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Digestive Conditions / Parasites
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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).
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Symptoms of parasitic infection |
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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 
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 this link.
Detection rates are a function of:
- Specimen collection and handling
- Number, kind and type of specimens examined
- Concentration procedures
- Staining procedures
- Macroscopic and microscopic examination techniques
- Quality of microscopes
- Use of advanced immunoassay methods
- Quality of training, frequency of practice and dedication of laboratory personnel.
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.
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. 
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).
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