Despite its name, Dientamoeba fragilis is not an ameba but an intestinal flagellate, most closely related to trichomonads. In human stool specimens, D. fragilis is almost always found solely as a trophozoite. However, the rare presence of putative cyst and precyst forms in clinical specimens has been reported; their transmission potential is being investigated. Other aspects of the transmission and pathogenicity of D. fragilis also are poorly understood.
The complete life cycle of Dientamoeba fragilis has not yet been elucidated; assumptions have been made on the basis of clinical observations and the biology of related species (in particular, Histomonas meleagridis, a parasite of galliform birds). Trophozoites are found in the lumen of the large intestine, where they multiply via binary fission, and are shed in the stool . Historically, only the trophozoite stage of D. fragilis had been detected. However, rare putative cyst and precyst forms have been described in human clinical specimens; whether and in what settings transmission to humans occurs via ingestion of such forms in contrast or in addition to other fecal-oral transmission routes is not yet known . Transmission via helminth eggs (e.g., via Enterobius vermicularis eggs) has been postulated .
Dientamoeba fragilis is primarily a parasite of humans. Trophozoites have been identified in some other mammals (e.g., non-human primates, swine), but the epidemiologic significance of these hosts is unknown.
Dientamoeba fragilis is found worldwide. Infection appears to be more common in children.
2. Clinical aspect
Not long after D. fragilis was described as a non-pathogenic amoeba in 1918, researchers began to question the assumptions made by Jepps and Dobell regarding the pathogenic nature of the organism. A study in the Philippines less than a year later in 1919 found three cases of D. fragilis in 100 symptomatic children (Haughwout and Horrilleno, 1920). The following year Jepps described ten cases of D. fragilis from 971 symptomatic soldiers at a war hospital (Dobell, 1940). These reports led to an increased interest in the parasite and five years later D. fragilis was reported and implicated as a potential pathogen throughout the world (Taliaferro and Becker, 1924).
Wenrich et al. (1936) reported an incidence of 4.3% of D. fragilis from 1060 university students in the USA. They found that there was a higher rate of gastrointestinal symptoms in the students infected with D. fragilis than those infected with Entamoeba histolytica, with diarrhoea and abdominal pain present in the majority of cases. However, it was not known at this time that E. histolytica consisted of two species, E. histolytica and Entamoeba dispar, the latter of which is considered to be non-pathogenic and much more common than the former.
The same year Hakansson (1936) described a case of D. fragilis infection in a 48-year-old physician (himself) who complained of gastrointestinal symptoms including pain in the upper abdomen, mucoid stool, loss of appetite and irritation of the rectum. After 2 weeks of recurrent symptoms he was treated with carbarsone, which led to complete resolution of symptoms and negative post-therapy stool samples. A year following these findings, Hakansson (1937) undertook a follow-up study where 12 patients with D. fragilis infections were treated with carbarsone, which resulted in complete resolution of symptoms with clearance of parasites.
In support of early findings, numerous studies over the following 75 years have subsequently shown the pathogenic potential of D. fragilis and demonstrated that it is a commonly encountered enteropathogen associated with signs of clinical disease such as diarrhea and other gastrointestinal complaints (Windsor and Macfarlane, 2005; Vandenberg et al., 2006; Kurt et al., 2008; Stark et al., 2010). Crotti and D’Annibale (2007) analysed stool specimens from 1989 subjects and while Giardia intestinalis was present in 1.8% of subjects, D. fragilis was detected in 4.1%. It was also demonstrated that D. fragilis was more commonly associated with clinical symptoms than G. intestinalis. More recently, Stark et al. (2010) examined 750 symptomatic and asymptomatic patients, detecting D. fragilis at a prevalence of 5.2%, more common than G. intestinalis. Similarly, most of the infected patients exhibited clinical symptoms largely consisting of diarrhea (30/36); loose stools (26/36); and abdominal pain/discomfort (28/36). Shedding of the parasite was found to be highly variable. Complete resolution of symptoms was observed in the majority of patients following treatments including iodoquinol, paromomycin, metronidazole or combination therapy (Stark et al., 2010). Chronic infections are reported, with one study indicating 32% of patients infected with D. fragilis present with symptoms greater than 2 weeks in duration (Stark et al., 2005). A recent study has also shown high rates of D. fragilis infection amongst close household contacts of patients with dientamoebiasis. A total of 30% of close human contacts tested for D. fragilis harbored the parasite, and the majority of these contacts (n = 80%) were symptomatic (Stark et al., 2012).
