AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Background

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).

Pathophysiology

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.

Frequency

International

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.

Mortality/Morbidity

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.

Age

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.

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

History

• Abdominal pain and diarrhea are the most common symptoms.
• • The most common complaints, abdominal pain and diarrhea, commonly occur together following infection with D fragilis.
  • In acute infection, duration of symptoms is 1-2 weeks.
  • • Diarrhea predominates in acute infection.¹
    • Diarrheal history may vary, with either consistently frequent stools (1-4 stools per day) or episodic occurrence of diarrhea.
    • Stools are greenish brown, and their consistency varies from watery to sticky.
    • Occasionally, mucus is noted in the stools, but hematochezia is unusual.
• In chronic infection, duration of symptoms is greater than 1-2 months.
• • Abdominal pain is the more common complaint.
  • In children, pain varies with regards to location, duration, and character.
• Other GI complaints include the following:²
• • Anorexia
  • Weight loss
  • Nausea
  • Vomiting
  • Bloating
  • Flatulence
  • Alternating constipation and diarrhea
• Nonintestinal complaints include the following:
• • Headache
  • Fever
  • Malaise
  • Fatigue
  • Irritability
  • Weakness
  • Pruritus
  • Urticaria

Physical

• No specific findings are present on physical examination.
• General abdominal tenderness may be noted in some children.

Causes

• The mode of transmission is believed to be through direct fecal-oral spread and, possibly, through the eggs of E vermicularis (pinworm).

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Other Problems to be Considered

Allergic gastroenteritis
Eosinophilic gastroenteritis
Celiac disease

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Lab Studies

• Blood tests
• • Blood test results are usually normal.
  • However, a CBC count with differential may reveal eosinophilia in as many as 50% of children infected with the parasite.
• Stool evaluation
• • The usual method for confirming the diagnosis is examination of a permanently stained smear of fresh feces, preserved immediately, for the morphologic characteristics of D fragilis trophozoites.
  • Newer, but experimental, techniques include immunofluorescence and real-time polymerase chain reaction (PCR) techniques.³ Culture is not routinely available.
  • Preferred stool preparation involves a fresh sample that is immediately preserved with polyvinyl alcohol fixative, sodium acetate-acetic acid-formalin fixative, or Schaudinn fixative.
  • Immediate preservation is necessary because, in unpreserved feces, the morphologic characteristics of the trophozoites do not persist, and they round up and become granular within 15 minutes at room temperature.
  • A single sample is diagnostic only 50-60% of the time.
  • Three separate samples increase the yield to 70-85%, and 6 separate samples increase the yield to 90-95%.
  • Ensure that stool samples are collected on alternate days because D fragilis can be excreted in a cyclic pattern similar to G lamblia.
  • The final portion of the stool evacuation may contain the most concentrated numbers of trophozoites.
  • Collect stool specimens before radiologic procedures that use barium because barium interferes with trophozoite detection and may do so for several weeks.
  • Other medications that can interfere with parasite detection include antibiotics, antiprotozoan medication, antimalarials, mineral oil, bismuth-containing preparations, and nonabsorbable diarrheal medications.
  • Process stool specimens in the laboratory with the formalin-ether sedimentation concentration technique and stain with either iron hematoxylin, trichrome, or celestin B.
• Diagnostic characteristics
• • Diagnostic characteristics are a pleomorphic trophozoite ranging in diameter from 5-15 mm (range, 4-30 mm) that contains 1-4 nuclei.
  • The most common form is binucleated. However, approximately 20-30% are uninucleated. Multinucleated forms also can be present.
  • The nuclei are distinctive, with several (4-8) chromatin granules clumped in the center of each nucleus.
  • The cytoplasm frequently contains numerous food vacuoles.

Imaging Studies

• Radiologic test findings are usually normal.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical Care

The goal of therapy is eradication of the parasite (see Medication).

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

The goal of therapy is eradication of the parasite. The drugs used are considered investigational by the US Food and Drug Administration because of a lack of clinical trials. Response rates for a single course of therapy are 70-90% in the limited data published.

Drug Category: Anthelmintics

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:

1. Inhibition of microtubules, causing irreversible block of glucose uptake
2. Tubulin polymerization inhibition
3. Depolarizing neuromuscular blockade
4. Cholinesterase inhibition
5. Increased cell membrane permeability, resulting in intracellular calcium loss
6. Vacuolization of the schistosome tegument
7. Increased cell membrane permeability to chloride ions via chloride channels alteration

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Further Outpatient Care

• Consider examination of stool specimens 3-4 weeks after therapy to determine if the parasite was eliminated.
• Examine fecal specimens from all family members (particularly siblings) of the index case for D fragilis and other parasites. In addition, examine for E vermicularis.
• Take the expense of ova and parasite (O&P) testing into account when considering follow-up and family member testing. A single stool sample for O&P testing costs approximately $80 in many US laboratories.

