Entamoeba coli

entamoeba coli

Entamoeba coli Entamoeba entamoeba coli trophozoites contain a single nucleus with a prominent karyosome that usually is eccentric in location, distinguishing them from E. histolytica and E. dispar trophozoites, which have a centrally located karyosome. From: Sleisenger and Fordtran's Gastrointestinal and Liver Disease (Ninth Edition), 2010 Related terms: • Entamoeba • Dysentery • Cyst • Entamoeba Histolytica • Blastocystis • Chloroquine • Morphology • Diarrhea • Escherichia entamoeba coli John E.

Bennett MD, in Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases, 2020 Epidemiology Syndromes of acute dysentery with fecal blood and pus have been well recognized since the days entamoeba coli Hippocrates. Dysentery is defined as frequent small bowel movements accompanied by blood and mucus, with tenesmus or pain on defecation. This syndrome, with or without fever, implies an inflammatory invasion of the colonic mucosa resulting from bacterial, cytotoxic, or parasitic destruction.

The pathologic changes of inflammatory colitis range from a superficial intense exudative inflammatory process involving the colonic mucosa, as seen in infection by shigellae or invasive E. coli organisms, to deeper, penetrating, flask-shaped ulcers with undermined edges, as seen in amebic dysentery. The pathogenesis of the inflammatory colitides may involve cytotoxic products of shigellae, 1 certain E.

coli strains, 2 clostridia, or other organisms. The epidemiologic patterns of acute dysenteric syndromes are influenced by the unusually low inoculum for infection required by organisms such as shigellae or amebas. As few as 100 shigellae or 10 cysts of enteric parasites, such as Entamoeba coli or Giardia lamblia, have been found to result in infection in adult volunteers.

3,4 In consequence, entamoeba coli is a substantial risk of person-to-person spread in daycare centers, 5 institutions, or other areas where nonhygienic conditions may allow direct fecal-oral spread. The cysts of parasites such as Entamoeba histolytica or Balantidium coli often resist chlorination and therefore entamoeba coli cause waterborne outbreaks of dysenteric illnesses. Saltwater or seafood exposure should lead to consideration of Vibrio parahaemolyticus as a potential cause of inflammatory colitis or of watery diarrhea, and farm or domestic animal exposure might lead to consideration of nontyphoid Salmonella spp., Campylobacter jejuni or Campylobacter coli, or Yersinia enterocolitica.

A study in children younger than 5 years in the United States found nontyphoid Salmonella, followed by Campylobacter, Y. enterocolitica, and E.

coli O157, were the most common bacterial enteric pathogens associated with illnesses. entamoeba coli When typhoid fever is present with diarrhea in an endemic area, the diarrhea is often inflammatory, with many fecal polymorphonuclear or mononuclear leukocytes seen on microscopic examination.

7 A recent multisite birth cohort study (Malnutrition and Enteric Disease Study [MAL-ED]) showed that norovirus GII, rotavirus, Campylobacter spp., astrovirus, and Cryptosporidium spp. exhibited the highest attributable burdens of diarrhea in the first year of life. In the second year of life the major pathogens were Campylobacter spp., norovirus GII, rotavirus, astrovirus, and Shigella spp. 8 Campylobacter spp. and EIEC were associated with dysentery.

Rotavirus and Shigella spp. were associated with fever, whereas rotavirus and norovirus GII were most associated with vomiting. A history of travel to areas of poor sanitation may implicate any of the aforementioned pathogens.

Finally, venereal exposure, particularly among men who have sex with men, may implicate gonococci, herpes simplex virus, Chlamydia trachomatis (including lymphogranuloma venereum serotypes), or Treponema pallidum as a cause of proctitis, or Campylobacter, Shigella, E. histolytica, or C. difficile as a cause of colitis. 9 A history of antibiotic intake and/or recent admission to a health care facility would strongly suggest C.

difficile infection (CDI), although community-acquired infection has been recognized as well. Peter J. Hotez, in Feigin and Entamoeba coli Textbook of Pediatric Infectious Diseases (Sixth Edition), 2009 DIAGNOSIS AND TREATMENT Entamoeba coli sometimes is difficult to distinguish from E. histolytica, particularly because the nuclear structures of their trophozoite stages are similar.

3 Some differences exist, however, including the karyosome, which is eccentric in Entamoeba coli, but central in E. histolytica, and the cytoplasm, which is coarse and seldom contains red blood cells in Entamoeba coli, in contrast to E.

histolytica. 3 The differences between the cyst stages of Entamoeba coli and E. histolytica (and Entamoeba dispar) are more apparent. The Entamoeba coli cyst typically has two to four times more nuclei than cysts in E.

histolytica. The Entamoeba coli cyst has been reported to become more refractive during fixation so that it often is visualized better in a wet preparation. 4 Generally, Entamoeba coli still is regarded by most investigators as a commensal organism.

In patients with persistent diarrhea whose diagnostic fecal evaluation reveals only the presence of Entamoeba coli, entamoeba coli a course of specific anti-amebic therapy is reasonable.

1 All of the Swedish patients were reported to respond to a 10-day course of diloxanide furoate in a dose of 500 mg three times daily. 7 Children also may respond to an equivalent pediatric dose of 20 mg/kg/day in three divided doses for 10 days. As of 1994, diloxanide furoate was entamoeba coli in the United States from the Centers for Disease Control and Prevention Drug Service.

Alternatively, two children from Ireland (where diloxanide furoate was unavailable) were treated successfully for Entamoeba coli–associated diarrhea with metronidazole. 2 B. Flagellates (Intestinal) Mark Feldman MD, in Sleisenger and Fordtran's Gastrointestinal and Liver Disease, 2021 Other Amebae That Infect the Human Intestine Ten other ameba species commonly infect the human GI tract. These include E. dispar, Entamoeba moshkovskii, Entamoeba bangladeshi, Entamoeba nuttalli, Entamoeba coli, Entamoeba hartmanni, Entamoeba gingivalis, Entamoeba polecki, Endolimax nana, and Iodamoeba bütschlii.

Dientamoeba fragilis (discussed in the following section), previously thought to be an ameba, is more closely related to the flagellated protozoan Trichomonas vaginalis than to the true amebae. 65 With the exception of E. gingivalis, which has no known cyst stage, all of these true amebae have simple 2-stage life cycles, consisting of an infectious cyst form and a motile trophozoite form. 65 E. dispar, E.

moshkovskii, E. bangladeshi, and E. nuttalli all appear identical to E. histolytica using a light microscope, and must be differentiated from E. histolytica based on biochemical, antigenic, or genetic differences. 1 E. dispar is a nonpathogenic protozoan parasite that is morphologically indistinguishable from E. histolytica by light microscopy. 1 An estimated 450 million people worldwide are infected with E. dispar, and infection with E.

dispar is approximately 10 times more prevalent than E. histolytica infection. 1,64,68 Although E. dispar has been demonstrated to cause mucosal ulcerations in animal models, it has not been demonstrated to cause human disease and does not require treatment. 1 E. moshkovskii, which is primarily thought to be a free-living ameba, also has cysts and trophozoites indistinguishable from E.

dispar and E. histolytica, except that trophozoites of E. histolytica might show erythrophagocytosis. A entamoeba coli prevalence of human E. moshkovskii infection has been demonstrated in some studies, and, although its causation of human disease is still controversial, infection by E. moshkovskii is associated with diarrhea entamoeba coli infants. 69-72 E. bangladeshi is a recently described species also morphologically identical to E. histolytica. Based on its small rRNA gene sequence, E.

bangladeshi is more closely related to E. dispar and E. histolytica than E. moshkovskii. Its pathogenic potential remains unknown. 73 E. nuttalli frequently causes invasive amebiasis in nonhuman primates, and symptomatic disease outbreaks have been described among animal caretakers.

74 There are currently no clinically available tests specific for E. moshkovskii, E. bangladeshi, or E. nuttalli. Blaine A. Mathison, Bobbi S. Pritt, in Reference Module in Biomedical Sciences, 2021 Entamoeba coli Entamoeba coli has a worldwide distribution and is one of the most commonly reported Entamoeba species in clinical specimens. Non-human primates may serve as reservoir hosts.

Trophozoites of E. coli measure 15–50 μm and have a single nucleus with irregular peripheral chromatin and a usually eccentric karyosome.

The cytoplasm is often described as “dirty” and may contain vacuoles and ingested food particles, including bacteria, yeast, and even other intestinal protozoa. Cysts are 10–35 μm in diameter. Immature cysts typically have a large glycogen vacuole and two nuclei. Mature cysts have eight nuclei, entamoeba coli hypernucleate forms having 16 or more nuclei. The presence of an Entamoeba cyst in human stool with more than four nuclei is pathognomonic for E.

coli ( Ash and Orihel, 2007). Rick D. Kellerman MD, in Conn's Current Therapy 2021, 2021 Entamoeba histolytica Entamoeba histolytica, the cause of amoebic dysentery and amebic liver abscess, is a worldwide pathogen of major clinical significance. Approximately 10% of the world’s population and up to 60% of children in highly endemic areas show serologic evidence of infection, and E. histolytica entamoeba coli estimated entamoeba coli cause 100,000 deaths per year globally. In the United States, infection is almost exclusively found among returned travelers, immigrants from endemic areas (especially Mexico and Central and South America), men who have sex with men (MSM), and institutionalized persons.

