract of humans. In humans, they may colonize the skin, oral cavity, pharynx, or gastrointestinal tract. Klebsiellae may be regarded as normal flora in many parts of the colon, intestinal tract and biliary tract, but the gut is also the main reservoir of opportunistic strains.

This bacterium has the potential to cause intestinal, lung, urinary tract, and wound infections in susceptible individuals, but Klebsiella overgrowth is commonly asymptomatic. K. pneumoniae, in particular, may cause diarrhea and some strains are enterotoxigenic. Infection has been linked to ankylosing spondylitis as well as myasthenia gravis (antigenic cross-reactivity), and these patients usually carry larger numbers of the organism in their intestines than healthy individuals. Klebsiella oxytoca has been found to be the cause of antibiotic-associated hemorrhagic colitis. These strains



have been shown to produce a cytotoxin that is capable of inducing cell death in various epithelial-cell cultures.

Klebsiella is also an infamously known nosocomial infectious agent, partially due to the ability of organisms to spread rapidly. Klebsiella accounts for approximately 3-7% of all hospital-acquired infections, placing it among the top eight pathogens in hospitals. Extraintestinal infection typically involves the respiratory or urinary tracts, but may infect other areas such as the biliary tract and surgical wound sites. K. pneumoniae and K. oxytoca are the two members of this genus responsible for most extraintestinal human infections.

Treatment of these species has become a major problem in most hospitals because of resistance to multiple antibiotics and potential transfer of plasmids to other organisms. Proper hand washing is crucial to prevent transmission from patient to patient via medical personnel. Contact isolation should be used for patients colonized or infected with highly antibiotic-resistant Klebsiella strains.

Klebsiella ozaenae and Klebsiella rhinoscleromatis are infrequent isolates that are subspecies of K. pneumoniae; however, each is associated with at unique spectrum of disease. K. ozaenae is associated with atrophic rhinitis, a condition called ozena, and purulent infections of the nasal mucous membranes. K. rhinoscleromatis causes the granulomatous disease rhinoscleroma, an infection of the respiratory mucosa, oropharynx, nose, and paranasal sinuses.

For the otherwise healthy individual, antimicrobial therapy is often unnecessary. Klebsiella thrives on a diet high in starch, so a low-starch diet may be helpful. A further caution is that Klebsiella thrives on Fructooligosaccharides (FOS) a class of oligosaccharides used as an artificial or alternative sweetener. Antibiotics may be indicated if symptoms are prolonged and in systemic infections. Refer to the bacterial sensitivities to identify the most appropriate pharmaceutical or natural agent.

Hogenauer C, Langner C, Beubler E, et al. Klebsiella oxytoca as a Causative Organism of Antibiotic-Associated Hemorrhagic Colitis. New England Journal of Medicine. December 2006;355;23.

Levy I et al. Nosocomial Infections After Cardiac Surgery in Infants and Children: Incidence and Risk Factors. J Hosp Infect. 2003;53(2):111-6.

Washington W, Allen S, Janda W, Koneman E, Procop G, Schreckenberger P, Woods, G. Koneman’s Color Atlas and Textbook of Diagnostic Microbiology, 6th edition. Lippincott Williams and Wilkins; 2006. pg 259-264.

Murray PR, Baron EJ, Jorgensen JH, Pfaller MA, Yolken RH. Manual of Clinical Microbiology, 8th edition. Washington, DC: ASM Press; 2003. pg 688-689.

Cultured Yeast

Yeast, such as Candida are normally present in the GI tract in very small amounts. Many species of yeast exist and are commensal; however, they are always poised to create opportunistic infections



and have detrimental effects throughout the body. Factors that contribute to a proliferation of yeast include frequent use of wide-spread antibiotics/low levels of beneficial flora, oral contraceptives, pregnancy, cortisone and other immunosuppressant drugs, weak immune system/low levels of sIgA, high-sugar diet, and high stress levels.

When investigating the presence of yeast, disparity may exist between culturing and microscopic examination. Yeast grows in colonies and is typically not uniformly dispersed throughout the stool. This may lead to undetectable or low levels of yeast identified by microscopy, despite a cultured amount of yeast. Conversely, microscopic examination may reveal a significant amount of yeast present, but no yeast cultured. Yeast does not always survive transit through the intestines rendering it unviable for culturing. Therefore, both microscopic examination and culture are helpful in determining if abnormally high levels of yeast are present.

