- Peter F Weller, MD, FACP
Peter F Weller, MD, FACP
- Editor-in-Chief — Infectious Diseases
- Section Editor — Tropical Medicine
- William Bosworth Castle Professor of Medicine
- Harvard Medical School
- Professor of Immunology and Infectious Diseases
- Harvard T. H. Chan School of Public Health
- Karin Leder, MBBS, FRACP, PhD, MPH, DTMH
Karin Leder, MBBS, FRACP, PhD, MPH, DTMH
- Section Editor — Travel Medicine
- Head of Infectious Diseases Unit
- Monash University, Australia
Dientamoeba fragilis is an anaerobic intestinal protozoan parasite. Historically, this organism was among a group of enteric protozoan parasites beginning with Giardia duodenalis (previously G. lamblia) that were initially believed to be commensals and not capable of causing symptomatic illness. As more information became available and antimicrobial agents were developed with activity against these parasites, it became clear that D. fragilis can cause an active infection, although it does not always result in symptomatic disease. (See "Epidemiology, clinical manifestations, and diagnosis of giardiasis" and "Blastocystis species" and "Nonpathogenic enteric protozoa".)
While the capacity of D. fragilis to cause symptomatic intestinal illness is increasingly recognized, there are a number of uncertainties surrounding D. fragilis [1,2]. How uniformly infection with this parasite causes symptoms is not known: in a Danish study, D. fragilis was detected in a greater proportion of fecal samples from the asymptomatic background population in Denmark than from subjects with symptoms . Moreover, the means by which this parasite is transmitted has not been fully defined. Finally, the diagnostic recognition of this parasite in fecal examinations requires specific processing and expertise; thus, it is possible that many infections with D. fragilis may go undiagnosed.
Ultrastructural, immunologic, and genetic analyses place D. fragilis in the family of protozoan flagellates, which includes Trichomonas [2,4]. Unlike other intestinal protozoan organisms that have both trophozoite and hardy cyst stages, for a long time D. fragilis was recognized to exist only as trophozoites. Trophozoites measure 7 to 12 micrometers in diameter, contain one or two nuclei, lack flagellae, and are minimally motile. However, cyst forms of D. fragilis have been identified in experimental mouse infections and in human fecal samples , suggesting that cystic forms are the transmissible infectious form of this organism.
There is genetic evidence for at least two variants of D. fragilis. However, it is unknown if these two differ in their pathogenicity .
Infections with D. fragilis are acquired by the fecal-oral route, but how fragile trophozoites survive outside of the body and do not succumb to stomach acid following ingestion are not fully understood (figure 1). Some investigators suggested that trophozoites might survive within and be ingested with the eggs of the pinworm Enterobius vermicularis. While this might explain coinfection in some children, it does not likely explain most D. fragilis infections. In addition, some studies have specifically failed to find a correlation between D. fragilis and E. vermicularis infections . The recognition of cyst forms of the parasite may be important for understanding transmission . In addition, sheep, pigs, and nonhuman primates have been identified as natural hosts of the genotypes found in humans, suggesting zoonotic potential for human transmission . (See "Enterobiasis (pinworm) and trichuriasis (whipworm)".)
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