Entamoeba dispar, Entamoeba bangladeshi, and Entamoeba moshkovskii are morphologically indistinguishable from E. histolytica. Although these species are usually considered nonpathological species. there have been increasing reports of E. moshkovskii infections associated with gastrointestinal symptoms in humans in endemic areas. Other Entamoeba, including Entamoeba hartmanni, Entamoeba coli, Entamoeba polecki, and others, can be individually identified on microscopy. Again these organisms are of uncertain pathogenicity and generally considered as commensal organisms, however, E.

polecki, Dientamoeba fragilis, and Iodaamopeba bütschlii have occasionally been associated with diarrheal illness. E. histolytica exists in two forms, the hardy cyst (infective form) characterized by four nuclei, and the trophozoite (responsible for invasive disease), which has a single nucleus and survives poorly outside the human body.

E. histolytica infection is acquired by ingestion of cysts in contaminated water or food or by fecal-oral contact. Acquisition of the parasite can result in asymptomatic infection (most common), diarrheal illness, or extraintestinal infection, the latter most commonly manifest as amebic liver abscess.

entamoeba coli

An appropriately robust layer of colonic mucin may be protective against symptomatic infection, whereas trophozoite attachment to the entamoeba coli epithelium results in penetration of the organism into the submucosal layer, where extensive tissue destruction can take place in the form of apoptosis and lysis of cells, hence the name “histolytica.” Symptoms of classic amebic dysentery usually begin insidiously over 1 to 3 weeks after infection.

Diarrhea is almost universal and typically consists of numerous small-volume stools that can contain mucus or frank blood, or both. Stools are almost always heme positive if not grossly bloody.

Abdominal pain and tenesmus are common; fever is present in approximately 30% of cases. Some patients have a chronic course characterized by weight loss, intermittent loose stools, and abdominal pain. Rare presentations of amebic dysentery include amebomas, which can mimic malignancy, and perianal ulcerations or fistulae.

Severe disease can occur in the form of fulminant colitis or toxic megacolon; the latter almost universally requires colectomy. Young age, pregnancy, corticosteroid use, malignancy, malnutrition, and alcoholism predispose to severe infection. Although persons with HIV infection or AIDS can develop invasive disease, E. histolytica does not appear to be a common opportunistic infection, and infection is curable in this population.

Frank E. Berkowitz, in Principles and Practice of Pediatric Infectious Diseases (Fourth Edition), 2012 The Pathogen Other amebas within this group are Entamoeba coli, Entamoeba hartmanni, Entamoeba polecki, and Iodamoeba buetschlii.

These organisms have the same life cycle ( Figure 262-1), characterized by a trophozoite stage, which lives in the colon, and a cyst stage, which is infectious. These organisms are differentiated from one another by their morphology.

1,2 E. nana trophozoites ( Figure 262-2) measure 5 to 12 µm in diameter. The cytoplasm is granular with multiple vacuoles that entamoeba coli ingested bacteria entamoeba coli debris.

entamoeba coli

The nucleus is small and when stained, the nuclear chromatin characteristically is distributed against the nuclear membrane. The mature cysts ( Figure 262-3) are ovoid to round in shape (similar in size to trophozoites), contain 4 nuclei, and also can have small, slightly curved chromatoid rods and glycogen vacuoles. Immature cysts containing 2 nuclei rarely are seen in stool specimens. Abinash Virk, in The Travel and Tropical Medicine Manual (Fourth Edition), 2008 NON-PATHOGENIC PROTOZOA Numerous other species of protozoa have been detected in human feces, including Entamoeba coli, Iodamoeba Bütschli, Endolimax nana, and Entamoeba hartmanni.

It is not unlikely that many of these ‘non-pathogens’ are capable of producing disease in the proper clinical setting. At the present time, however, identification of one of these organisms in the stool is more useful as a marker of exposure to fecal-contaminated food or water. Their presence should prompt a more exhaustive search for pathogens such as Giardia or E. histolytica, which may be present in the stool in much smaller numbers. Nonflagellated intestinal protozoa can be further subdivided into entamoeba coli groups: ● Entamoeba histolytica.

● Entamoeba coli. ● Endolimax nana. ● Iodamoeba butschlii. ● Blastocystis hominis. E. histolytica is pathogenic. Other Entamoeba is typically not pathogenic, but may cause diagnostic confusion with E. histolytica. E. histolytica exists as trophozoites or cysts. Morphologic characteristics of the trophozoite stage include: ● 20–30 µm in size. ● Outer clear ectoplasm and inner granular endoplasm. ● A nucleus with a karyosome at the center. ● Clear area around the karyosome.

● May have red cells in the cytoplasm. Humans are infected with food and water contaminated with mature (quadrinucleate) cysts. Infection may also be transmitted by anal-genital and oral-genital route. The cysts excyst in the small intestine thus producing trophozoites. These colonize the mucosal surfaces of the large intestine. In the intestine they may remain asymptomatic.

In others they may cause invasive intestinal amebiasis, resulting in blood and mucus in stool with diarrhea (acute amebic dysentery). Also, some intestinal amebiasis may take a chronic form with intermittent diarrhea and abdominal pain. In some the trophozoites may enter into entamoeba coli portal circulation and entamoeba coli hepatic amebiasis and subsequent amebic liver abscess.

Amebic abscess may rupture through the right diaphragm and cause pulmonary amebiasis. Various intestinal nonflagellated protozoa are listed in Table 10.2. Protozoa Cyst Trophozoite Entamoeba histolytica Pathogenic 10–20 µm, peripheral, fine evenly distributed chromatin; 2–4 nuclei with small central karyosome 12–60 µm, may have red blood cells within cytoplasm Entamoeba coli Nonpathogenic, larger than E.

histolytica 10–35 µm, coarse, clumped unevenly arranged peripheral chromatin, 8–16 nuclei entamoeba coli large eccentric karyosome 15–50 µm, sluggish compared to E. histolytica Endolimax nana Nonpathogenic 5–10 µm with 2–4 nuclei; no peripheral chromatin 6–12 µm; single nucleus with large central karyosome Iodamoeba butschlii Nonpathogenic 5–20 µm; single nucleus with no peripheral chromatin 8–20 µm Blastocystis hominis Debatable whether they are intestinal commensals or true pathogens; possible link between this protozoa and irritable bowel syndrome (IBS) Lynne S.

Garcia, in Hunter's Tropical Medicine and Emerging Infectious Diseases (Tenth Edition), 2020 Diagnosis Differentiation of this organism from either Entamoeba histolytica/E. dispar/E. moshkovskii/E. bangladeshi or Entamoeba coli is rarely accomplished on the basis of a wet preparation examination and is difficult even with the permanent stained smear ( Fig.

99.4). 9 The nuclear morphology of the trophozoite is almost a composite of those of E. histolytica/ E. dispar/E. moshkovskii/E. bangladeshi and E. coli. Without some of the cyst stages for comparison, it would be very difficult to identify this organism to the species level on the basis of the trophozoite alone.

The cyst normally has only a single nucleus, chromatoidal material like that seen in E. histolytica, and, frequently, an inclusion body. This mass tends to be round or oval and is not sharply defined on the edges. The material, which is not glycogen, remains on the permanent stained smear and stains less intensely than nuclear material or chromatoidal bars. Lorna Entamoeba coli. . William Stauffer, in Immigrant Medicine, 2007 Intestinal parasites Gastrointestinal parasites are commonly found on screening stool examinations of immigrants and refugees.

Frequently encountered nonpathogens are Endolimax nana, Entamoeba coli, Entamoeba hartmanni, Iodamoeba butschlii, Chilomastix mesnili, and Blastocystis hominis. With the possible exception of Blastocystis hominis, these organisms are considered nonpathogenic and should not be treated.

Common organisms considered pathogens include Giardia lamblia, Entamoeba histolytica, Trichuris trichiura, Hymenolepis nana, Ascaris lumbricoides, hookworm, Strongyloides stercoralis, Schistosoma species, and Dientamoeba fragilis ( Table 12.7).

Other, more unusual, parasitic infections are occasionally identified, such as the fluke infections (i.e. Ophisthorchis spp.). Prevalence of parasites in refugee children in Buffalo, New York, was 21.8% (19/87), 13 similar to that seen in refugees of all ages in Minnesota (22%, 462/2129).

25 A higher percentage was found in refugee children in Portland, Maine, 43.7% (38/87). 12 About a third (31.1%, 75/241) of refugee children in Miami–Dade County, Florida, had pathogens entamoeba coli on stool O&P.

33 Empiric overseas pre-departure treatment of refugees in sub-Saharan Africa with albendazole has been ongoing since 1999 (excluding pregnant women and those <2 years of age). Reductions in detection of intestinal parasites were seen in a before-and-after study of refugees arriving in Massachusetts. 34 Significant reductions in both helminths and protozoa including hookworm, Trichuris, Ascaris, and Entamoeba histolytica were observed.

It should be noted that in this population eosinophilia is frequently residual from a parasitic infection prior to departure. In fact, eosinophilia in this pretreated group has only a 12% positive predictive value for the subsequent detection of a potentially pathogenic parasite in the stool.

Newer comprehensive treatment regimen recommendations aimed at empiric treatment of Strongyloides stercoralis and Schistosoma spp. may broaden the overseas treatment and will empirically treat most cestode, nematode, and trematode parasites. Routine examination of stool for ova and parasites (stool O&P) is currently recommended for individuals arriving from the developing world or who resided in refugee camps or areas where sanitation services were disrupted due to natural disasters or political conditions.

Any person with symptoms suggesting a gastrointestinal parasite regardless of their prior living conditions should also be tested. Eosinophilia is also strongly suggestive of infection with parasites. The specificity of eosinophilia in a nontreated refugee (absolute eosinophil count above 400–500/microliter) has been shown to be greater than 95%. 35 While multiple stool specimens increase the likelihood of finding a pathogen, the entamoeba coli number is not clear. 36–38 One to three specimens should be adequate in most cases.