Dysbiotic Yeast

Yeast was cultured from this stool specimen and the amount is considered to be dysbiotic. A positive yeast culture and sensitivity to prescriptive and natural agents is helpful in determining which anti-fungal agents to use as part of a therapeutic plan for chronic yeast syndrome. When investigating the presence of yeast, disparity may exist between culturing and microscopic examination. Yeast grows in colonies and is typically not uniformly dispersed throughout the stool. This may lead to undetectable or low levels of yeast identified by microscopy, despite a significant amount of yeast cultured.

Microscopic yeast

Microscopic examination has revealed yeast in this stool sample. The microscopic finding of yeast in the stool is helpful in identifying whether the proliferation of fungi, such as Candida albicans, is present. Yeast is normally found in very small amounts in a healthy intestinal tract. While small quantities of yeast (reported as rare or few) may be normal, yeast observed in higher amounts (moderate to many) is considered abnormal.

An overgrowth of intestinal yeast is prohibited by beneficial flora, intestinal immune defense (secretory IgA), and intestinal pH. Beneficial bacteria, such as Lactobacillus colonize in the intestines and create an environment unsuitable for yeast by producing acids, such as lactic acid, which lowers intestinal pH. Also, lactobacillus is capable of releasing antagonistic substances such as hydrogen peroxide, lactocidin, lactobacillin, and acidolin.

Many factors can lead to an overgrowth of yeast including frequent use of antibiotics (leading to insufficient beneficial bacteria), synthetic corticosteroids, oral contraceptives, and diets high in sugar. Although there is a wide range of symptoms which can result from intestinal yeast overgrowth, some of the most common include brain fog, fatigue, reccurring vaginal or bladder infections, sensitivity to smells (perfumes, chemicals, environment), mood swings/depression, sugar and carbohydrate cravings, gas/bloating, and constipation or loose stools.

A positive yeast culture (mycology) and sensitivity to prescriptive and natural agents is helpful in determining which anti-fungal agents to use as part of a therapeutic treatment plan for chronic colonic yeast. However, yeast are colonizers and do not appear to be dispersed



uniformly throughout the stool. Yeast may therefore be observed microscopically, but not grow out on culture even when collected from the same bowel movement.

Parasites

Parasites were detected by microscopic examination in this stool specimen. Intestinal parasites are abnormal inhabitants of the GI tract that live off and have the potential to cause damage to their host. Factors such as contaminated food and water supplies, day care centers, increased international travel, pets, carriers such as mosquitoes and fleas, and sexual transmission have contributed to an increased prevalence of intestinal parasites.

In general, acute manifestations of parasitic infection may involve diarrhea with or without mucus and/or blood, fever, nausea, or abdominal pain. However, these symptoms do not always occur. Consequently, parasitic infections may not be diagnosed and eradicated. If left untreated, chronic parasitic infections can cause damage to the intestinal lining and can be an unsuspected cause of illness and fatigue. Chronic parasitic infections can also be associated with increased intestinal permeability, irritable bowel syndrome, irregular bowel movements, malabsorption, gastritis or indigestion, skin disorders, joint pain, allergic reactions, decreased immune function, and fatigue.

Murray MT. Stomach Ailments And Digestive Disturbances. Rocklin, CA: Prima Publishing;1997.

Gittleman AL. Guess What Came to Dinner Parasites And Your Health. New York, NY: Penguin Group; 2001.

Trichuris trichiura (whipworm)

Trichuris trichiura eggs were identified in this specimen. Trichuris trichiura is a nematode that infects the large intestine. Infection is spread via the fecal-oral route. The parasite is found principally in the tropics and subtropics. Mild asymptomatic infections are common in rural parts of the southeastern USA.

Light infections are often asymptomatic. Heavy infections cause abdominal pain, anorexia, and diarrhea and may retard growth. Very heavy infections may cause weight loss, anemia, and rectal prolapse in children and parturient women.

No drug treatment is required for asymptomatic or light infections. Mebendazole (100 mg bid x 3 days, adult dose) or albendazole (400 mg qd x 3 days, adult dose) are used for more severe infections. These drugs should not be used during pregnancy. Natural agents include quassia and black walnut.