Deterrence/Prevention

Control measures to limit spread of parasites include the following:

• Disinfect surfaces and equipment handled by children infected by the parasite.
• Disinfect diapering areas.
• Separate diapering areas from food preparation sites.
• Educate about handwashing techniques.
• Improve personal hygiene.
• Separate symptomatic individuals.

Patient Education

• Educate patient and caregivers about the importance of effective handwashing techniques.

MISCELLANEOUS

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

Medical/Legal Pitfalls

• Failure to diagnose is the major potential legal pitfall. This is particularly true in the rare occurrence that failure to thrive ensues.

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• References

1. Cuffari C, Oligny L, Seidman EG. Dientamoeba fragilis masquerading as allergic colitis. J Pediatr Gastroenterol Nutr. Jan 1998;26(1):16-20. [Medline].
2. Johnson EH, Windsor JJ, Clark CG. Emerging from obscurity: biological, clinical, and diagnostic aspects of Dientamoeba fragilis. Clin Microbiol Rev. Jul 2004;17(3):553-70, table of contents. [Medline].
3. Verweij JJ, Mulder B, Poell B, van Middelkoop D, Brienen EA, van Lieshout L. Real-time PCR for the detection of Dientamoeba fragilis in fecal samples. Mol Cell Probes. Oct-Dec 2007;21(5-6):400-4. [Medline].
4. Butler WP. Dientamoeba fragilis. An unusual intestinal pathogen. Dig Dis Sci. Sep 1996;41(9):1811-3. [Medline].
5. Frenkel LM. Dientamoeba fragilis infection. In: Textbook of Pediatric Infectious Diseases. Vol 2. 4^th ed. Elsevier Health Sciences; 1998:2403-6.
6. Grendon JH, DiGiacomo RF, Frost FJ. Descriptive features of Dientamoeba fragilis infections. J Trop Med Hyg. Oct 1995;98(5):309-15. [Medline].
7. Keystone JS, Yang J, Grisdale D, et al. Intestinal parasites in metropolitan Toronto day-care centres. Can Med Assoc J. Oct 1 1984;131(7):733-5. [Medline].
8. Kurt O, Girginkardesler N, Balcioglu IC, Ozbilgin A, Ok UZ. A comparison of metronidazole and single-dose ornidazole for the treatment of dientamoebiasis. Clin Microbiol Infect. Jun 2008;14(6):601-4. [Medline].
9. Medical Letter on Drugs and Therapeutics. Drugs for parasitic infections. Med Lett Drugs Ther. Mar 6 1992;34(865):17-26. [Medline].
10. Norberg A, Nord CE, Evengard B. Dientamoeba fragilis--a protozoal infection which may cause severe bowel distress. Clin Microbiol Infect. Jan 2003;9(1):65-8. [Medline].
11. Preiss U, Ockert G, Broemme S, Otto A. On the clinical importance of Dientamoeba fragilis infections in childhood. J Hyg Epidemiol Microbiol Immunol. 1991;35(1):27-34. [Medline].
12. Shein R, Gelb A. Colitis due to Dientamoeba fragilis. Am J Gastroenterol. Oct 1983;78(10):634-6. [Medline].
13. Spencer MJ, Garcia LS, Chapin MR. Dientamoeba fragilis. An intestinal pathogen in children?. Am J Dis Child. Apr 1979;133(4):390-3. [Medline].
14. Spencer MJ, Millet VE, Garcia LS, et al. Parasitic infections in a pediatric population. Pediatr Infect Dis. Mar-Apr 1983;2(2):110-3. [Medline].
15. Stark DJ, Beebe N, Marriott D, et al. Dientamoebiasis: clinical importance and recent advances. Trends Parasitol. Feb 2006;22(2):92-6. [Medline].
16. Turner JA. Giardiasis and infections with Dientamoeba fragilis. Pediatr Clin North Am. Aug 1985;32(4):865-80. [Medline].
17. Vandenberg O, Peek R, Souayah H, Dediste A, Buset M, Scheen R. Clinical and microbiological features of dientamoebiasis in patients suspected of suffering from a parasitic gastrointestinal illness: a comparison of Dientamoeba fragilis and Giardia lamblia infections. Int J Infect Dis. May 2006;10(3):255-61. [Medline].
18. Vandenberg O, Souayah H, Mouchet F, Dediste A, van Gool T. Treatment of Dientamoeba fragilis infection with paromomycin. Pediatr Infect Dis J. Jan 2007;26(1):88-90. [Medline].

Article Last Updated: Jul 24, 2008