Strongyloides is present in many parts of the world and is difficult to detect on stool O&P: even three properly collected stool examinations only identify half of entamoeba coli infected.

Autoinfection can result in entamoeba coli lasting decades. This is of concern due to the risk of disseminated infection and death when patients become immunosuppressed from human immunodeficiency virus (HIV) infection, malignancy, or medications (steroids, chemotherapy).

Most infected individuals will have eosinophilia. This parasite should be considered when a patient has eosinophilia with no source identified in the stool. In this case, serologic evaluation may identify the infection and lead to appropriate treatment.

Entamoeba dispar cysts cannot be distinguished from E. histolytica by microscopy. An asymptomatic refugee who has E. histolytica/dispar complex identified should have serologic evaluation and/or stool antigen testing and undergo treatment only if the diagnosis of Entamoeba coli. histolytica is confirmed. In many settings, these tests may not be available, and some experts choose to treat these patients with a 7-day course of paromomycin to assure eradication of potentially harmful cysts.

Collection of stool will be done in the home, and specimen containers contain toxic preservative material. Clear instructions should be given to patients in their own language via an interpreter if necessary to avoid receipt of unusable specimens and inadvertent exposure to entamoeba coli preservative. Recently, the Centers for Disease Control and Prevention established recommendations for presumptive treatment of strongyloidiasis and schistosomiasis for Sudanese refugees.

39 These recommendations were based on findings of a serosurvey showing that almost 70% of the Lost Boys and Girls of Sudan tested positive for schistosomiasis or strongyloidiasis and over 20% tested positive for both. Current recommendations are presumptive treatment for all Sudanese entamoeba coli who are not pregnant or lactating and do not have evidence of neurocysticercosis. For those not tested for Loa loa, recommended treatment is a 7-day course of albendazole (400 mg twice a day) for those over 1 year of age and two doses of praziquantel (20 mg/kg 6–8 hours apart) for those 4 years of age and over.

For those who have tested negative for Loa loa and weigh more than 15 kg, ivermectin (200 mcg/kg, one dose) was recommended for treatment of strongyloidiasis.

Those persons over 1 year of age were also recommended to receive one dose of albendazole (600 mg) for treatment of other intestinal parasites and the above noted dose of praziquantel for schistosomiasis. Testing for schistosomiasis and strongyloidiasis is available at the Centers for Disease Control and Prevention for persons who meet the exclusion criteria for presumptive treatment. It is unclear at this time whether these recommendations are being followed by those seeing refugees and immigrants from Sudan, or whether these recommendations entamoeba coli be generalized to include other immigrant groups.

Many experts who screen refugees prefer to make specific diagnoses and generate targeted treatment plans, while entamoeba coli the course of eosinophilia over time. The most important finding to come of entamoeba coli studies may be to prompt clinicians to consider screening high-risk asymptomatic individuals, even those without eosinophilia, for parasitic diseases, especially strongyloidiasis.

• About ScienceDirect • Remote access • Shopping cart • Advertise • Contact and support • Terms and conditions • Privacy policy We use cookies to entamoeba coli provide and enhance our service and tailor content and ads. By continuing you agree to the use of cookies. Copyright © 2022 Elsevier B.V. or its licensors or contributors. ScienceDirect ® is a registered trademark of Elsevier B.V. ScienceDirect ® is a registered trademark of Elsevier B.V. none
( Grassi, 1879) Entamoeba coli is a non-pathogenic species of Entamoeba that frequently exists as a commensal parasite in the human gastrointestinal tract.

E. coli (not to be confused with the bacterium Escherichia coli) is important in medicine because it can be confused during microscopic examination of stained stool specimens with the pathogenic Entamoeba histolytica. [1] This amoeba does not move much by the use of its pseudopod, and creates a " sur place (non-progressive) movement" inside the large intestine.

Usually, the amoeba is immobile, and keeps its round shape. This amoeba, in its trophozoite stage, is only visible in fresh, unfixed stool specimens. Sometimes the Entamoeba coli have parasites as well.

One is the fungus Sphaerita spp. This fungus lives in the cytoplasm of the E. coli. [2] While this differentiation is typically done by visual examination of the parasitic cysts via light microscopy, new methods using molecular biology techniques have been developed.

[3] The scientific name of the entamoeba coli, E. coli, is often mistaken for the bacterium, Escherichia coli. Unlike the entamoeba coli, the amoeba is mostly harmless, and does not cause as many intestinal problems as some strains of the E. coli bacterium. To make the naming of these organisms less confusing, "alternate contractions" are used to name the species for the purpose making the naming easier; for example, using Esch. coli and Ent. coli for the bacterium and amoeba, instead of using E.

coli for both. [4] [5] Entamoeba coli cyst with more than 4 nuclei The presence of E.coli is not cause in and of itself to seek treatment as it is considered harmless. [6] However, when a person becomes infected with this benign entamoeba, other pathogenic organisms may have entamoeba coli introduced as well, and these other pathogens might cause infection or illness. [7] Morphology [ edit ] Stages of the Entamoeba coli parasite Entamoeba species all come in monogenetic forms, or having one generation lifecycles.

E. coli has "three distinct morphological forms exist airing the life cycle-Trophozoite, Pre-cystic stage and Cystic stage". This lifecycle gives rise to the general way of how Entamoeba species form. This parasite has one large nucleus with a entamoeba coli membrane surrounding the nucleus. There are many chromatin inside the nucleus, and one large, irregular-shaped karyosome. [8] The chromatin is clumped, and uneven in disperse inside the nucleus.

The parasite forms by binary fission like most Entamoeba spp. [9] The mature cyst is the infective stage, and is known to survive longer than those of E. histolytica. The cysts can survive three to four months outside the host's body after desiccation. [8] The cysts cause infection by consuming contaminated food and drinks like waste water. Sometimes insects and rodents carry the parasite to cause infection in the food and drinks.

Excystation happens once the cysts are ingested, and travel to the large intestine. [2] Diagnosis [ edit ] E. coli trophozoites can be distinguished by their wide and tapered pseudopodia. They are often mistaken for E. histolytica due to their overlap in size. The cysts are distinguished by noticing the eight nuclei found in the mature form. [10] To diagnosis for E. coli, a stool sample is usually tested. This is the best method to check to see if the parasite is E.

coli and not E. histolytica. This usually involves checking the cysts for the size, shape, and the number of nuclei. E. coli has cysts in size to 10 to 35 micrometers, the shape is irregular, oval with a shell-like appearance that is more uniformed compared to E. histolytica, and has up entamoeba coli eight nuclei in the cyst compared to the four nuclei of E. histolytica. To the untrained eye of by inexperienced microbiologists, "tetranucleate cysts of Entamoeba coli can be mistaken for mature cysts of Entamoeba histolytica" Often " a tetranucleate Entamoeba coli cyst is larger than a mature cyst of Entamoeba histolytica, can be variable in shape, and has nuclear peripheral chromatin and karyosome composed of irregular granules" in this matter of comparison.

To make a diagnosis for any Entamoeba species, usually a wet mount is created "by finding the characteristic cysts in an iodine stained, formol-ether concentration method or by detecting the characteristic trophozoites in a wet preparation or a permanent stained preparation" to see what they may look like.

[11] Also, these stains of trichrome can be used to mount the cysts of any Entamoeba spp. [12] Other tests can be used to diagnosis for Entamoeba spp. These tests involve the use of laboratory methods.

Some of these laboratory tests include: the use of light microscopy, culture methods, isoenzyme analysis, antibody detection tests, antigen detection tests, immunochromatographic assays, and DNA-based diagnostic tests.

[13] Some uses of microscopy also involve the use of transmission electron microscopy and scanning entamoeba coli microscopy. Usually, the cysts are freeze fractured to insure that the samples are easier to look at to compare Entamoeba spp. [14] The DNA-based diagnostic tests include the use of DNA extraction, PCR, microarrays, and typing methods.For example, one DNA-based diagnostic test that is changing how Entamoeba spp. is being diagnosis faster and more accurate is by using the "Reverse Line Hybridization Assay" test.

This test main purpose is to detect and different Entamoeba spp. in stool samples in order to find the causative agent of amoebic dysentery, E.

histolytica. This test involves the use of gene sequencing, and seeing what different genomes each Entamoeba coli spp. has to help detect the deadly E. histolytica. [15] Pathology [ edit ] E. coli are mostly harmless parasites, and do not cause harm to the host. However, there have been cases of internal bleeding. Usually, the cytoplasm of the E. coli "does not contain red blood cells, except in the rare case of patients with intestinal hemorrhage" that leads to blood in the stools of these patients.

This may lead to intestinal lesions. Other problems that E. coli causes are usually result from having too many in the large intestine. For example, large populations of E. coli may lead to "dyspepsia, hyperacidity, gastritis, and indigestion"; these are common problems of most intestinal parasites. [8] Treatment [ edit ] There is generally no need to treat for E. coli, due to the rarity of this parasite becoming infectious. In one exceptional situation, E.

coli was found to be infectious: in northern Europe, stool samples and electron microscopy revealed large populations of the amoeba within a group of patients with persistent diarrhea. [16] Some types of treatments may need entamoeba coli be used due to large populations. Some arsenical compounds are shown to treat the trophozoite stage, like carbarsone.

[8] Other compounds used to treat large populations of E. coli include diloxanide furoate, and this usually is used in antiamebic therapy. [16] See also [ edit ] • Amoebiasis References [ edit ] • ^ Sodeman WA (1996). "Intestinal Protozoa: Amebas". In Baron S; et al. (eds.). Baron's Medical Microbiology (4th ed.). Univ of Texas Medical Branch. ISBN 978-0-9631172-1-2. • ^ a b "Atlante dei protozoi intestinali umani - sezione AMEBE identificazione microscopica di Giovanni Swierczynski e Bruno Milanesi".