References:

Sanford JP. The Sanford Guide to Antimicrobial Therapy. 35th edition. Gilbert DN, Moellering Jr, RC, Sande MA, eds. Hyde Park (VT): Antimicrobial Therapy Inc; 2005.

Abramowicz, M. The Medical Letter On Drugs and Therapeutics. Drugs For Parasitic Infections. New



Rochelle (NY): The Medical Letter, Inc.

Beers, M. H., & Berkow, R. (Eds.). The Merck Manual of Diagnosis and Therapy Online. http://www.merck.com/mrkshared/mmanual/section13/chapter161/161a.jsp, Accessed August, 2005.

CDC Division of Parasitic Diseases website. http://www.cdc.gov/ncidod/dpd/default.htm, Accessed August, 2005.

Garcia, LS. Diagnostic Medical Parasitology. 4th ed. Washington DC: ASM; 2001; 6.

Leber AL, Movak SM In: Murray PR, Baron EJ, Pfaller MA, Tenover FC, Yolken RH, eds. Manual of Clinical Microbiology. 7th ed. Washington DC: ASM Press; 1999; 1401.

Giardia lamblia

Giardia lamblia trophozoites or cysts were identified in this specimen. Giardia lamblia is a flagellated protozoan that infects the small intestine. Cysts are passed in stool and spread by the fecal-oral route. Waterborne transmission is the major source of giardiasis. In the USA, giardiasis is one of the most common intestinal infections.

Many cases are asymptomatic. However, these persons pass infective cysts and need to be treated. Symptoms of acute giardiasis generally appear 1 to 3 wk after infection. Symptoms are usually mild and include watery malodorous diarrhea, abdominal cramps and distention, flatulence and eructation, intermittent nausea, epigastric pain and greasy stools that tend to float. Low-grade fever, chills, malaise, and headaches may be present. Malabsorption of fat and sugars can lead to significant weight loss in severe cases.

The treatment of choice is metronidazole (250 mg tid x 5 days for adults, 15 mg/kg/day in 3 doses x 5d for pediatrics). Paromomycin (25-35 mg/kg/day in three dosesx 7 days) is the alternative for treating G. lamblia during pregnancy. Other therapeutic alternatives include tinidazole (2g once, adult dose), and furazolidone (100 mg qid x 7-10 days, adult dose). Natural substances include berberine, grapefruit seed extract, and quassia. Fatty foods should be avoided, as Giardia feeds on bile salts.

Additional Information:

CDC. Giardiasis Surveillance, United States, 1992-1997. MMWR 2000;49,SS-7:1-13. Lengerich EJ, Addiss DG, Juranek DD. Severe giardiasis in the United States . Clin Infect Dis 1994;18:760-3.

Addiss DG, Davis JP, Roberts JM, Mast EE. Epidemiology of giardiasis in Wisconsin . Increasing incidence of reported cases and unexplained seasonal trends. Am J Trop Med Hyg 1992;47:13-9.

Addiss DG, Juranek DD, Spencer HC. Treatment of children with asymptomatic and nondiarrheal Giardia infection. Pediatr Infect Dis J 1991;10:843-6.

Bartlett AV, Englander SJ, Jarvis BA, Ludwig L, Carlson JF, Topping JP. Controlled trial of Giardia lamblia: Control strategies in day care centers. Am J Public Health 1991;81:1001-6.

Kreuter AK , Del Bene VE, Amstey MS. Giardiasis in pregnancy. Am J Obstet Gynecol



1981;40:895-901.

References:

Sanford JP. The Sanford Guide to Antimicrobial Therapy. 35th edition. Gilbert DN, Moellering Jr, RC, Sande MA, eds. Hyde Park (VT): Antimicrobial Therapy Inc; 2005.

Abramowicz, M. The Medical Letter On Drugs and Therapeutics. Drugs For Parasitic Infections. New Rochelle (NY): The Medical Letter, Inc.

Beers, M. H., & Berkow, R. (Eds.). The Merck Manual of Diagnosis and Therapy Online. http://www.merck.com/mrkshared/mmanual/section13/chapter161/161a.jsp, Accessed August, 2005.

