Parasites
by Dr. Gary Farr on 23 May 2002

What is it?/Characteristics/Cause

Intestinal Parasites

{what_is_it}

The two major classifications, predator and scavenger, are differentiated by their nutritional relationships.7 Further modification leads to symbiosis and commensalism. Parasitism is where the host is injured through the activities of the parasite during an intimate and protracted relationship between the two.

Some organisms have a changing interaction with their host — sometimes as a parasite and sometimes commensal.

Few people realize the enormous impact of parasites and diarrheal diseases on human health. Diarrheal diseases ( bacterial as well as parasitic) constitute the greatest worldwide cause of morbidity and mortality.1 Numerous studies show parasitic infection up to 99% in undeveloped countries.2

In the United States, diarrheal diseases caused by intestinal infections are the third leading cause of morbidity and mortality. Most Americans have grown up with modern sanitation, and it is often assumed parasitic infections are encountered only in impoverished foreign countries.3 According to Neva, "The United States citizen can acquire amebiasis, giardiasis, pinworms, and strongyloides, for example, without so much as a passport application."4

The increase in worldwide travel, coupled with increasing immigration into the United States, contributes to the spread and incidence of parasitic infections. In a study of outpatients at the Gastroenterology Clinic in Elmhurst, N.Y., a 74% incidence of parasites was found.5 A total of 20% of this population harbored pathogens. One survey of public health laboratories reported that 15.6% of specimens examined contained a parasite.6 At Great Smokies Diagnostic Laboratory, almost 30% of specimens examined are positive for a parasite.

The prevalence of parasitic infections in the United States is difficult to quantify. Most figures are underestimates that can be traced to inadequate parasitologic training of physicians and laboratory technicians.3 As detection methods become more accurate and sophisticated, physicians are recognizing the increased incidence of parasitic infection and its relationship to a broad spectrum of diseases.

Common Protozoal Parasites

Information on parasites is available in several excellent texts.24,32 The protozoa that parasitize the intestinal lumen belong to five groups: amoebae, flagellates, ciliates, coccidia and microsporidia. Most are transmitted through fecally contaminated food, water or other materials. Contaminated water supplies are a particular problem because many cysts are not killed by usual levels of chlorination.

Blastocystis hominis

Blastocystis hominis is the most prevalent parasite but often isn’t detected due to poor laboratory techniques. 33 At Great Smokies Lab, Blastocystis is found in more than 20% of clinical specimens.34 The weight of evidence supports treating it as a potential pathogen (disease causing organism).35 Together with other weak pathogens, it is associated with many chronic conditions, including irritable bowel, chronic fatigue and arthritic/rheumatoid complaints.

Three forms have been identified, and the vacuolated form is most commonly seen in fecal specimens. Blastocystis has been found to produce gastrointestinal cramps, vomiting, sleeplessness, nausea, weight loss, lassitude, dizziness, flatus, anorexia, and pruritus. B. hominis is often found in patients with classic symptoms of irritable bowel syndrome.36 Treatment with metronidazole has been found to eradicate the organism.

Blastocystis hominis may be highly variable in its pathogenicity (its ability to cause disease). The organism is present in a number of healthy individuals, and an asymptomatic carrier state has been postulated. 37 In many patients with gastrointestinal illness, this organism is the only identifiable parasite, and these patients improve when Blastocystis is eradicated.35 We find its presence highly correlates with gastrointestinal symptoms; and, along with others, suggest it may be a pathogen in symptomatic patients.14,38

Dientamoeba fragilis

Dientamoeba fragilis, a pathogenic flagellate and one of the most frequent parasitic infections, often goes undetected due to poor laboratory technique.39-41 Symptoms include diarrhea and abdominal discomfort. It resides in the colon, has a cosmopolitan distribution, is found as a trophozoite and has no cyst stage. Transmission is by direct ingestion of the trophozoite and can be found within the eggs of some helminths, especially pinworms.