Atlas-protozoa.com. Retrieved 2015-12-03. • ^ Verweij JJ, Laeijendecker D, Brienen EA, van Lieshout L, Polderman AM (2003). "Detection and identification of entamoeba species in stool samples by entamoeba coli reverse line hybridization assay".

J. Clin. Microbiol. 41 (11): 5041–5.

entamoeba coli

doi: 10.1128/JCM.41.11.5041-5045.2003. PMC 262518. PMID 14605136.

entamoeba coli

• ^ Pometto, Anthony; Shetty, Kalidas; Paliyath, Gopinadhan; Levin, Robert E. (2005-10-11). Food Biotechnology (Second ed.).

p. 9. ISBN 9781420027976. Retrieved 2015-12-03. • ^ "Entamoeba". Microscope-microscope.org. Retrieved 2015-12-03. • ^ "CDC - Nonpathogenic (Harmless) Intestinal Protozoa - Biology". Cdc.gov. 2015-03-17. Retrieved 2015-12-03. • ^ "CDC - DPDx - Intestinal Amebae". Cdc.gov. 2013-11-29. Retrieved 2015-12-03. • ^ a b c d Saritha Pujari (2015-11-14). "Parasite Entamoeba Coli : Life Cycle, Mode of Infection and Treatment".

Yourarticlelibrary.com. Retrieved 2015-12-03. • ^ Don Lehman. "Diagnostic Parasitology; E. coli". Udel.edu. Retrieved 2015-12-03. • ^ "Intestinal Protozoa". Tulane.edu. 2015-06-03. Retrieved 2015-12-03. • ^ Jim McMorran; Damian Entamoeba coli Stew McMorran; Steve Youngmin; Ian Wacogne; Jon Pleat; Clive Prince. "Entamoeba coli - General Practice Notebook". Gpnotebook.co.uk. Retrieved 2015-12-03. • ^ "CDC - DPDx - Intestinal Amebae - Images".

Cdc.gov. 2013-11-29. Retrieved 2015-12-03. • ^ Fotedar R, Stark D, Beebe N, Marriott D, Ellis J, Harkness J (2015-09-28). "Laboratory Diagnostic Techniques for Entamoeba Species". Clin. Microbiol.

Rev. 20 (3): 511–32, table of contents. doi: 10.1128/CMR.00004-07. PMC 1932757. PMID 17630338. • ^ Chávez-Munguía, Bibiana; Martínez-Palomo, Entamoeba coli (2011-08-25). "High-Resolution Electron Microscopical Study of Cyst Walls of Entamoeba spp". Journal of Eukaryotic Microbiology.

entamoeba coli

58 (6): 480–486. doi: 10.1111/j.1550-7408.2011.00576.x. PMID 21883633. S2CID 19124321. • ^ Verweij JJ, Laeijendecker D, Brienen EA, van Lieshout L, Polderman AM (2015-09-28). "Detection and Identification of Entamoeba Species in Stool Samples by a Reverse Line Hybridization Assay".

J. Clin. Microbiol. 41 (11): 5041–5. doi: 10.1128/JCM.41.11.5041-5045.2003. PMC 262518. PMID 14605136. • ^ a b Hotez, Peter (July 2000). "The other intestinal protozoa: Enteric infections caused by Blastocystis hominis, Entamoeba coli, and Dientamoeba fragilis".

Seminars in Pediatric Infectious Diseases. 11 (3): 178–181. doi: 10.1053/pi.2000.6228. Further reading [ edit ] Edit links • This entamoeba coli was last edited on 1 May 2022, at 18:36 (UTC). • Text is available under the Creative Commons Attribution-ShareAlike License 3.0 ; additional terms may apply.

By using this site, you agree to the Terms of Use and Privacy Policy. Wikipedia® is a registered trademark of the Wikimedia Foundation, Inc., a non-profit organization. • Privacy policy • About Wikipedia • Disclaimers • Contact Wikipedia • Mobile view • Developers • Statistics • Cookie statement • • none
Continuing Education Activity Entamoeba coli is one of many non-pathogenic protozoa found in humans. It is transmitted through fecal-oral contact, and the mature cyst can be found in entamoeba coli water.

Typically, these protozoa inhabit the large intestinal tract and can be identified in diagnostic stool specimens. This activity highlights the role of the interprofessional team in the evaluation and treatment of Entamoeba coli. Objectives: • Identify the etiology of Entamoeba coli infection. • Explain the evaluation of Entamoeba coli infection.

• Review the management options available for Entamoeba coli. Introduction Entamoeba coli is one of many non-pathogenic protozoa found in humans. [1] It is transmitted through fecal-oral contact, and the mature cyst can be found in contaminated water. [2] Typically, these protozoa inhabit the large intestinal tract and can be identified in diagnostic stool specimens.

[3] It is essential to differentiate Entamoeba coli, a nonpathogenic protozoan, from those that cause significant disease. The complete name of the protozoan is usually used to avoid confusion with the bacterium Escherichia coli.

Etiology Entamoeba coli is transmitted through fecal-oral contact. [4] Typically, mature cysts are ingested from contaminated water and food sources. [5] Epidemiology Entamoeba coli is global in its distribution, with the highest prevalence in regions with inadequate sanitation, typically in rural areas.

[5] Older studies entamoeba coli the United States reported a prevalence of 4.2% among all stool samples sent to diagnostic laboratories in 1987.

[6] [7] Intestinal parasitic diseases are common in developing countries. In a hospitalized population in Iran, random stool samples showed a prevalence of Entamoeba coli infection in 4.6%. [8] A random non-hospitalized rural community in Iran showed a 2.9% prevalence.

[9] In a secluded population in Iran, it is 6.8%.

entamoeba coli

{INSERTKEYS} [10] However, other areas have reported a prevalence of 11.4%. [11] Turkey reported a prevalence of 11.5%. [12] Rural areas of India had reported a prevalence of 21.8%. [13] In a hospitalized population in Sudan, the prevalence was 7%.

[14] In a study of 193 children in Malawi, East Africa, Entamoeba coli was found in approximately 10.4% of the sample. [5] In a random school population in Sudan, the prevalence was 7.5%. [15] In some rural school communities in Colombia, the prevalence can be as high as 25.7% to 35%.

[16] [17] Rural areas in Yucatan, Mexico, had a school children prevalence of 26.5%. [18] Rural communities in Ecuador had a prevalence in schoolchildren of 34.0%.

[19] Even in developed countries, the prevalence can be high. In Swiss children, a prevalence of 8% has been reported. [20] Fresh vegetables can carry parasites and infect a person when consumed unwashed or washed with contaminated water. A study in Tunisia showed that fresh vegetable samples contain helminth eggs and protozoan cysts eggs in 12.5% of the cases; Entamoeba coli was found in 1.6%.


entamoeba coli

{INSERTKEYS} [21] In another study in the United Arab Emirates, helminths eggs and protozoa cysts were detected in 15.1% of the samples; Entamoeba coli composed 18.2% of that percentage. [22] This fact demonstrates that safe handling of raw vegetables should be maintained and is recommended.

Pathophysiology Entamoeba coli, similar to other Entamoeba specifies, has three distinct morphological forms: trophozoite, pre-cystic stage, and cystic stage. [2] The trophozoite form, which measures 20 to 25 μm, is minimally mobile. [23] The core of the trophozoite is slightly oval in shape with a nucleus surrounded by a thick membrane. Within this membrane, chromatin granules surround the large, eccentric, and irregular karyosome.

The cytoplasm contains large vacuoles and is typically granular with easily distinguishable ectoplasm and endoplasm. The amoeba produces short, blunt pseudopods, which are projections from the granular cytoplasm, allowing limited mobility. When they surround bacteria and food particles, these pseudopods ingest them and form phagosomes through phagocytosis. In this stage, red blood cells and other bacteria and parasites can be found in the amoeba.

Ingestion of red blood cells by Entamoeba coli is rare but may be seen. [24] Entamoeba coli can swallow other organisms, such as Giardia lamblia, which may compete for its food source. [23] [25] There have been cases of hyperparasitization with spores of the Sphaerita species fungus. [26] Sphaerita species appear as tightly packed clusters within the cytoplasm, measuring approximately 0.5 to 1.0 μm producing degenerative changes in the host's protoplasm, especially in the nucleus.

The pre-cyst form begins when the trophozoite starts to slightly change its shape, becoming more spherical and containing two nuclei. The cyst is typically 10 to 35 μm in diameter and is a colorless spherical shape. [23] Their cytoplasm is still granular, but the vacuoles are absent.

In the binucleate state, the glycogen vacuole is formed. The most distinguishing feature of the Entamoeba coli is the eight-core nuclei, which develops as the cyst begins to mature. In the octonucleate cystic form, the glycogen vacuole is reabsorbed. Occasionally, the nuclei may replicate until it has 16 nuclei in total.

The mature cyst is rich in glycogen with a refractile wall. [27] Colonization of the host first begins with the ingestion of mature cysts through contaminated food and water sources, typically via fecal-oral contamination. The cyst is hard due to its strong cell wall and can survive up to weeks in an external environment, and this quality allows it to survive the stomach's acidic environment.

Cysts release trophozoites in the small intestine forming daughter trophozoites that are minimally motile and migrate to the colon. Entamoeba species, like most of the protozoans, reproduce by binary fission to form two daughter cells.

Trophozoites in the colon multiply by undergoing binary fission and slowly reduce in size to first transform into the pre-cyst phase and then to the cyst phase. These cysts undergo mitosis until it becomes octonucleated or occasionally developing 16 nuclei. Host feces release mature octonucleate cysts of Entamoeba coli. Trophozoites found in the stool outside the body are rapidly destroyed, and if ingested, would not survive exposure to the gastric environment. History and Physical Most patients with Entamoeba coli infestation remain asymptomatic, and often, the protozoan is discovered incidentally.