CDC Division of Parasitic Diseases website. http://www.cdc.gov/ncidod/dpd/default.htm, Accessed August, 2005.

Garcia, LS. Diagnostic Medical Parasitology. 4th ed. Washington DC: ASM; 2001; 6.

Leber AL, Movak SM In: Murray PR, Baron EJ, Pfaller MA, Tenover FC, Yolken RH, eds. Manual of Clinical Microbiology. 7th ed. Washington DC: ASM Press; 1999; 1401.

Giardia Lamblia

Giardia lamblia was detected by enzyme immunoassay in this specimen. Giardia lamblia is a single-celledparasite (protozoa), which is the most frequent cause of non-bacterial diarrhea in the United States. The Centers for Disease Control and Prevention (CDC) estimates that as many as 2.5 million cases of Giardia infection occur annually in the U.S., or almost one for every 100 persons [1]. Symptomatic individuals may experience diarrhea, abdominal cramps, dehydration, malabsorption, loss of appetite,anemia, and/or weight loss 1-2 weeks following the ingestion of one or more cysts. Typically, symptomswill last 1-2 weeks and most acute infections are self-limiting. Some individuals may be completely asymptomatic. Approximately 40% of patients diagnosed with giardiasis will demonstrate disaccharide intolerance, particularly lactose, that may last up to six months. Chronic cases of giardiasis may last months to years, and are more difficult to treat. Chronic giardiasis may lead to a malabsorption syndrome, weight loss, and general weakness and fatigue. Resistance to drug treatment is common; however, Metronidazole (Flagyl) is quite effective.

Giardia lives in the intestines of infected humans or animals. Contamination with Giardia from soil, food, water, or surfaces can occur from contact with feces from infected sources. Giardia is not spread by contact with blood. Giardia is recognized as one of the most common causes of waterborne outbreaks [2]. Prevalence of giardiasis in adults has been estimated to be 4-7%, most of which are asymptomatic [3]. Higher prevalence rates have been reported in children [4] and homosexual men [5,6]. According to the Food and Drug Administration, the higher prevalence of giardiasis in children vs. adults suggests that many individuals have a lasting immunity following infection [7]. Person to person transmission is common in day-care centers where diapering is done, as well as ininstitutions for mentally handicapped patients.



http://www.cdc.gov/ncidod/dpd/parasites/giardiasis/factsht_giardia.htm

http://vm.cfsan.fda.gov/~mow/chap22.html

1. Giardiasis Surveillance-United States, 1992-1997. Centers for Disease Control and Prevention, August 2000.2. MMWR CDC Surveill Summ. 1998;47(5):1-34.3. Kappus KD, Ludgren RG, Juranek DD. Intestinal Parasitism in the United States: update on a continuing problem. Am J Trop Med Hyg 1994;50(6):705-13.4. Addiss DG. Evaluation of a commercially available enzyme-linked immunoabsorbent assay for Giardia lambia antigen in stool. J Clin Micro 1991;29(6):1137-1142.5. Esfandiari A, Swartz J, Teklehaimanot S. Clustering of giardiosis among AIDS patients in Los Angeles County. Cell Mol Biol 1997;43(7):1077-83.6. Esfandiari A, Jordan WC, Brown CP. Prevalence of enteric parasitic infection among HIV-infected attendees of an inner city AIDS clinic. Cell Mol Biol 1995;41 Suppl 1:S19-23.7. The Bad Bug Book. US Food & Drug Administration, Center for Food Safety and

Lysozyme

The level of lysozyme, a biomarker of inflammation, is elevated in this specimen. Lysozyme is an enzyme that catalyzes the hydrolysis of specific glycosidic bonds in mucopolysaccharides that constitute the cell wall of gram-positive bacteria. Lysozyme is an antibacterial defense present in the G.I. tract and is secreted by granulocytes, macrophages, Paneth cells, and Brunner’s Glands as well as normal colonic crypt cells [1]. The main source for fecal lysozyme is the intestinal granulocytes.