Unfortunately, study into the pathological manifestations of D. fragilis infections is hampered by the lack of a suitable animal model, despite previous attempts using macaques, cats, chickens and rats, none of which have been reproducible (Dobell, 1940; Knoll and Howell, 1946; Barratt et al., 2011a). However no recent studies in the last 75 years have attempted to establish animal models for the further study of D. fragilis. In addition, while a large proportion of infected individuals present with gastrointestinal illnesses, clinical presentations of D. fragilis frequently show variability and asymptomatic carriage can occur. Intermittent shedding of the organism is common among patients therefore care must be taken and correct diagnostic procedures used for definitive diagnosis. Numerous studies have also reported that treatments which eliminate the organism lead to clinical improvement (cited by Windsor and Johnson, 1999; cited by Johnson et al., 2004; Stark et al., 2010) and as such, D. fragilis needs to be included as a part of routine laboratory diagnostics for the differential detection of enteric protozoa.
Uncertain. There are two main theories of how D. fragilis spreads.
D. fragilis may be spread through contamination of hands, objects or food with infected faeces. The parasite is then taken in by the mouth.
Alternatively, D. fragilis may be spread by threadworms (pinworms). D. fragilis might be protected by threadworm eggs. Threadworms are caught when someone swallows the worm’s eggs. Threadworm eggs hatch inside the bowel, where they live, then travel out through the anus (back passage) to lay their eggs on the skin there at night time. Threadworm eggs may be picked up on the fingers and transferred to the mouth if the person scratches their bottom or does not wash their hands after going to the toilet. Threadworm eggs may also fall off into bedding or clothing, or be wafted into the air, settling on many surfaces in the home or school.
Dientamœba fragilis est un parasite intestinal responsable d’infection. L’infection se contracte par contact avec les selles d’une personne infectée.
Où et chez qui survient-elle ?
On trouve le parasite dans le monde entier. Dientamœba fragilis est plus fréquente dans des environnements où les conditions d’hygiène sont insuffisantes. C’est la principale cause d’infection intestinale chez les touristes dans les zones tropicales et subtropicales.
Comment la reconnaître ?
L’infection peut ne pas provoquer de symptômes. Le délai entre la contamination et les premiers symptômes est habituellement de 7 à 14 jours.
Les symptômes intestinaux sont à l’avant-plan. Chez l’enfant, l’infection peut provoquer des maux de ventre persistants et de la diarrhée. Une perte de poids est également possible.
Comment le diagnostic est-il posé ?
Le médecin peut poser le diagnostic sur la base d’une analyse de selles prélevées trois jours différents.
Que pouvez-vous faire ?
Une bonne hygiène des mains est essentielle pour éviter la contamination. Se laver les mains après chaque passage aux toilettes, avant de manger, lors de la préparation des repas.
Que peut faire le médecin ?
Le traitement de l’infection à Dientamoeba fragilis consiste à administrer un médicament antiparasitaire. Le métronidazole est le plus couramment utilisé en Belgique.
Although Dientamoeba fragilis is not a parasite which is commonly spoken of, recent research identifies not only a significant prevalence but also that, unlike many intestinal bacteria which produce no symptoms in patients, Dientamoeba fragilis usually does.
In a study concerning Australian 6,750 patients with gastrointestinal issues who had stool samples analyzed, 0.9 percent of them tested positive for Dientomoeba fragilis. The most common symptoms manifesting in these patients were diarrhea and abdominal pain. This survey reflects several others and confirms that D. Fragilis is often found in patients with gastric issues and also those where there is a recurring problem.
It would seem that that not only is Dientomoeba fragilis a significant causation of digestive issues, but that it can be prominent even in environments which are considered to have high sanitary standards. This is due to the same study establishing that only 10% of the patients affected by the bacteria had undergone travel to countries where sanitation was considered to be substandard.