[27] It is important in those patients with diarrhea symptoms to obtain a thorough history and physical exam. Patients may rarely show gastrointestinal symptoms such as loose stools, colicky abdominal pain, and flatulence. [28] Some patients can complain of gastritis, indigestion, dyspepsia, or hyperacidity if the amoeba is in large amounts in the gastrointestinal tract.

Stools are usually non-bloody and without mucus. Symptoms may persist for a long time; however, they are generalized and nonspecific for Entamoeba coli.

Evaluation Ova and parasite testing can be performed to help distinguish between different amoebae species. Testing via microscopy will show the presence of protozoa; however, it is essential to differentiate between Entamoeba coli and the pathogenic amoeba, Entamoeba histolytica.

[23] Stool examination via ova and parasite testing is the most common form of analysis and evaluation. [4] [23] Stool examination with ova and parasite testing typically requires three stool specimens for best sensitivity and specificity. [2] Wet smears may result in difficulty in observing the Entamoeba coli cyst due to the refractile wall. [27] On initial microscopy, the cyst of Entamoeba coli typically has eight nuclei, while Entamoeba histolytica typically has four.

The peripheral chromatin is coarse and irregularly clumped for Entamoeba coli and fine, evenly distributed for Entamoeba histolytica. The karyosome of Entamoeba coli is irregular, large, and eccentric, with Entamoeba histolytica having a small, round, and centrally located karyosome. More advanced tests are available, usually to differentiate between pathogenic and nonpathogenic Entamoeba species.

These advanced tests include isoenzyme analysis, antibody detection test, antigen detection test, immunochromatographic assays, and electron microscopy.

[23] DNA based methods tests include polymerase chain reaction, microarray, and reverse line hybridization assay; however, they are not always available. [29] Reverse line hybridization assay is the fastest and most specific method of DNA analysis.

[29] The test allows for the determination of multiple strains of protozoa and showed intraspecific variation in Entamoeba coli. Treatment / Management Treatment is not indicated for Entamoeba coli infection. [27] Supportive care should be provided for patients, and proper hygiene should be maintained.

An alternate source should be sought for patients with symptoms. If the patient is symptomatic and no other organism or causes are found, treatment may be indicated. For those with persistent symptoms and no other infection source, treatment can be initiated. In one study, patients with gastrointestinal symptoms for many years with no other diagnosis were found to consistently had Entamoeba coli in the stool and were treated with diloxanide furoate 500 milligrams three times daily for ten days.

[28] After treatment, symptoms were resolved, and the stool was tested again with no signs of Entamoeba coli infection. Metronidazole 400 mg orally three times a day is also effective. Patients typically stop developing symptoms within five days. Differential Diagnosis Patients with only Entamoeba coli in stool are typically asymptomatic. [27] Differential diagnosis of diarrheal disease is vast but can include: • Bacterial pathogens: Escherichia coli, Shigella, Salmonella, Campylobacter, and Clostridium difficile • Inflammatory bowel disease • Ischemic bowel disease The differential diagnosis for cyst or protozoa in the stool can include: [2] [23] • Entamoeba histolytica • Chilomastix mesnili • Endolimax nana • Entamoeba dispar • Entamoeba hartmanni • Entamoeba polecki • Iodamoeba buetschlii Prognosis The prognosis of patients with Entamoeba coli is excellent, as most patients are asymptomatic.

[27] Complications Complications from Entamoeba coli infection are limited as patients are usually asymptomatic. [27] There are no long-term complications documented.

The presence of nonpathogenic protozoa suggests contaminated food or water sources or poor fecal-oral hygiene.

[2] [23] Consultations The following consultations are required: • Internal medicine • Epidemiology • Microbiology laboratory • Pharmacy • Social worker Deterrence and Patient Education If Entamoeba coli are found in stool samples, it may persist for days to years.

Treatment is typically not needed. Patients can reduce the chances of getting parasitic infections such as Entamoeba coli by maintaining proper hand hygiene and avoiding contaminated food and water. Entamoeba coli is found globally and more prevalent in areas with poor sanitation. [4] [5] Hygiene promotion lowers the risk of reinfection more than medication treatment alone. [30] When traveling to areas with a high prevalence of low sanitation: • Avoid drinking tap or well water.

Avoid ice cubes, which are commonly made from tap water. • Avoid eating raw fruits and vegetables that are cleaned with tap or well water. • Avoid street vendors. • Drink bottled beverages and use bottled water to brush your teeth. • Wash hands with soap and water frequently, particularly after touching animals, before eating, and after using the restroom.

• Boil water before drinking. • Use gloves if you need to touch feces. {/INSERTKEYS}

entamoeba coli

Pearls and Other Issues • Entamoeba coli is one of many non-pathogenic protozoa found in humans. • It is transmitted through fecal-oral contact. • Typically, mature cysts are ingested from contaminated water and food sources. • The highest prevalence occurs in areas with inadequate sanitation, typically in rural areas.

• Entamoeba coli has three distinct morphological forms: trophozoite, pre-cystic stage, and cystic stage. • The most distinguishing feature is the eight-core nuclei, which develops as the cyst begins to mature. • The cyst is hard due to its strong cell wall and can survive up to weeks in an external environment.

• Trophozoites found in the stool outside the body are rapidly destroyed, and if ingested, would not survive the gastric environment. • Most patients with Entamoeba coli infestation remain asymptomatic, and often protozoan is discovered incidentally. • Patients may rarely show gastrointestinal symptoms such as loose stools, colicky abdominal pain, and flatulence.

• Ova and parasite testing can be completed to help distinguish between different amoebae species. • It is essential to distinguish between Entamoeba coli and the pathogenic amoeba, Entamoeba histolytica.

• Stool samples should be taken at different times to ensure adequate specimens for testing. • Reverse line hybridization assay is the fastest and most specific method of DNA analysis. • Treatment is not indicated for Entamoeba coli infection. • If the patient is symptomatic and no other organism or causes are found, treatment may be indicated. • Patients can reduce the chances of getting parasitic infections such as Entamoeba coli by maintaining proper hand hygiene.

Enhancing Healthcare Team Outcomes Entamoeba coli is a common protozoan found in stool worldwide. It is essential to identify and differentiate this non-pathologic protozoan from those causing significant disease.

Infection with Entamoeba coli is a sign of fecal-oral contamination. Prevention through proper hand hygiene and avoidance of contaminated food and water. Patient education through multiple medical professionals, such as nursing staff, pharmacists, and physicians, is essential so patients can reduce infection chances.

Patients should be advised to see physicians for further workup if gastrointestinal symptoms develop. This illustration of a composite photomicrograph reveals the ultrastructural details seen in two stages of the life cycle of the parasite, Entamoeba coli, including its cystic stage in the lower right, which was stained with iodine, and its Giemsa-stained, vegetative, trophozoite stage at center left. Used with permission from CDC Public Health Image Library This photomicrograph of an iron-hematoxylin-stained specimen, revealed the presence of two amoebic organisms in their cystic stages of their development.

In this focal plane, the smaller Entamoeba histolytica cyst (top), contained four nuclei, and two bluntly-tipped chromatoid bodies, while six nuclei could be detected in the larger Entamoeba coli cyst (bottom), which also contained two chromatoid bodies as well. Used with permission from the CDC Public Health Image Library, contributed by Mae Melvin, MD. This photomicrograph of an iron-hematoxylin-stained specimen, revealed the presence of a mature, Entamoeba coli cyst, which contained five visible nuclei, each with its eccentrically located karyosome, and peripherally located chromatin.

Used with permission from the CDC Public Health Image Library, contributed by Mae Melvin, MD. This trichrome-stained photomicrograph, depicted a mature, Entamoeba coli cyst, containing five, clearly visible nuclei, and a what may have been a sixth nucleus, which was outside the focal plane, and therefore, out of focus.

The cyst also contained a visible chromatoid body. Used with permission from the CDC Public Health Image Library, contributed by Mae Melvin, MD.
OVERVIEW: What every clinician needs to know Parasite name and classification Entamoeba histolytica – protozoan entamoeba coli E.

histolytica is one of three morphologically identical species of Entamoeba commonly found in humans; the others are E.

dispar and E. moshkovskii. Only E. histolytica causes invasive disease in humans; the others are non-pathogenic. Asymptomatic infection should be treated because of the potential risk of progression to invasive disease, the risk of spread to family entamoeba coli, and the potential impact on Public Health. Current U.S. treatment guidelines recommend for asymptomatic infection: Iodoquinol 650 mg PO three times a day for 20 days in adults and 30-40 mg/kg/d PO in three divided doses for 20 days in children OR paromomycin 25-35 mg/kg/d PO in three divided doses for 7 days in adults and children OR diloxanide furoate 500 mg PO three times a day for 10 days in adults and 20 mg/kg/d PO in three divided doses for 10 days in children.

• Intestinal amoebiasis The goals of treatment for intestinal amoebiasis are two-fold: to treat the invasive disease (using tissue agents) and to eradicate intestinal carriage of the organism (using luminal agents). Metronidazole is often used for treating the invasive component of intestinal amoebiasis, with a reported cure rate of approximately 90%.

Tinidazole has a similar efficacy and has been shown in a Cochrane review to reduce clinical failure with fewer adverse events as compared to metronidazole entamoeba coli the treatment of amoebic colitis. Current U.S. treatment guidelines recommend as first line treatment either metronidazole 500-750 mg PO three times daily for 7-10 days in adults and 35-50 mg/kg/d PO in three divided doses for 7-10 days in children OR tinidazole 2g PO once daily for 3 days in adults and 50 mg/kg/d PO in a single dose for 3 days in children.