Moderate elevations in fecal lysozyme are commonly associated with significant overgrowth of enteropathogens such as years or dysbiotic bacteria. Markedly elevated levels of fecal lysozyme have been identified in colonic inflammatory bowel disease (IBD), such as Crohn’s disease and ulcerative colitis as well as other non-IBD G.I. diseases with diarrhea, compared to healthy controls [2,3]. In Crohn’s disease, excess lysozyme may be a result of active secretions of macrophages in the lamina propria, and monocytic cells in the granulomas (sites of G.I. inflammation) [4]. In ulcerative colitis, it has been postulated that elevations in fecal lysozyme may be secondary to intestinal loss of granulocytes and their secretory granules [5]. Additionally, Paneth cell metaplasia, a phenomenon that occurs with various inflammatory conditions of the large intestine, may be a minor contributor to fecal lysozyme elevations [5]. Paneth cells are part of the intestinal epithelial lining found in the deepest part of intestinal cryptwhich are the crypts of Lieberkühn. Paneth cells contain lysozyme in their secretory granules, and combined with their phagocytic capability, help to regulate intestinal microbial flora [5].

Lysozyme is helpful in the determination of colonic inflammatory activity rather than small bowel disease [2]. Slightly elevated levels of lysozyme may be treated with anti-inflammatory agents or by removing the antagonist, such as enteroinvasive microorganisms or allergens. Moderate to high levels of lysozyme



(>2,000) may indicate an active inflammatory bowel condition which often requires further testing such as colonoscopy. To rule out IBD, check fecal lactoferrin levels (elevated with IBD). 1. Saito H, Ksajima T, Masuda A, et al. Lysozyme localization in human gastric and duodenal epitheleum. Cell Tissue Res 1988; 251:3-7-313.2. Van der Sluys Veer A, Brouwer J, Biemond I, et al. Fecal lysozyme in assessment of disease activity in inflammatory bowel disease. Dig Dis & Sci. 1998;43(3):590-5.3. Klass HJ, Neale G. Serum and faecal lysozyme in inflammatory bowel disease. Gut 1978;19:233-9.4. Geboes K, Van den Oord JJ, Rutgeerts P, et al. Immunohistochemical identification of lysozyme in pseudopyloric gland metaplasia in Crohn’s disease. Hepatogastroenterology 1986;90:1121-8. 5. Stamp GWH, Poulsom R, Chung LP, et al. Lysozyme gene expression I inflammatory bowel disease. Gastroenterol 1992;103:532-538.

Fecal Lactoferrin

The level of fecal lactoferrin, a biomarker of serious gastrointestinal inflammation, is abnormally high in this fecal sample. Fecal lactoferrin is elevated in association with Inflammatory Bowel Disease (IBD) such as Ulcerative Colitis (UC) or Crohn’s Disease (CD)[1,2], but NOT Irritable Bowel Syndrome (IBS)[1,3]. Therefore, assessment of fecallactoferrin levels enables distinction between IBD and non-inflammatory IBS. Such distinction is critical because, although both IBD and IBS may share some common symptoms such as diarrhea, abdominal cramping and weight loss, the diseases are treated quite differently. IBD may become life threatening, requires life long treatment and possibly surgery. In contrast, IBS is often effectively treated with dietary restrictions, stress reduction and medication.

Gastrointestinal inflammation associated with IBD is associated with increased infiltration of activated neutrophils into the mucosa and increased release of lactoferrin into the gut[1,4,5]. Patients with inflammation of the GI tract, such as IBD (but not IBS), exhibit elevated lactoferrin concentrations in the feces[1].

Clinical studies have shown that fecal lactoferrin levels of healthy persons are similar to IBS patients, but markedly increased in patients with active IBD[1,3]. Patients with IBD oscillate between active and inactive disease states, and fecal lactoferrin levels increase 2-3 weeks prior to onset of clinical symptoms[6]. During remission and effective treatment, fecal lactoferrin decreases significantly. Therefore disease activity, and efficacy of treatment can be monitored by following fecal lactoferrin levels. The test can be ordered separately to track disease activity in patients with IBD.

Moderately elevated levels of fecal lactoferrin can occur, with fecal red blood cells andleukcytes, in association with invasive enterpathogens [7,8]. Such levels would beexpected to be much lower than those associated with the active phase of IBD. Therefore,with moderately elevated levels of fecal lactoferrin, one should check for the presence ofenteropathogens (eg. Shigella, Campylobacter, Clostridium difficile).