Amoeba

Amoeba including Endolimax nana, Entamoeba histolytica, E. coli and E. hartmanni are cosmopolitan in distribution. E. histolytica is linked to acute diarrhea and GI distress. However, individuals may harbor E. histolytica without obvious symptoms. Lesser known organisms Entamoeba coli, E. hartmanni and Endolimax nana are associated with chronic GI symptoms, although not generally recognized as pathogens. There is an association between E. nana infection and reactive arthritis.42 Variations in an organism’s virulence and/or the host resistance may explain variations in the degree of pathogenicity.

There are two forms of amoeba — the motile trophozoite and the cyst - and transmission is by ingestion of the cyst stage. The cyst, the infective form of the organism, resists environmental changes and may spread from person to person or indirectly via food or water. Symptoms occur primarily with tissue invasion and include intermittent diarrhea and constipation, flatulence and cramping. Intestinal infection symptoms include mild diarrhea, food intolerance, fatigue and dysentery.

Giardia lamblia

Giardia lamblia, a flagellate with cosmopolitan geographic distribution, is found in duodenal contents and bile. In the duodenum it can be demonstrated in the mucosal crypts where it attaches itself to the mucosal cells, causing gastroenteritis. When swept into the fecal stream, the trophozoite encysts. Consequently, most fecal specimens contain the encysted parasite rather than the flagellated trophozoite form, which is usually found only in severe diarrhea. In the cyst (resistant) form, they spread the disease from host to host by fecal/oral routes, either directly (as between children in day-care centers or between sexual partners) or by food and water.43 Waterborne epidemics involve mountain streams, well water and even some chlorinated community water systems.

Iodamoeba butschlii

Iodamoeba butschlii is an amoeba with a low pathogenicity associated with chronic complaints. It has a cosmopolitan distribution and is located in the lumen of the colon and cecum. Transmission is by ingestion of the cyst stage.

Fungal conidia

Fungal conidia are yeast. They are very small (two to four microns), have considerable structure (typically with pointed ends and an interior vacuole), and are difficult to culture. The few studies on this organism cite its ability to ferment complex polysaccharides to produce alcohol. In a recent review of Great Smokies’ parasitology results, we found fungal conidia in 5.4% of the samples.44 They were more prevalent in women and frequently found in the absence of other parasites. Almost all the patients suffered from gastrointestinal complaints, but diarrhea (38%), gas (33%), and bloating (33%) were most common.

At this time we know little about fungal conidia pathogenicity. Our advice is to put fungal conidia in the same category as Blastocystis hominis or yeast overgrowth and treat (or not treat) with the same criteria.

Intestinal helminths

Intestinal worms are a leading cause of morbidity and mortality and usually diagnosed by detection of eggs or larvae in fecal specimens. Some of the more common helminths are Nematodes, including Enterobius vermicularis, Ascaris lumbricoides, Trichuris trichiura, Necator americanus and Strongyloides stercoralis.

Shown below are microscopic images of actual parasites:

Click on each image for a larger image
This image shows a small parasite on the wall of the large intestine. Endolimax nana Endolimax nana Entamoeba histolytica Entamoeba histolytica

{characteristics}

In general, a parasite interferes with the host's vital processes through secretions, excretions or other products.7 These products include proteolytic enzymes that erode the intestinal wall, enterocytotoxins (from E. histolytica), and serotonin-like products.8

Parasitic infections can trigger autoimmune reactivity. The parasite might cause tissue destruction, thus releasing high amounts of self antigens which stimulate the autoreactivity.9

Symptoms/Medical Dx/Medical Tx

{symptoms}

The most common symptoms of intestinal parasitic infections are abdominal pain and moderate or severe diarrhea, but there is a wide range of both acute and chronic effects (see sidebar).