It is recommended that patients with invasive amoebiasis should be given a luminal agent after treatment with a tissue agent to eliminate any surviving organisms in the colon. Luminal agents entamoeba coli to eradicate intestinal carriage of the organism include Paromomycin, Diiodohydroxyquin (iodoquinol) and diloxanide furoate. Metronidazole (or tinidazole) and paromomycin should be given sequentially, not concurrently, since the diarrhea that is a common entamoeba coli effect of paromomycin can make it difficult to assess the patient’s response to therapy.

Entamoeba coli U.S. treatment guidelines recommend as first line treatment either iodoquinol 650 mg PO three times a day for 20 days in adults and 30-40 mg/kg/d PO in three divided doses for 20 days in children OR paromomycin 25-35 entamoeba coli PO in three divided doses for 7 days in both children and adults.

• Amoebic liver abscess Both tissue and luminal agents are also used in the treatment of amoebic liver abscess. Metronidazole has been reported to be very effective, with cure rates of 95% and reports of resolution of fever, pain, and anorexia within 72-96 hours. Tinidazole is also very effective, with several studies reporting a single dose of 2 g daily for 2-5 days was as effective as, or more effective than, metronidazole.

Fewer side effects were reported with tinidazole. Current U.S. treatment guidelines recommend as first line either metronidazole 750 mg PO tid for 7-10 days (35-50 mg/kg/d in children) OR tinidazole 2 g once PO daily for 5 days (50 mg/kg/day in children 3 years of age or older). Luminal agents used are paromomycin, iodoquinol, and diloxanide furoate.

Doses are identical to those mentioned in the section on intestinal amoebiasis. • Treatment failures have been reported with metronidazole with most failures attributed to incorrect diagnosis, unsuitable choice of drug, or poor compliance rather than drug resistance. However, laboratory studies have shown that the indiscriminate use of antiamoebic drugs can result in the development of metronidazole-resistant E.

histolytica strains in the laboratory. • Intestinal amoebiasis Other nitroimidazoles Other nitroimidazole drugs, such as ornidazole and secnidazole, have been used successfully in the treatment of E. histolytica and have been recommended as alternative antiamoebic drugs to metronidazole. These drugs are entamoeba coli readily available than metronidazole or tinidazole Secnidazole has been successfully used in the treatment of uncomplicated amoebic colitis in Brazil as a single dose of 2 g for 5 days.

Nitazoxanide A promising new drug to treat E. histolytica is nitazoxanide, which has been shown to have an efficacy between 69 and 96%. A study in Egypt showed treatment with a 3-day course of nitazoxanide was effective (94% efficacy) compared to placebo in the treatment of intestinal amoebiasis. A total of 94% of patients treated with nitazoxanide were free of Entamoeba histolytica in two post-treatment stool specimens compared with only 43% of patients receiving placebo.

According entamoeba coli the latest U.S. treatment guidelines, nitazoxanide is not FDA-approved for the treatment of amoebiasis. • Amoebic liver abscess Utrasound-guided needle aspiration Use of image-guided needle aspiration in the treatment of amoebic liver abscess is controversial.

A 2009 Cochrane review comparing metronidazole alone with metronidazole plus aspiration was inconclusive. Several authors have suggested that aspiration may be used in patients who are slow to respond to metronidazole therapy, patients with large entamoeba coli abscesses (due to risk of rupture into the pericardium), and severely ill patients in whom an accelerated clinical course and large abscesses make rupture seem imminent.

Nitaxozanide A small study of seventeen adults with hepatic amoebiasis demonstrated encouraging results, with all seventeen patients responding to nitaxozanide therapy. Further studies are warranted. What are the clinical manifestations of infection with E. histolytica? • Asymptomatic infection Between 80 and 90% of infected individuals are asymptomatic; however, it is important to note that 4-10% of asymptomatic individuals infected with E.

histolytica develop disease in the subsequent year. • Intestinal amoebiasis (amoebic colitis) Patients with amoebic colitis can present with symptoms ranging from mild diarrhea to fulminant colitis.

entamoeba coli

The onset is often gradual, and entamoeba coli frequently report several weeks of symptoms. Presenting features of amoebic colitis include: Diarrhea (94-100%) Bloody stools (70%) Abdominal pain (12-80%) Weight loss (44%) Fever greater than 38°C (10%) Intestinal amoebiasis can also present with: Asymptomatic colitis Fulminant colitis–reported in about 0.5% of cases Amoeboma–reported in approximately 1.5% of all cases Toxic megacolon–reported in about 0.5% of cases • Amoebic liver abscess Amoebic liver abscess is the most common extra-intestinal manifestation of amoebiasis and is a result of spread via the portal venous system.

Amoebic liver abscesses are ten times more common in men than women and are rare in children. Other risk factors include travel to endemic areas and a history of alcohol abuse. Presenting features of amoebic liver abscess include: Fever (85-98%) Right upper quadrant pain (84-100%) Hepatomegaly (30-80%) Diarrhea (20-35%) Cough (10-30%) Other reported symptoms include malaise, nausea, vomiting, weight loss, and anorexia.

Jaundice is uncommon, reported in approximately 5% of cases. The presence of jaundice suggests the existence of large or multiple abscesses, bacterial superinfection, and hepatic derangement and may indicate a poorer prognosis. Patients with amoebic liver abscess may have concurrent intestinal amoebiasis, but more often they have no bowel symptoms and stool microscopy is usually negative for E.

histolytica trophozoites and cysts. • Other extra-intestinal sites Pleuropulmonary involvement Pulmonary symptoms include cough (87-100%), pleuritic chest pain (50-100%), hemoptysis entamoeba coli, and dyspnea (20-25%). In the case of a hepatobronchial fistula, patients may have a cough productive of copious amounts of brown sputum. Cardiac involvement Cardiac symptoms include chest pain and dyspnea. Brain involvement Clinical features have been reported to include headache, vomiting, seizures, mental state changes, neck stiffness, and motor deficits.

Urinary tract problems; genital disease, including rectovaginal fistulae; perianal disease; and cutaneous lesions entamoeba coli been described as case reports. • Amoebic colitis Fever Abdominal tenderness Weight loss Per-rectal bleeding or bloody stools • Amoebic liver abscess Hepatomegaly is the most important physical sign and varies depending on the size and site of the lesion.

There may be a palpable hepatic mass. Hepatic tenderness may be diffuse or localized. Do other diseases mimic its manifestations? • Amoebic colitis Salmonellosis (infection with Salmonella spp) Shigellosis (infection with Shigella spp) Campylobacter infections Giardiasis (Giardia lamblia infection) Cytomegalovirus colitis Escherichia coli infections Cryptosporidiosis (Cryptosporidium parvum infection) Cyclosporiasis (Cyclospora cayetanensis infection) Irritable bowel syndrome Inflammatory entamoeba coli disease Ischemic colitis Diverticulitis Balantidium coli • Ameboma Ileo-caecal tuberculosis Carcinoma of bowel • Amoebic Liver Abscess Pyogenic liver abscess Hepatoma Acute cholecystitis Parasitic cysts (such as hydatid disease) What laboratory studies should you order and what should you expect to find?

Results consistent with the diagnosis: • Leukocytosis without eosinophilia, mild anemia, and raised alkaline phosphatase are the most common findings in amoebic liver abscess. Other abnormalities include elevated levels of bilirubin. • Positive fecal occult blood test is seen in at least 70% of patients with amoebic colitis.

Results that confirm the diagnosis • There is no worldwide gold standard test for the diagnosis of amoebiasis because of the lack of availability of certain tests in developing world settings and the diversity of presentations of intestinal and extra-intestinal amoebiasis in which different testing methods have variable sensitivity and specificity.

• Stool microscopy may be difficult to interpret because of the inability to differentiate between different species of Entamoeba.

However, in the presence of symptoms of acute colitis, it can be presumed there is infection with E. entamoeba coli. • Stool antigen tests are increasingly used for diagnosis, although there are conflicting reports of the sensitivity and specificity of stool antigen testing in developing versus developed world settings.

• Serology has limitations in differentiating between acute and past infection with E. histolytica. • Polymerase chain reaction (PCR)-based approaches are generally considered the method of choice in developed countries and have been strongly endorsed by the World Health Organization (WHO). However, these methods may not be available in all clinical settings.

• The non-invasive diagnosis of amoebic liver entamoeba coli is challenging, as most patients at the time of diagnosis do not have concurrent intestinal infection with E.

histolytica and fecal testing is negative in the majority of patients. • Stool samples, tissue samples Stool microscopy Examination of a minimum of three stool samples is recommended, with a detection rate of 85-95% reported. Microscopy is confounded with false positives, because E. histolytica is microscopically indistinguishable from the nonpathogenic entamoeba species E.

dispar and E. moshkovskii. Finding trophozoites containing ingested red blood cells (RBC) has previously been considered diagnostic for amoebic colitis. However, these are not seen in the majority of patients and have also been found in vitro and in vivo when E. dispar was found. Most entamoeba coli with amoebic liver abscess do not have concurrent intestinal infection at the time of diagnosis, and fecal testing is negative in the majority of patients.

Treatment based on stool microscopy is reasonable if there are consistent clinical symptoms, but, in asymptomatic infections, stool microscopy results may be difficult to interpret.

Culture Culture has a significant entamoeba coli rate and is technically difficult, so it not routinely performed. Stool antigen detection Entamoeba coli antigen detection is generally performed using antigen-based enzyme-linked immunosorbent assay (ELISA) kits.