Guidelines for interpreting the results of this test are provided by the results of a large multi-center clinical study which evaluated fecal lactoferrin levels in 180 patients suffering with IBS and IBD (UC and CD) compared to 56 healthy controls.

FECAL LACTOFERRIN GROUP # of SPECIMENS mean mcg/ml +/- SE

Inactive UC 41 67 +/- 24

Active UC 31 815 +/- 789

Inactive CD 26 239 +/- 83

Active CD 51 672 +/- 242

IBS 31 1.3 +/- 0.3

Healthy Controls 55 1.6 +/- 0.4

1. Kane, S.V., Sandborn, W.J., Rufo, P.A., et al. Am. J. Gastroenterol. (2003)98(6):1309-14.2. Sugi, K., Saitoh, O., Hirata, I., et al. Am. J. Gastroenterol. (1996)91(5):927-33.3. Buderus, S., Lohmann, N., Boone, J. et al. Suppl. Gastroenterol. (2002)122:A-219:St392.4. Baveye, S., Elass, e., Mamurer, J. et al. Clin. Lab. Med. (1999) 37:281-6.5. Fine, K.D., Ogunji, G., Niehaus, M. et al. Am J. Gastroenterol. (1993):1300-05.6. Walker, T., Sandborn, W., Boone, J., et al. Am J. Gastroenterol. (2003)98:S246:7427. Huicho, L., Garaycochea, V., Uchima, N. et al. Ped. Infect. Dis. J. (1997)16(7):644-7.8. Guerrant, R.L., Araujo, V., Soares, E. et al. J. Clin. Microbiol. (1992)30(5):1238-42.

White Blood Cells (WBCs)

The number of WBCs in this specimen is higher than expected. Elevated levels of white blood cells in the stool are an indication of an inflammatory process resulting in the infiltration of leukocytes within the intestinal lumen. This could be the result of an inflammatory disorder such as



Colitis [1,2] or Crohn’s disease [2]. Enteroinvasive bacteria such as Campylobacter, Shigella, and Salmonella, and enteropathogenic parasites such as Giardia, Blastocystis, Cryptosporidium, and Entamoeba can be a cause of inflammation to the mucosal lining and have been isolated in the presence of fecal leukocytes. WBCs are often accompanied by mucus and blood in the stool [3-5]. Other conditions that may produce WBCs in the stool include localized abscesses and anal fistulas [6]. A positive WBC result requires identification and eradication of the cause of inflammation and possible anti-inflammatory therapy.

1. Zins BJ, Tremaine WJ, Carpenter HA. Collagenous colitis: mucosal biopsies and association with fecal leukocytes. Mayo Clin Proc 1995;70(5):430-3.2. Seva-Pereira A, Franco AO, de Magalhaes AF, et al. Diagnostic value of fecal leukocytes in chronic bowel disease. Rev Paul Med 1994;112(1):504-6. 3. Patwari Ak, Deb M, Dudeja M, Jayasheela M, et al. Clinical and laboratory predictors of invasive diarrhoea in children less than five years old. J Diarrhoeal Dis Res 1993;11(4):211-6.4. Hossain MA, Albert MJ. Effect of duration if diarrhoea and predictive values of stool leukocytes and red blood cells in the isolation of different serogroups and serotypes of Shigella. Trans R Soc Trop Med Hyg 1991;85(5):664-6.5. Larrosa-Haro A, Ruiz-Perez M, Aguilar-Benavides S. Utility of studying feces for the diagnosis and management of infants and preschool children with acute diarrhea. Salud Publica Mex 2002;44(4):328-34.6. Becker W, Fischbach W, Jenett M, et al. 111In-oxine-labelled white blood cells in the diagnosis and follow up of Crohn’s disease. Klin Wochenschr 1986;64(3):141-8.

Mucus

Mucus was detected in this specimen. The presence of pus or mucus in the stool may result from prolonged irritation to the intestinal mucosa and may be secondary to a proliferation of GIenteropathogens such as bacteria [1-3], yeast [4], or parasites [4,5]. It can also be associated with an inflammatory bowel condition [6,7]. Mucus is also secreted by the intestinal mucosa in response to parasympathetic excitability such as spastic constipation, mucus colitis, neoplasm of the rectum, or villous adenoma of the colon [8]. A positive mucus result requires treatment of the cause of inflammation and possibly anti-inflammatory therapy. Microbial and microscopic studies of the stool are useful detecting dysbiotic bacteria, fungi, or parasites. Localized abscesses and inflammatory disorders should also be ruled out.