 

Symptoms of parasitic infection

 

Giardiasis is an interesting model for the systemic effects of gastrointestinal parasites. Giardia lamblia, although capable of causing acute illness (diarrhea), can hide in the GI tract for years with few symptoms.10 Among the common systemic complaints of this disease are fatigue and anorexia. It is reasonable to suspect that many long-term effects are due to phenomena occurring at or within the mucosal membranes. Zinneman reported that giardiasis is associated with reduced secretory IgA, a primary mucosal defense mechanism against foreign infections.11 Moreover, Giardia lamblia is known to be a cause of malabsorption, suggesting a decreased mucosal permeability. Giardiasis, however, is associated with asthma, urticaria, arthritis and uveitis, suggesting increased mucosal permeability.12

It could be hypothesized that giardiasis results in altered permeability — increased permeability to some types of molecules and decreased permeability to other types. Decreased secretory IgA levels, either as a cause or as a consequence of this phenomenon, would result in increased susceptibility to secondary infections and systemic symptoms.

The most common symptom of parasite infection is diarrhea, with abdominal pain as second most common symptom.10,13 Other symptoms include flatulence, foul-smelling stools, cramps, distention, anorexia, nausea, weight loss, belching, heartburn, headache, constipation, vomiting, fever, chills, bloody stools, mucus in stools and fatigue.10 Although specific symptoms are associated with certain organisms (e.g. fever with malaria), most symptoms can be present with almost any parasite. In addition, there is an increasing number of parasite cases with systemic complaints not traditionally thought to be caused by parasites. Endolimax nana has been associated with urticaria, and Blastocystis hominis with infective arthritis.14

Substantial literature associates parasites with allergy, but it isn't known whether parasites enhance the probability of getting allergies or whether being allergic predisposes one to parasitic infection.15 Two reports associate Trichuris infection with diminished mental development in children and recovery of mental function after treatment.16,17 Leo Galland, M.D. reported intestinal protozoans as an unsuspected cause of chronic illness and fatigue. 18,19 Potentially pathogenic protozoa were detected in 27% of a group of urban patients with irritable bowel syndrome.20 Organisms included B. hominis, D. fragilis, G. lamblia, E. histolytica and Entamoeba coli. Cryptosporidium, a supposed weak pathogen most frequently causing a self-limited diarrhea in adults, is a major cause of diarrheal disease in the pediatric population.21 Cryptosporidiosis has been associated with reactive arthritis and acute pancreatitis.22,23

Pathogenicity

Among the many organisms classified as parasites, only some are referred to as “pathogens.” In fact, the classification of organisms as pathogens continues to fluctuate. Few people realize that only a few decades ago Giardia lamblia, the leading cause of intestinal parasitic infections in the United States, was not considered a pathogen.24 More recently, Cryptosporidium, a well-known pathogen in animals, was identified as a human pathogen. Today, a controversy continues about the status of Blastocystis hominis. Next to yeast, B. hominis is the most frequently observed organism in fecal samples.

Part of the problem in classifying parasites is defining "pathogen" and "commensal." Many individuals harbor pathogens such as Giardia lamblia or Entamoeba histolytica but don't have discernible gastrointestinal symptoms. And conversely, the apparent pathological effects of supposed commensals such as Entamoeba coli or Endolimax nana have been reported.25-28

One hypothesis to explain variable pathogenicity is that distinct pathogenic and nonpathogenic strains of organisms appear morphologically identical.29 Another hypothesis postulates pathogenic and nonpathogenic states of an organism and proposes mechanisms whereby modulators related to the microenvironment or the host could switch the parasite from one state to the other.29

The true nature of pathogenicity, however, may rest in both hypotheses. Pathogenicity may vary depending on the parasite itself, the host, and the microecological environment where the parasite lives.