Because this pathogen is one which responds to treatment reflecting that of other commensal microflora when an overgrowth or pathogenic problem occurs, then three aspects should be focused upon when providing a natural treatment:
1) Eliminate the pathogen
2) Support the beneficial microflora so it can assist in overwhelming the pathogen naturally
3) Support the immune system so the natural defense mechanism of the body can also overwhelm the pathogen
Although infections from other forms of pathogen are often shown to be opportunistic in that they will, particularly in the case of yeasts, invade a person whose immune system is somehow impaired, this appears not the be the case with D. Fragilis. Studies have shown that the pathogen is shown to predominate in people, who although they may be ill, have no problem with their immune system. However this does not mean that the immune system should not be supported in this instance only that it is less important when it comes to this particular overgrowth.
Neither when it comes to infection by this pathogen does it seem to leave the patient unaffected as it does with others which show that people can have the bacteria but no symptoms. In the control group used no patient had the infection, and correspondingly they did not have symptoms either. However it did sometimes exist in affected patients at the same time as other pathogens which produce atypical reactions and which do affect those who are immune deficient so it is best to treat both as a possibility.
To clear the pathogen naturally it is necessary to approach it by both dietary means and preferably natural supplements which can support the natural defense system of the body.
Firstly it helps to starve the pathogen by reducing the amount of sugar intake. This is done through an elimination process which means that initially you abstain from ingesting all sugars wherever possible. This includes not only basic sugars but also those in junk and packaged food, baked goods, fruit, dairy and alcohol. When it comes to dairy sugar it must also be remembered that often it appears as lactose in many foods which can include tinned goods. Many people remark that they do not eat dairy in the form of milk, cheese or similar products, however simply by eliminating these does not mean you are eliminating lactose which is the problematic issue. Remember to check all labeling on products, including supplements and other drugs, to see if lactose is included in the ingredient list.
The one exception to excluding dairy is that of probiotics. Although many natural practitioners have long since recommended taking a probiotic daily this has, until recently, not been in the remit of orthodox medicine. However now studies are being performed which prove that patients taking a probiotic even in conjunction with a prescribed drug, see much better improvements in many illnesses which arise from pathogenic infestation and cause gastric distress.
Yogurt, probiotic drinks and even kefir if you can find it, are really essential in building up the beneficial bacteria in the body and restoring the balance within the digestive tract which helps to overwhelm the pathogen in the most natural way possible.
After 2 weeks on the elimination diet, and if symptoms have improved substantially, then you can start reintroducing certain foods. However when it comes to alcohol, sweet stuff and candy, junk food and sodas, it is highly recommended that these are excluded for much longer if not permanently where it is reasonable.
Taking a supplement with the elimination diet can also help. Canxida Remove and Canxida Restore both provide ingredients which are natural and which are proven to help fight digestive disturbances relating to pathogenic overgrowth. Restore contains many probiotics which can support the healthy gut flora and Remove contains ingredients such as Black Walnut and garlic which are known to naturally overwhelm pathogens. Garlic in particular is also known to breach biofilms where pathogens are now known to hide and neither does it trigger these pathogens to strengthen their reserves against attack. This is a situation which is known now to occur with many chemically synthesized drugs including antibiotics and antifungals. It also contains numerous other natural ingredients in addition to many other compounds which will also support the immune system and others such as Betaine Hydrochloride which assist with balancing the pH of the digestive tract. This is also necessary to help absorb undecylenic acid which is a natural and extremely effective antifungal derived from the castor bean, but which needs an acidic rather than alkaline environment to work.
When it comes to ingesting products which can induce and aggravate infections caused by pathogens then we must also look at medications. Those which are known to cause problems either directly or indirectly include: antacids, proton pump inhibitors, corticosteriods, NSAIDs and oral contraceptive pill. All of these can negatively influence the natural balance of the intestinal gut flora or pH of the digestive tract. This means that the beneficial microflora which usually far outnumber the pathogenic organisms lose their natural ability to overwhelm pathogens seeking to damage the body.
Considering the number of people suffering from gastrointestinal disturbances due to pathogenic organisms, it may well be worth discussing alternative treatments with your clinician.
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