1. Patwari Ak, Deb M, Dudeja M, Jayasheela M, et al. Clinical and laboratory predictors of invasive diarrhoea in children less than five years old. J Diarrhoeal Dis Res 1993;11(4):211-6.2. Nelson EA, Mok TC, Yu LM. Retrospective comparison of management of gastro-enteritis in hospitalized children. Ann Trop Paediatr 2002;22(2):165-71. 3. de Boissieu D, Chaussain M, Badoual J, et al. Small bowel overgrowth bacterial overgrowth in children with chronic diarrhea,



abdominal pain, or both. J Pediatr 1996;128(2):203-7.4. Mishra OP, Dhawan T, Singla PN, et al. Endoscopic and histopathological evaluation of preschool children with chronic diarrhea. J Trop Pediatr 2001; 47(2):77-80.5. Larrosa-Haro A, Ruiz-perez M, Aguilar-Benavidas. Utility of studying feces for the diagnosis and management of infanmts and preschool children with acute diarrhea. Salud publica Mex 2002;44(4):328-24.6. Kwan AC, Hu WH, Chan YK, et al. Prevalence of irritable bowel syndrome in Hong Kong. J Gastroenterol Heapatol 2002;17(11):1180-6.7. Pan G, Lu S, Han S. A study on the symptoms and diagnostic criteria of irritable bowel syndrome in Chinese. Zhonghua Nei Ke Za Zhi 1999;38(2):81-4.8. Fischbach. A manual of laboratory and diagnostic tests. Philadelphia:

Secretory IgA (sIgA)

The concentration of sIgA is abnormally high in this fecal specimen. Immunological activity in the gastrointestinal tract can be assessed using secretory immunoglobulin A (sIgA). Secretory IgA is the predominant antibody or immune protein the body manufactures and releases in external secretions such as saliva, tears, and milk [1]. It is also transported through the epithelial cells that line the intestines out into the lumen. Secretory IgA represents the first line of defense of the GI mucosa and is central to the normal function of the GI tract as an immune barrier [1]. As the principal immunoglobulin isotype present in mucosal secretions, sIgA plays an important role in controlling intestinal milieu which is constantly presented with potentially harmful antigens such as pathogenic bacteria, parasites, yeast, viruses, abnormal cell antigens, and allergenic proteins [1]. Secretory IgA antibodies exert their function by binding to antigenic epitopes on the invading microorganism limiting their mobility and adhesion to the epithelium of the mucus membrane [2]. This prevents the antigens from reaching systemic circulation allowing them to be excreted directly in the feces.

Elevated fecal sIgA is an appropriate response to an antigenic presence. Microbial and microscopic studies of the stool are useful in identifying if bacteria, yeast, or parasites are present. Eradication of the pathogenic microorganisms will bring sIgA back down into the normal range. Elevated sIgA levels have been observed in the absence of bacteria, yeast or parasites, in individuals with atopic conditions such as food allergies, urticaria, and dermatitis.

References:

1. Crago SS, Tomasi TB. Mucosal Antibodies, Food Allergy and Intolerance. Bailliere Tindall/W.B. Saunders 1987;167-89.2. Roberts JA. Factors predisposing to urinary tract infections in children. Ped Neph 1996;10:517-522.3. Carins J, Booth C. Salivary immunoglobulin-A as a marker of stress during strenuous physical training. Aviat Space Environ Med 2002;73(12)1203-7. 4. Teodosio MR, Oliveira ECM. Urinary secretory IgA after nutritional



rehabilitation. Braz J Med Biolog Res 1999;32-421-4265. Alverdy J. Effects of glutamine-supplemented diets on immunology of the gut. J Parent Enteral Nutr 1990;14(4):1095-1135.6. Burke DJ, et al. Glutamine-supplemented total parenternal nutrition improves gut function. Arch Surg 1989;24:2396-2399.7. Alverdy JA. The effect of total parenternal nutrition on gut lamina propria cells. J Parent. Enteral Nutr 1990;14(suppl).8. Qamar A, Aboudola S, Warny M, et al. Saccharomyces boulardii stimulates intestinal immunoglobulin A immune response to clostridium difficile toxin A in mice. Infect Immun 2001;69(4):2762-5.9. Buts JP, Bernasconi P, Vaerman JP, et al. Stimulation of secretory IgA and secretory component of immunoglobulins in small intestine of rats treated with Saccharomyces boulardii. Dig Dis Sci 1990;35(2):251-6.