As noted by Markell: "The diet or nutritional status of the host may be of major importance in determining the outcome of a parasitic infection. The general nutritional status of the host may be of considerable importance both in determining whether or not a particular infection will be accompanied by symptoms, and in influencing their severity if present."7

Factors relevant to the parasite include production of toxins, cytolytic ability and adherence.30 Factors related to the host include immune competence, secretory IgA levels, T and B lymphocyte levels, gut motility and permeability. Affecting both the parasite and the host are the stool transit time and microenvironment (pH, fat and fiber content, the health and number of bacterial organisms making up the normal flora, and the ability of normal flora to compete for nutrients with potential pathogens). 31

{med_dx}

The diagnosis of most parasitic infections depends on the laboratory.43 For intestinal parasites, morphological demonstration of diagnostic stages is the principal means of diagnosis. The emerging area of immunodiagnostic techniques is of growing importance.

We commonly utilized Great Smokies Diagnostic Lab to determine parasitic infestations, although through the use of reflex testing (below), the parasite reflex may read independent of the lab findings. We can order a diagnostic kit and send to you to determine if you have a parasite infection. For more information regarding the Comprehensive Digestive Stool Analysis go to {cdsa}this link.

Detection rates are a function of:

Many studies show that detection rates dramatically increase with the sophistication of detection procedures, such as adding concentration, flotation, appropriate preservatives, specialized permanent stains and other methods.45-47

Various studies show that when increasing from a single specimen to multiple specimens, detection increases from less than 50% to more than 95%.46-48

In addition to using formed stools as a specimen, purged samples (induced by oral purgative) provide valuable specimens.49 Recent reports show that a rectal mucosal swab specimen aids in detection of certain parasites.

Computer-enhanced video microscopy also aids in identification and provides the physician with a picture of organisms found.

Various immunoassay techniques are now available, increasing detection of both intestinal and bloodborne parasites. Some tests detect antibody presence, while some detect antigens or use nucleic probes.

When to suspect parasitic infections

Office diagnosis of parasitic infections requires physicians to check for such symptoms as diarrhea, unexplained fever, cough, itching or rash of the skin, abdominal pain and bloody stools.

Certain people are at particular risk for infection, including those who recently traveled outside the United States and individuals who are immuno-compromised.50-52

In addition to diarrhea, the most common symptom, other symptom complexes may suggest parasitic infection. For example, amoebic colitis can mimic Crohn’s disease of the colon and ulcerative colitis.53 Fulminant amoebic colitis may be present with rectal bleeding and colonic ulcerations and can be difficult to differentiate from inflammatory bowel disease.54 Inflammatory bowel disease patients can also be carriers of amoebae. Because steroids can provoke amoebic activity and cause a fulminating colitis, it is necessary to determine if amoebae exist.

Recent reports suggest that intestinal infections with Giardia lamblia and Blastocystis hominis cause symptoms identical to those observed in patients with inflammatory bowel disease.55 Leo Galland, M.D. analyzed the prevalence using rectal swabs.56 Treatment led to resolution of symptoms in approximately 90% of the study population. As more data becomes available, stool examination for parasites may become an integral part of the evaluation of patients with inflammatory bowel disease or other undiagnosed gastrointestinal complaints.

{med_tx}

Antiparasitic drugs, while effective, are powerful pharmacologic agents to be taken with careful consideration.

Therefore, nutritional and other approaches to parasite infestation are worth noting. Leitch et al. reported that dietary fiber reduces the rate of intestinal infection by Giardia lamblia.58 The authors speculate that fiber induces mucus secretion and reduces the attachment of trophozoites. It may also affect the growth of bacterial flora, pH and the competition for nutritional resources among organisms. Measures that build and restore the gastrointestinal immune system are worthwhile interventions. Modification of bowel flora, bowel environment and digestive enzymes act synergistically in eradicating parasites.

