Dientamoeba Fragilis Infection 

Updated: Jul 31, 2018
Author: Maria A Garcia Fernandez, MD; Chief Editor: Russell W Steele, MD 

Overview

Practice Essentials

Dientamoeba fragilis is a nonflagellate trichomonad parasite 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. D fragilis has been detected in untreated sewage.[1]

The mode of transmission is not well understood, and conflicting evidence has been published.[2]  Surveys of various mammals and birds have only identified nonhuman primates as natural hosts and never in domestic pets; however, recently a high prevalence of infection has been reported in pigs.[3]  Thus, there is a possible zoonotic transmission of this parasite, although most infections are believed to be through direct fecal-oral spread and, possibly, through co-infection 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.

The life cycle of D fragilis is shown in the image below.

This is an illustration of the assumed life cycle This is an illustration of the assumed life cycle of Dientamoeba fragilis, the cause of a protozoan parasitic infection.

Epidemiology

Frequency

International

Estimated prevalence in the general population in the United States and in other developed countries is most commonly 2-5%. 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.

A prospective study from Spain that included 44 D. fragilis patients and their 97 household contacts reported that 50.5% of household contacts had a positive PCR for D. fragilis. The study also reported that patients with children were more associated with coinfection.[4]

Mortality/Morbidity

Colonization may occur without development of disease, and, in adults, asymptomatic colonization was once thought to be present in 75-85% of individuals infected by the parasite. More recently, it is not believed that asymptomatic carriage is as prevalent as once thought and in children symptomatic disease develops in as many as 90% of those colonized. In 2014, new research was presented at the 24th European Congress of Clinical Microbiology and Infectious Diseases (ECCMID) that questioned the pathogenicity of the parasite.[5]

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 and abdominal pain. 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.

 

Presentation

History

Abdominal pain and diarrhea are the most common symptoms in patients with Dientamoeba fragilis infection.[6] In acute infection, diarrhea is the predominant symptom, which lasts 1-2 weeks.[7] 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. Chronic infection is diagnosed when duration of symptoms is greater than 1-2 months. The most common symptom in chronic infection is abdominal pain.

Other GI complaints include the following[8] :

  • 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

Nonspecific findings are present on physical examination though 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). Pigs have recently been identified as a natural host for D fragilis,[3] raising the possibility of transmission from porcine waste and the parasite has also been identified in untreated wastewater.[1]

 

DDx

Diagnostic Considerations

A study by Krogsgaard et al suggested that Dientamoeba fragilis is not directly involved in the pathogenesis of irritable bowel syndrome (IBS). In analyzing fecal samples from 124 persons with IBS symptoms and 204 controls, the investigators found that a greater proportion of the control samples carried D. fragilis (35%) than did samples from the IBS subjects (23%).[9]

Differential Diagnoses

 

Workup

Laboratory Studies

Blood tests

Blood test results are usually normal in patients with Dientamoeba fragilis infection. 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.[10] 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

Medical Care

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

 

Medication

Medication Summary

The goal of therapy is eradication of the parasite Dientamoeba fragilis. 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, with higher rates of treatment failures reported following the use of metronidazole as compared with other antimicrobials. There is no consensus as to best clinical practice due to lack of large-scale, randomized trials. A 2014 randomized study found no evidence to support routine metronidazole treatment of D. fragilis –positive children with chronic gastrointestinal symptoms.[11]

A study reported that exposure to metronidazole was found to confer decreased risk of D. fragilis infection; however, similar associations were found for antimicrobials not commonly used to treat D. fragilis, such as broad-spectrum penicillin, fluoroquinolones, and macrolides. In contrast, mebendazole exposure was associated with increased risk.[12]

A study by Boga et al suggested that in patients with D. fragilis infection, coinfection with E vermicularis may somehow protect D. fragilis from eradication by drug therapy. If so, according to the investigators, this would indicate that patients coinfected with the two parasites should be treated for both simultaneously.[13]  Current recommendations for therapy include one of the following drugs: iodoquinol (drug of choice), tetracycline, paromomycin or metronidazole. Availability of iodoquinol and paromomycin in the United States is limited. Newer agents secnidazole and ornidazole appear effective in single dosage with fewer side effects and longer half-lives while ronidazole, tinidazole and nitazoxanide show in vitro activity against D. fragilis.[14, 15, 16, 17]

Anthelmintics

Class Summary

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

Metronidazole (Flagyl)

Imidazole ring-based antibiotic active against various anaerobic bacteria and protozoa.

Tetracycline (Sumycin)

Inhibits bacterial protein synthesis by binding with 30S and, possibly, 50S ribosomal subunits.

Iodoquinol (Yodoxin)

Amebicide used in treatment of D fragilis.

Paromomycin (Humatin)

Amebicidal and antibacterial aminoglycoside obtained from strain of Streptomyces rimosus; active in intestinal amebiasis.

 

Follow-up

Further Outpatient Care

Consider re 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. The expense of ova and parasite (O&P) testing must be taken into account when considering follow-up and family member testing since a single O&P test 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.

 

Questions & Answers

Overview

What is Dientamoeba fragilis and how is it transmitted?

What is the pathophysiology of Dientamoeba fragilis infection?

What is the global prevalence of Dientamoeba fragilis infection?

What is the morbidity associated with Dientamoeba fragilis infection?

Which age groups have the highest prevalence of Dientamoeba fragilis infection?

Presentation

Which clinical history findings are characteristic of Dientamoeba fragilis infection?

What are the GI signs and symptoms of Dientamoeba fragilis infection?

What are the nonintestinal signs and symptoms of Dientamoeba fragilis infection?

Which physical findings are characteristic of Dientamoeba fragilis infection?

How is Dientamoeba fragilis infection transmitted?

DDX

What conditions should be considered in the diagnosis of Dientamoeba fragilis infection?

What are the differential diagnoses for Dientamoeba Fragilis Infection?

Workup

What is the role of blood tests in the diagnosis of Dientamoeba fragilis infection?

What is the role of stool evaluation in the diagnosis of Dientamoeba fragilis infection?

What is the role of imaging studies in the diagnosis of Dientamoeba fragilis infection?

Treatment

What is the goal of therapy for Dientamoeba fragilis infection?

Medications

What is the role of medications in the treatment of Dientamoeba fragilis infection?

Which medications in the drug class Anthelmintics are used in the treatment of Dientamoeba Fragilis Infection?

Follow-up

What is included in long-term monitoring for Dientamoeba fragilis infection?

How is Dientamoeba fragilis infection prevented?

What is included in patient education about Dientamoeba fragilis infection?