Short Chain Fatty Acids (SCFAs)

The relative and/or total amounts of SCFAs are abnormal in this specimen. In infants, microbial colonization and subsequent SCFA production is a gradual process which is largely determined by environmental exposure, maternal gut microflora, breastfeeding, and possibly genetics [1]. The establishment of an adequate distribution of healthy flora in the gut is crucial in the health of both infants and adults because of the ”competitive exclusion” process of dysbiotic flora [1]. Healthy microflora, such as Lactobacillus and Bifidus generate large amounts of SCFAs (acetic, proprionic, butyric, and valeric) which decrease the pH of the intestine and therefore make the environment unsuitable for pathogens, including bacteria and yeast [1]. SCFAs are the end product of the bacterial fermentation process of dietary fiber by beneficial flora in the gut and play an important role in the prevention of intestinal dysbiosis [1].

The amount and types of SCFAs produced by colonic bacteria will depend on factors such as type offiber consumed and overall intestinal health. For example, more SCFAs in general are produced bygums and pectins than oat fiber or corn bran; more propionate and butyrate are produced by bacterial activity on gums than pectins [2]. Antibiotic-induced diarrhea may be secondary to decreased colonic fermentation of carbohydrates and decreased overall production of SCFAs [3].

Studies show that SCFAs have numerous implications in gut physiology and health. SCFAs decrease inflammation, stimulate healing, and contribute to normal cell metabolism and differentiation [4].Acetate, propionate and butyrate have been demonstrated to potentially improve the microcirculation in the intestinal mucosa thereby improving its growth and repair [5,6]. Rectal irrigation with SCFAs can result in improvement of ulcerative colitis [7]. Butyrate and propionate contribute toapoptosis of colorectal cells by increasing the production of reactive oxygen species in the gut [8]. Butyrate also has a positive effect on the differentiation of colonocytes, and this may account for the protective effect of dietary fiber against colorectal cancer [9]. Probiotics and increased dietary fiber can improve/normalize SCFA status.

1. Lispki E. Digestive Wellness. New Canaan(CN):Keats Publishing;1996.2. Titgemeyer EC, Bourquin LD, Fahey GC Jr, et al. Fermentability of various fiber sources by human fecal bacteria in vitro. Am J Clin Nutr 1991;53(6):1418-24.



3. Clausen MR, Bonnen H, Tvede M, et al. Colonic fermentation to short- chain fatty acids is decreased in antibiotic-associated diarrhea. Gastroenterol 1991;101(6):1497-504.4. Hickman MA. Interventional nutrition for gastrointestinal disease. Clin Tech Small Anim Pract 1998;13(4):211-6.5. Mortesen FV, Nielsen H, Aalkjaer C, et al. Short chain fatty acids relax isolated resistance arteries from the human ileum by a mechanism dependent on anion-exchange. Pharmacol Toxicoli 1994;75(3-4):181-5.6. Mortesen FV, Nielsen H, Mulvaney MJ, et al. Short chain fatty acids dilate isolated human colonic reistance arteries. Gut 1990;31(12):1391-4.7. Breuer RI, Buto SK, Christ ML, et al. Rectal irrigation with short-chain fatty acids for distal ulcerative colitis. Preliminary report. Dig Dis Sci 1991;36(2):185-7.8. Giardina C, Inan MS. Nonsteroidal anti-inflammatory drugs, short-chain fatty acids, and reactive oxygen metabolism in human colorectal cells. Biochim Biophys Acta 1998;1401(3):277-88.9. Basson MD, Sgambati SA. Effects of short-chain fatty acids on human rectosigmoid mucosal colonocyte brush border enzymes. Metabolism 1998;47(2):133-4.


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