Gastrointestinal amebiasis (an infection of the large intestine caused by tiny one- celled parasites classified as Entamoeba histolytica) is treated with nitroimidazole drugs, which kill amebas in the blood and in the wall of the intestine. These drugs include metronidazole in the United States, and tinidazole or ornidazole in other countries. Metronidazole is usually given for 10 days, either orally (by mouth) or intravenously (directly into the veins). To kill amebas living inside the lumen of the intestine, three luminal drugs are also available: iodoquinol, paromomycin, and diloxanide furoate. These luminal drugs are used in patients with active gastrointestinal symptoms and also in asymptomatic carriers (persons who pass amebas in their stools without having symptoms of amebiasis).

CRA Dx/Nutritional Tx

{nut_tx}

Mirelman reported that allicin, the active principle of garlic extract, is an inhibitor of growth for Entamoeba histolytica.59 Other studies suggest its effectiveness with other parasites as well.

Other reports claim that berberine, the active ingredient of goldenseal (Hydrastis), oregon grape root (mahonia aquifolium), and Barberry (Berberis vulgaris) are effective against Entamoeba histolytica and compare favorably to Quinacrine HCl in the treatment of giardiasis.60,61

Quassia appears to be another useful anti-helminthic, which anecdotally has been used successfully for Ascaris lumbricoides, amoebic dysentery and giardiasis. An advantage of Quassia is its low toxicity.62,63

The following supplements may be indicated:

{cra_tx}

The following reflexes will often be active:

These reflexes should be tested and treated with the proper supplementation. You should take this preliminary free test or be examined by a licensed practitioner for testing. A liver/gallbladder flush and intestinal detoxification program may also be recommended.

Diet/Chiropractic Tx/Exercise & Prevention

{diet}

In order for parasites to be able to "set up house" in a person's body, there must be an altered intestinal ecosytem exisiting. Avoid "junk" and "white trash" food. White trash food is food that is made from white flour that has no natural food value in terms of vitamins and minerals. White trash food tends to make the intestinal tract more alkaline where parasites can thrive.

If food allergies are present these will need to be tested.

{chiro_tx}

The nervous system, along with the links to the digestive system play an integral part in the digestive process. Go {chiropractic}here for additional information regarding chiropractic.

{prevention} {fre_test_digest}

Use our {find_doctor} NutritionLocator to find a doctor in your area.