Antigen entamoeba coli has a number of advantages over microscopy, including the ability to differentiate between species of Entamoeba, rapidity of testing, and greater sensitivity. Several studies in regions of the world in which E. histolytica is endemic have reported high sensitivities between 95 and 100% with stool antigen detection kits.

However, these results have not been reproduced in non-endemic areas in which sensitivities as low as 0-38% have been reported when compared with PCR. Stool antigen detection kits are relatively cheap and simple to perform and are a viable option for resource limited settings without access to PCR and where serology is less useful.

Colonic biopsy Colonic biopsy may be helpful in the diagnosis of amoebic colitis if other diagnostic tests are negative.

The detection rate of trophozoites on histopathologic examination of biopsy specimens from patients with amoebic colitis varies in different reports from all to only some patients. Aspiration and culture entamoeba coli fluid from amoebic abscesses Amoebic pus is often described as having a classic “anchovy paste” or “chocolate sauce” appearance; however, the color can vary from pink to dark brown.

Aspirated pus is usually sterile, although bacterial superinfection can occur. The microscopy detection rate of active trophozoites varies from 0 to 100% in different series. • Other tests PCR PCR, particularly real-time PCR, is a costly procedure compared with fecal microscopy and antigen-based detection tests and is not available in most clinical settings.

PCR, including real-time PCR, is able to identify Entamoeba histolytica in a variety of clinical specimens, including feces, tissues, and liver abscess aspirates. PCR has been shown to be 100% specific compared to isoenzyme analysis from culture and significantly more sensitive than microscopy or culture in the diagnosis of Entamoeba histolytica and Entamoeba dispar.

PCR has also been reported approximately 100 times more sensitive than the best ELISA stool antigen detection kit currently available. The detection of E.

histolytica DNA by PCR in aspirates from liver abscesses has been reported to show high sensitivity. A recent study has also reported that detection of E. histolytica DNA in blood, urine, and saliva by PCR may assist in the diagnosis of liver abscess. Serology Serology is also useful for diagnosing amoebiasis. Many different assays have been developed for the detection of antibodies, including indirect haemagglutination (IHA), agar gel diffusion, counterimmunophoresis indirect immunofluorescence assay (IFA), and ELISA.

Serum antibodies to E. histolytica are usually detectable within 5-10 days of acute infection. Serum IgG antibodies persist for years, whereas serum IgM levels generally become negative within 6-12 months of treatment.

Between 10-35% of uninfected individuals in endemic areas have anti-amoebic antibodies due to previous, often undiagnosed infection with E. histolytica. Consequently, negative serology in these populations helps exclude disease, but positive serology is difficult to interpret as it does not distinguish between acute infection and past exposure to the parasite. Techniques reported to have excellent sensitivity and specificity include ELISA, indirect hemagglutination (IHA), and immunofluorescence.

Agar gel diffusion and counterimmunophoresis are less sensitive than IHA but are inexpensive and, in most patients, only remain positive for 6-12 months, which may make them more useful in endemic areas. Amoebic serology is highly sensitive (94%) and specific (95%) for the diagnosis of liver abscess; however, a false-negative serological test can be obtained early during infection (within the first 7-10 days).

entamoeba coli

Immunochromatographic assays The Triage parasite panel (TPP; Biosite Diagnostic Inc., San Diego, CA) is an immunochromatographic assay for the simultaneous detection of antigens specific for Giardia lamblia, E. histolytica/E. dispar, and Cryptosporidium parvum. Several studies have reported high sensitivity compared to microscopy; however, a lower sensitivity has been reported when compared to PCR or ELISA. The TPP is unable to differentiate between E.

histolytica, E. dispar, and E. moshkovskii and, therefore, has limited clinical application. • Histopathology Pathological findings in amoebic colitis include mucosal entamoeba coli, multiple discrete ulcers separated by normal colonic mucosa, diffusely inflamed and edematous mucosa, and necrosis and perforation of the intestinal wall. Typically, trophozoites of E. histolytica are seen within the inflammatory debris or localized to the advancing edges of ulcers. The classically described “flask-shaped” amoebic ulcer is caused by lateral spread of trophozoites after invasion of the submucosa.

Histopathology in amoebic liver abscesses demonstrates well circumscribed regions of dead hepatocytes, liquefied cells, and cellular debris. A ring of connective tissue, with few inflammatory cells and amoebic trophozoites, which usually surrounds the lesion. Amoeba can be found at the edge of the lesion but are rarely detected in the pus or within the abscess cavity itself. Hepatocyte death is thought to be mediated by lysis of neutrophils by E.

histolytica, which causes release of cellular mediators. The lysis of neutrophils may also explain the paucity of inflammatory cells in typical histopathology of amoebic liver abscess. What imaging studies will be helpful in making or excluding the diagnosis of amoebiasis?

• Imaging techniques, such as ultrasound, CT, and MRI, have excellent sensitivities for the detection of liver abscess entamoeba coli can help to support the diagnosis; however, there are no findings specific for amoebic liver abscess on imaging. • Ultrasound ($) Ultrasound is cheap, accessible, and noninvasive. It is very sensitive in the diagnosis of liver abscess (approximately 95%) but lacks specificity. Abscesses are seen as well-defined hypoechoic areas in the liver parenchyma, which are homogenous in appearance with rounded edge.

The majority of patients have single abscesses of variable size located in the right liver lobe, predominantly within segments six to eight. Multiple abscesses or abscesses located in the left liver lobe are found less frequently but are more likely to result in severe and complicated clinical courses. The vast majority of successfully treated abscesses completely resolve to a sonographically normal parenchymal pattern; however, 7-10% of patients may still have typical residual lesions 1-13 years after resolution of clinical symptoms.

• Plain films (x-ray) ($) Abdominal x-rays may be useful in toxic megacolon, where there is total or segmental non-obstructive dilatation of the colon to an external diameter greater than or equal to 6 cm.

In patients with perforation, free gas may be seen under the diaphragm. In amoebic liver abscess, patients may have an elevated right hemidiaphragm on x-ray or a right-sided pleural effusion. • Barium enema ($) Generally, the radiographic findings in the colon are nonspecific and may be observed in diseases other than amoebiasis.

However, a barium enema can pick up perforation, luminal narrowing in amoeboma, and dilatation of the colon in toxic megacolon. Patients with amoebic colitis may have focal short segmental colitis with skip areas or diffuse colitis. The right side of the colon tends to be more severely involved, invariably sparing the terminal ileum. • Computed Tomography (CT) ($$) Entamoeba coli is slightly more sensitive in the diagnosis of liver abscess than ultrasound but is more expensive and may not be as readily entamoeba coli in endemic areas Contrast-enhanced CT shows a low-density mass that may have a peripheral solid component and central liquefied component of different densities.

Chest CT imaging is useful in the investigation and diagnosis of pleuropulmonary amoebiasis. • Magnetic Resonance Imaging (MRI) ($$$$) MRI in sensitive in identifying amoebic liver abscesses. Amoebic liver abscess appears as a low signal intensity lesion on T1-weighted and high signal intensity on T2-weighted images.

It may be unilocular or multiloculated. • Gallium Scan ($$) A Gallium scan may be helpful in differentiating an amoebic liver abscess from a pyogenic abscess. Amoebic liver abscesses do not contain neutrophils, therefore, gallium scanning reveals a cold lesion, sometimes with a bright rim. Conversely, a pyogenic abscess would have increased gallium uptake in the center. • Entamoeba coli and/or Colonoscopy ($$) The appearance of the colon in amoebic colitis ranges from non-specific mucosal thickening and inflammation to classic flask-shaped amoebic ulcers.

Colonoscopy must be performed with care because of the risk of perforation. Scrapings or biopsy specimens taken from the edge of ulcers may be positive for cysts or trophozoites on microscopy, and antigen testing for E. histolytica may be positive. • $ = 60-125; $$ 125-500; $$$ 500-1,000; $$$$ > 1,000 What complications can be associated with this infection, and are there additional treatments that can help to alleviate these complications? Complications can be grouped into those that occur in intestinal amoebiasis (amoebic colitis, amoeboma, toxic megacolon, peritonitis, and cutaneous amoebiasis) and those that occur in extra-intestinal amoebiasis (amoebic liver abscess, splenic abscess, brain abscess, empyema, and pericarditis).

Complications of Intestinal Amoebiasis: • Fulminant amoebic colitis Fulminant colitis occurs in approximately 0.5% of cases. Clinical presentation is characterized by profuse bloody diarrhea, fever, pronounced leukocytosis, and widespread abdominal pain, and it is often complicated by bowel necrosis leading to perforation.

Signs of peritonitis (e.g., guarding, rebound tenderness) may be present. A case series of 50 adult patients in Colombia with fulminant colitis, reported an intestinal perforation rate of approximately 75% and a mortality rate greater than 40%. Treatment is with nitroimidazoles, and early surgical management is frequently required, along with broad spectrum antibiotics in patients with intestinal perforation.

Pregnant women, immunocompromised individuals, and patients receiving corticosteroids are especially at risk of fulminant disease. • Amoeboma Localized colonic infection can result in the formation of a mass of granulation tissue called an amoeboma. Amoeboma is an uncommon complication of intestinal amoebiasis, occurring in approximately 1.5% of all cases.

Symptoms and signs include localized tenderness and pain and concurrent amoebic colitis, and/or amoebic liver abscess may be seen. Amoeboma is important to be aware of, as it can mimic colon cancer. • Toxic megacolon, seen in approximately 0.5% of cases Toxic megacolon is a potential complication of any form of colitis, and the differential diagnosis includes both inflammatory and infectious causes.

It is defined as total or segmental entamoeba coli dilatation of the colon to an external diameter greater than or equal to 6 cm associated with systemic toxicity.

