Updated: Jul 24, 2008
Dientamoeba fragilis is a nonflagellate trichomonad parasite and is one of the smaller parasites that can live in the human large intestine. Unlike most other intestinal protozoa, its life cycle has no cyst stage; thus, infection between humans occurs during the trophozoite stage. Organisms move most actively in fresh feces but quickly round up when left standing, are sensitive to an aerobic environment, and die and dissociate when placed in saline, tap water, or distilled water. The mode of transmission is believed to be through direct fecal-oral spread and, possibly, through coinfection of eggs of Enterobius vermicularis (ie, pinworm).
Organisms infect mucosal crypts of the large intestine that are located close to the mucosal epithelium, from the cecum to the rectum; however, the cecum and proximal colon are usually affected. This parasite is not known to be invasive and does not cause cellular damage. It may invoke an eosinophilic inflammatory response in the colonic mucosa; thus, symptoms are related to the superficial colonic mucosal irritation. Similar to some other parasites (eg, Cyclospora cayetanensis, Giardia lamblia, Cryptosporidium parvum), the parasite D fragilis has been demonstrated to cause disease in humans regardless of their immune status.
Estimated prevalence in the general population in the United States and in other developed countries is most commonly 2-4%. However, much higher prevalence rates (19-69%) have been reported in specific populations, such as individuals living in crowded conditions (eg, institutions, communal living), individuals living in conditions with poor hygiene, and those traveling to developing countries.
Colonization may occur without development of disease. In adults, asymptomatic colonization is present in 75-85% of individuals affected by the parasite. In children, the opposite is true; disease develops in as many as 90% of those colonized.
No specific mortality is associated with this enteropathogen. Morbidity related to acute infection occurs in the first 1-2 weeks of the disease, with symptomatology predominated by diarrhea. Chronic infection occurs after 1-2 months of illness and is manifested by abdominal pain.
Infection may occur at any age. The most common age at which infection has been reported in children is 5-10 years. Interestingly, E vermicularis (pinworm) infection can also occur in the same age group.
| Amebiasis | Irritable Bowel Syndrome |
| Campylobacter Infections | Isosporiasis |
| Colitis | Lactose Intolerance |
| Cyclosporiasis | Malabsorption Syndromes |
| Enteroviral Infections | Protein Intolerance |
| Escherichia Coli Infections | Salmonella Infection |
| Gastroenteritis | Somatoform Disorder: Pain |
| Giardiasis | Soy Protein Intolerance |
| Intestinal Protozoal Diseases |
Allergic gastroenteritis
Eosinophilic gastroenteritis
Celiac disease
The goal of therapy is eradication of the parasite (see Medication).
Parasite biochemical pathways are different from the human host; thus, toxicity is directed to the parasite, egg, or larvae. Mechanism of action varies within the drug class. Antiparasitic actions may include the following:
Imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa.
500-750 mg PO tid for 10 d
20-40 mg/kg/d PO divided tid for 10 d; not to exceed 2 g/d
Cimetidine may increase toxicity of metronidazole; may increase effects of anticoagulants; may increase toxicity of lithium and phenytoin; disulfiramlike reaction may occur with PO ingested ethanol
Documented hypersensitivity; first trimester of pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Contraindicated in first trimester of pregnancy; adjust dose in hepatic disease; monitor for seizures and development of peripheral neuropathy
Inhibits bacterial protein synthesis by binding with 30S and, possibly, 50S ribosomal subunits.
500 mg PO qid for 10 d
40 mg/kg/d PO divided qid for 10 d; not to exceed 2 g/d
Bioavailability decreases with antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate; can decrease effects of PO contraceptives, causing breakthrough bleeding and increased risk of pregnancy; can increase hypoprothrombinemic effects of anticoagulants
Documented hypersensitivity; severe hepatic dysfunction
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Photosensitivity may occur with prolonged exposure to sunlight or tanning equipment; reduce dose in renal impairment; consider drug serum level determinations in prolonged therapy; use during tooth development (last one half of pregnancy through age 8 y) can cause permanent discoloration of teeth; Fanconilike syndrome may occur with outdated tetracyclines
Amebicide used in treatment of D fragilis.
650 mg PO tid for 20 d
30-40 mg/kg/d PO divided tid for 20 d; not to exceed 2 g/d
None reported
Documented hypersensitivity; hepatic damage
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Avoid long-term use because optic neuritis, optic atrophy, and peripheral neuropathy have been reported; use caution in patients with thyroid disease
Amebicidal and antibacterial aminoglycoside obtained from strain of Streptomyces rimosus; active in intestinal amebiasis.
25-35 mg/kg/d PO divided tid for 7 d
Administer as in adults
Nephrotoxic potential may increase with concurrent administration of other aminoglycosides, penicillins, cephalosporins, amphotericin B, and loop diuretics
Documented hypersensitivity; intestinal obstruction
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Because of narrow therapeutic index and toxic hazards associated with extended administration, do not use for long-term therapy; caution in renal failure, hypocalcemia, myasthenia gravis, and conditions that depress neuromuscular transmission; adjust dose in renal impairment
Control measures to limit spread of parasites include the following:
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Dientamoeba fragilis, D fragilis, Enterobius vermicularis, pinworm, trichomonad parasite, intestinal protozoa, large intestine parasite, Cyclospora cayetanensis, Giardia lamblia, Cryptosporidium parvum, diarrhea
David R Mack, MD, FRCPC, Professor, Departments of Pediatrics and Biochemistry, Microbiology, and Immunology, University of Ottawa Faculty of Medicine; Head, Division of Gastroenterology, Hepatology, and Nutrition, Department of Pediatrics, Children's Hospital of Eastern Ontario, Canada
David R Mack, MD, FRCPC is a member of the following medical societies: American Gastroenterological Association, Canadian Association of Gastroenterology, and North American Society for Pediatric Gastroenterology and Nutrition
Disclosure: Nothing to disclose.
Michael D Nissen, MBBS, BMedSc, FRACP, FRCPA, Associate Professor in Biomolecular, Biomedical Science & Health, Griffith University; Director of Infectious Diseases and Unit Head of Queensland Paediatric Infectious Laboratory, Sir Albert Sakzewski Viral Research Centre, Royal Children's Hospital
Michael D Nissen, MBBS, BMedSc, FRACP, FRCPA is a member of the following medical societies: American Academy of Pediatrics, American Society for Microbiology, Pediatric Infectious Diseases Society, Royal Australasian College of Physicians, and Royal College of Pathologists of Australasia
Disclosure: Nothing to disclose.
Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner
Martin Weisse, MD, Program Director, Associate Professor, Department of Pediatrics, West Virginia University
Martin Weisse, MD is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, and Pediatric Infectious Diseases Society
Disclosure: Nothing to disclose.
Robert W Tolan Jr, MD, Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine
Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility
Disclosure: GlaxoSmithKline Honoraria Speaking and teaching; MedImmune Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; sanofi pasteur Honoraria Speaking and teaching; Baxter Healthcare Honoraria Speaking and teaching
Russell W Steele, MD, Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine
Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association
Disclosure: None None None
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