References

References

1 Thorne GM. Infect Dis Clin North Am 1988;2(3):747-51.
2 Gonçalves JF et al. Rev Inst Med Trop Sao Paulo 1990;32(6):428-35.
3 Dalton HP et al. Interpretive Medical Microbiology 1986;501.
4 Neva FA. Parasitic diseases of the GI tract in the United States. DM 1972 (June 3).
5 Wajsman R et al. Prevalence of B. hominis and other parasites in an immigrant population. Presentation at American College of Gastroenterology, 56th Annual Meeting, October 13-15, 1991.
6 Johnston TS. Drug Intell Clin Pharm 1981; 15(2):103-10.
7 Markell EK et al. Medical Parasitology 1986. 6th Edition:6-9.
8 Guerrant R. Parasitic causes of disease. Textbook of Secretory Diarrhea. Raven Press, NY 1990;273-80.
9 Abu-Shakra M. Autoimmunity 1991; 9(4):337-44.
10 Wolfe MS. Clin Microbiology Review 1992; 5(1):93-100.
11 Zinneman HH et al. Dig Dis 1972;17(9):793-7.
12 Gillon J. Qtr J Med, NS LIII 1984; (Winter) 209:29-39.
13 Jones JE. Primary Care 1991;18(1):1-12.
14 Lee MG et al. Ann Rheum Dis 1990; 49(3):192-3.
15 Moqbel R et al. Clin Exp Allergy 1990;20:611-8.
16 Callender JEM et al. Lancet 1992; 339:181.
17 Nokes C et al. Lancet 1992;339:500.
18 Galland L et al. J Nut Med 1990;1:27-31.
19 Galland L. J Adv Med 1989;2(4):539-52.
20 Galland L. Intestinal protozoan and Irritable Bowel Syndrome. Presentation at Am Acad Family Pract, Oct 1992; San Diego, CA.
21 White DG et al. Brit Med J 1990; 300(March):774-7.
22 Hay EM et al. Brit Med J 1987;295(July):249.
23 Hawkins SP et al. Brit Med J 1987; 294(Feb):483.
24 Sun T. Color Atlas and Textbook of Diagnostic Parasitology. 1988.
25 Wahlgren M. Lancet 1991;337:675.
26 Corcoran GD et al. Lancet 1991;338:254.
27 Veraldi S et al. Int J Derm 1991;30:376.
28 Rolston KVI et al. N Engl J Med 1986; (July 17):192.
29 Ravdin JI. Am J Trop Med Hyg 1989;41(3):40-8.
30 Ravdin JI. Clin Res 1990;38(2):215-25.
31 Lee MJ. Nutr Cancer 1991;75-6.
32 Ash LR et al. Atlas of Human Parasitology. 1980; Second Edition.
33 Lee MJ. J Clin Microbiology 1991; Sep:2089.
34 Fleming C et al. Poster presentation at ASCP/CAP Spring Meeting 1991; March 2-7, Nashville, Tenn.
35 Zierdt CH. Clin Microbiol Rev 1991;4(1):61-79.
36 Johanson JF et al. Am College Gastroenterol, 57th Ann Mtg, Oct 1992; Miami Beach, FL.
37 Doyle PW et al. J Clin Microbiol 1990; 28(1):116-21.
38 Babb RR et al. West J Med 1989;151(5):518-9.
39 Grendon JH et al. Public Health Rep May-June 1991;106(3):322-5.
40 Yang J et al. Am J Trop Med Hyg 1977; 26(1):16-22.
41 Kean BH et al. Am J Dig Dis 1966;II(9):735-46.
42 Burnstein L et al. J Rheumatology;10:514-5.
43 Balows A et al. Manual of Clinical Microbiology 1991; 5th Edition. 702:754-6.
44 Lee M et al. Identification and characterization of the yeast Kloeckera in human stool samples. Presentation at ASM 92nd General Meeting, May 26-30, 1992, New Orleans, LA.
45 Gardner BB et al. J Clin Micro 1980; 12(5):656-8.
46 Sawitz WG et al. Am J Trop Med 1942; 22:131-6.
47 Markell EK et al. Medical Parasitology 1986; 6th Edition. 336.
48 Ash LR et al. Parasites: a guide to laboratory procedures and identification. 1987; 4-5.
49 Dowell LB. Off J AMT 1961;(Jan-Feb):23-5.
50 Owen RL. Parasitic diseases. Gastrointestinal Disease:Pathophysiology, Diagnosis, Management. 1989: 1402-18.
51 Smith PD et al. Ann Intern Med 1992; 116(1):63-77.
52 Kotler DP et al. Ann Intern Med 1990; 113(6):444-9.
53 Korelitz BI. J Clin Gastroent 1989;11(4):373-5.
54 Radvin JL. J Infect Dis 1989;159:420-9.
55 O'Gorman MA et al. Am J Gastroenterol 1989;84:1192.
56 Galland L et al. Am J Gastroenterol 1989; 84:1181.
57 The Medical Letter. Drugs for parasitic infections. December 1993;35(911):111.
58 Leitch GJ et al. Am J Trop Med Hyg 1989; 41(5):512-20.
59 Mirelman D et al. J Infec Dis 1987: 156(1):243-4.
60 Subbaiah TV et al. Nature 1967; 215:527-8.
61 Gupte S. Am J Dis Child 1975;129:866.
62 Kirby GC et al. Biochem Pharmacol 1989; 38(24):4367-74.
63 Phillipson JD et al. Trans Royal Society Trop Med Hyg 1991;85:18-21.

© Copyright 2000-2005, BecomeHealthyNow.com, Inc. All rights reserved.