Trends in Parasitology
Volume 22, Issue 2, February 2006, Pages 92-96
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Dientamoebiasis: clinical importance and recent advances

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Dientamoeba fragilis, an unusual single-celled parasite that was described first in 1918, is found worldwide in the gastrointestinal tract of humans. D. fragilis has emerged from obscurity recently because it is now recognized as a common cause of chronic diarrhoea and is treatable with drugs. Recent molecular studies have described D. fragilis as having two genotypes. Diagnostic tests, based on conventional and real-time PCR, have been developed that will provide a rapid, sensitive and specific diagnosis of D. fragilis. These tests will also aid the elucidation of the host distribution and the life cycle of this pathogen.

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A neglected cause of diarrhoea

Dientamoeba fragilis is a pathogenic human intestinal protozoan parasite that was first described in the scientific literature in 1918 by Jepps and Dobell (cited by Johnson et al. [1]). More than 87 years since the discovery of D. fragilis, the amount of scientific knowledge acquired about this organism when compared with other protozoans pales into insignificance. Its life cycle and mode of transmission are unknown and no animal models or axenic culture systems have been developed. However,

Morphological characteristics

D. fragilis is a pleomorphic trophozoite (Figure 1), ranging in size from 4–20 μm (typically 5–15 μm). The trophozoites of D. fragilis are typically binucleate, with only 30–40% uninucleate. No cyst stages have been reported [2].

In stained smears, using iron–haematoxylin or trichrome stains, the nuclear membrane is delicate and does not possess any peripheral chromatin. The karyosome contains chromatin granules, varying in number from four to eight, often appearing as chromatin packets. The

Taxonomy

Jepps and Dobell, in 1918, argued that because this organism had been found to have a binucleated form and no cyst stage, it was not only a new species, but also a distinct new genus of parasite. Hence, the name D. fragilis was suggested and is still in use today (Box 1). These authors placed this new protozoan in the family Entamoebidae (cited by Johnson et al. [1]).

Using only light microscopy, staining and culture techniques, Dobell also recognized the close structural similarities between

Clinical aspects

Initially, Jepps and Dobell concluded that this parasite was nonpathogenic; however, researchers questioned the pathogenicity of D. fragilis almost immediately.

In many clinical circles, there is still resistance to accepting the disease-causing potential of this organism, and many doubt its clinical significance as a human pathogen. Although this organism is still struggling to gain acceptance as a significant pathogen, the evidence supporting its pathogenicity is overwhelming and the continued

Transmission

The mode of transmission of D. fragilis is not known. Dobell postulated that, because H. meleagridis – which is transmitted from bird to bird by the eggs of the nematode Heterakis gallinae – and D. fragilis are morphologically similar, they might have similar modes of transmission. Several studies have examined a role for the transmission of D. fragilis in the ova of Enterobius vermicularis and found a high level of co-infection 17, 18, 19. More recent studies have rejected the hypothesis of E.

Molecular epidemiology and genetic diversity

By using PCR-restriction fragment length polymorphism (PCR–RFLP) analysis of ribosomal genes of 12 D. fragilis isolates grown in a xenic culture system, the researchers found that organisms currently being reported as D. fragilis represent at least two significantly different genetic entities – genotypes 1 and -2 [25]. Eleven clinical samples were genotype 1, whereas one clinical sample and the American Type Culture Collection (ATCC) strain Bi/pa (ATCC 30948) were genotype 2. Johnson and Clarke

Diagnostic techniques

In wet preparations, D. fragilis appears as a nonspecific rounded mass, and the nuclear structure cannot be seen in either saline or iodine preparations (cited by Windsor and Johnson [12]). As trophozoites degenerate rapidly, prompt fixation of the specimen is necessary. Successful diagnosis of D. fragilis is closely associated with the use of permanent stains of faecal smears.

Many different stains and fixatives have been used successfully with D. fragilis, the most common being polyvinyl

Therapy

Many studies have shown that the elimination of D. fragilis using antimicrobial agents usually relieves clinical symptoms [12]. As such, the treatment of symptomatic patients with D. fragilis infections is warranted.

Iodoquinol (diiodohydroxyquin) has been widely used to treat D. fragilis infections, particularly in North America [36]. Metronidazole has also been shown to be effective in treating D. fragilis infections [37], and successful eradication of both symptoms and parasite were obtained

Further study

Numerous clinical and epidemiological studies have substantiated D. fragilis as a significant enteropathogen. It is, therefore, surprising that so little research has been undertaken on this organism.

Clifford Dobell, one of the first parasitologists to describe D. fragilis, wrote the following about this organism in 1940 [2]:

To the protozoologist – if not to the physician – D. fragilis is now, perhaps, the most interesting of all the intestinal amoebae of man: for we know less about it than

Future perspectives

Of all the pathogenic protozoan parasites that infect humans, only a small amount of knowledge has been acquired over the years on D. fragilis. Its life cycle and mode of transmission are unknown. No animal models or axenic culture systems have been developed for the study of this organism. The diagnostic tests available for this organism are limited compared with other protozoa.

More research is needed on the epidemiology, clinical signs (such as IBS) and pathology associated with

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