Joint surgical and medical management are critical. Mortality is increased following perforation. Colectomy is indicated if the dilatation persists beyond the first 24 hours of admission in association with pyrexia and tachycardia.

Amoebic colitis has also been reported in asymptomatic patients. In a cohort of 5193 Japanese patients undergoing colonoscopy for investigation entamoeba coli positive fecal occult blood tests, 4 were found to have amoebic ulcerative lesions in the caecum and ascending colon, none of whom had abdominal symptoms. Complications of Extra-intestinal Amoebiasis and Hematogenous Spread • Pleuropulmonary involvement Pleuropulmonary involvement can result from atelectasis and development of a sympathetic transudative pleural effusion, rupture of a liver abscess into the chest cavity leading to empyema, or hematogenous spread resulting in parenchymal infection.

It is the second most common extra-intestinal manifestation of amoebiasis after hepatic involvement Symptoms include cough (87-100%), pleuritic chest pain (50-100%), hemoptysis (44-50%) and dyspnea (20-25%). If a hepatobronchial fistula develops, patients may have a cough productive of entamoeba coli amounts of brown sputum containing necrotic material and occasionally amoebic trophozoites. Physical examination may reveal hepatic enlargement and tenderness, dullness to percussion (particularly in the right lung base), and diminished or absent breath sounds.

Fever may be present in 82-100% of patients. In chronic cases, patients may be severely emaciated and digital clubbing may be prominent. It is common to hear a pleural friction rub in patients with an amoebic liver abscess extending to the pleura. • Cardiac involvement Cardiac involvement is rare but has a mortality entamoeba coli approximately 30%. It results from liver abscess rupture into the pericardium and can present with signs and symptoms of pericarditis (chest pain, pericardial rub, dyspnea, tachycardia) or cardiac tamponade.

• Brain involvement Cerebral amoebiasis is a rare cause of brain abscess thought to result from hematogenous dissemination from the colon via hepatic, pulmonary, or vertebral veins. Infection of the central nervous system (CNS) without hepatic involvement is rare, and the incidence of brain abscesses in patients with confirmed amoebic liver abscesses has been reported to vary from 0.6 to 8.1%.

Clinical features have been reported to include headache, vomiting, seizures, mental state changes, neck stiffness, and motor deficits. • Urinary tract problems; genital disease, including rectovaginal fistulae; perianal disease; and cutaneous lesions have been described as case reports. Other complications • Lactose malabsorption is significantly more common in individuals infected with E.

histolytica and passing cysts compared with control subjects. • Amoebiasis has also been linked with malnutrition in children. What is the life cycle of the parasite, and how does the life cycle explain infection in humans? • Entamoeba histolytica has two morphological forms: the infectious cyst and the invasive trophozoite, both of which may be found in the feces of infected patients (cysts are typically found in formed stool, whereas trophozoites are typically found in diarrheal stool) (see Figure 1).

• Infection occurs when the cysts are ingested in fecal-contaminated food, water, or by hands. Transmission can also occur through exposure to fecal matter during sexual contact. Entamoeba cysts are relatively environmentally resistant and entamoeba coli survive for days to weeks in the external environment. • Excystation occurs in the small intestine, and trophozoites are released; they migrate to the large intestine where they multiply by binary fission • In asymptomatic carriers, the trophozoites remain confined to the intestinal lumen, and cysts are passed in stools.

• When the trophozoites invade the intestinal mucosa, patients typically present with intestinal disease. • Spread of trophozoites through the bloodstream to extra-intestinal sites, such as the liver, brain, and lungs, results in pathologic manifestations involving these organs (extra-intestinal disease).

Figure 1. Entamoeba coli cycle of Entamoeba histolytica from the CDC DPDx Website (http://www.dpd.cdc.gov/dpdx/) Transmission, risk factors and prevalence • Entamoeba histolytica can be transmitted by ingestion of contaminated water or food; via the fecal-oral route (via fomites or person-to-person spread); or via oral, anal, and oral-genital sexual practices.

• Limited data are available on seasonal variation in incidence of E. histolytica infection • Deficiencies in hygiene and sanitary practices and overcrowding are predisposing factors for entamoeba coli • Entamoeba histolytica is found worldwide and remains an important health problem in developing countries in which sanitation, infrastructure, and health education are not adequate.

Entamoeba coli, E. histolytica is also seen in developed countries, predominantly due to immigration and increases in international entamoeba coli. • Endemic countries include Mexico, India, Bangladesh, South Africa, some Central and South American countries, and Asian Pacific countries.

• Hepatic amoebiasis is endemic entamoeba coli Thailand, India, Egypt, and South Africa. In a single hospital in Vietnam, more than 1200 cases of hepatic amoebiasis were identified during an 8-year period. The incidence is also high in Central and South America, particularly in Mexico and in the Amazon regions of Brazil.

• Recent studies using techniques able to isolate E. histolytica from the other species, such as ELISA, PCR, and isoenzyme analysis, have demonstrated prevalence of intestinal amoebiasis ranging from 1 to 76% in a diverse range of patient populations. • In developed countries, high-risk groups include travelers, immigrants from endemic areas, and men who have sex with men (MSM).

• Amoebic liver abscesses are ten times more common in men than women and are rare in children. Other risk factors include travel to endemic areas and a history of alcohol abuse. They are most common in adults in their fourth and fifth decades of life Travelers to endemic areas Travelers to any endemic area may entamoeba coli Entamoeba, but travelers to Asia seem at most risk.

Patients can present with amoebic liver abscess months to years after travel or residency in an endemic area, so a careful travel history is extremely important. Men who have sex with men (MSM) Oral, anal, and oral-genital sexual practices are reported to predispose MSM to infection with E. histolytica. Pregnant women, immunocompromised individuals, and patients receiving corticosteroids are especially at risk of fulminant disease. • Infection control and prevention issues Anti-infective prophylaxis entamoeba coli not recommended.

No vaccination is currently available. • Travelers to endemic areas should avoid drinking local water and should eat only cooked food or peeled fruit. • Cysts are resistant to low doses of chlorine or iodine, so, if safe bottled water is unavailable, water should be boiled.

• Prevention of amoebic infection could be accomplished by improvements in sanitation, a clean water supply, health education, and public health measures entamoeba coli identify and treat carriers. There are no epidemiologically significant animal carriers. How does this organism cause disease? • Trophozoites of E. histolytica adhere to colonic epithelial cells via a specific lectin, the galactose/N-acetylgalactosamine lectin.

This lectin also seems to play a role in immunity, with one study from Bangladesh indicating that children with a mucosal IgA response against the lectin had 86% fewer new infections during a 1-year period than children without this response. • Colitis results after penetration of the trophozoite through the intestinal mucous layer.

E. histolytica trophozoites are cytolytic and are able to kill both epithelial cells and inflammatory cells. This is thought to be medicated by a number of mechanisms, including: Secretion of proteinases by the trophozoites Lysis of target cells via a contact-dependent mechanism Induction of programmed cell death (apoptosis) Formation of amoebapores, small peptides capable of forming pores in lipid bilayers Changes in intestinal permeability, probably via disruption of tight-junction proteins WHAT’S THE EVIDENCE for specific management and treatment recommendations?

Abba, K, Sinfield, R, Hart, C, Garner, P. “Pathogens associated with persistent diarrhea in children in low and middle income countries: systematic review”.

BMC Infect Dis. vol. 9. 2009 June 10. pp. 88 Ahmad, N, Khan, M, Hoque, M, Haque, R, Mondol, D. “Detection of Entamoeba histolytic DNA from liver abscess aspirate using polymerase chain reaction (PCR): a diagnostic tool for amoebic liver abscess”. Bangladesh Med Res Council Bull. vol. 33. 2007. pp. 13-20. Aikat, B, Bhusnurmath, S, Pal, A. entamoeba coli pathology and pathogenesis of fatal hepatic amoebiasis – a study based on 79 autopsy cases”.

Trans Roy Soc Trop Med Hygiene. vol. 73. 1979. pp. 188-92. Ali, K, Clark, C, Petri, W. “Molecular epidemiology of amebiasis”. Infect Gen Evolution. vol. 8. 2008. pp. 698-707. Aristizabal, H, Acevedo, J, Botero, M. “Fulminant amebic colitis”. World J Surg. vol. 15. 1991. pp. 216 Bakshi, JS, Ghiara, JM, Nanivadekar, AS.

“How does tinidazole compare with metronidazole? A summary report of Indian trials in amoebiasis and giardiasis”. Drugs. vol. 15. 1978. pp. 33-42. Blackwell, V, Travis, S. “Toxic dilatation of the Colon”. Med. vol. 39. 2011. pp. 105-7. Blessmann, J, Binh, H, Hung, D, Tannich, E, Burchard, G. “Treatment of amoebic liver abscess with metronidazole alone or in combination with ultrasound-guided needle aspiration: a comparative, prospective and randomized study”.

Trop Med Int Health. vol. 8. 2003. pp. 1030-4. Blessmann, J, Buss, H, Nu, P, Dinh, B, Ngo, Q, Van, A, Alla, M, Jackson, T, Ravdin, Entamoeba coli, Tannich, E. “Real time PCR for detection and differentiation of Entamoeba histolytica and Entamoeba dispar in faecal samples”.

J Clin Microbiol. vol. 40. 2002. pp. 4413-7. (Evaluation of several hundred stool samples from areas of amebiasis endemicity in Vietnam and South Africa. PCR was 100% specific compared to entamoeba coli analysis or culture and significantly more sensitive than entamoeba coli or culture in the diagnosis of Entamoeba histolytica and Entamoeba dispar.) Blessmann, J, Van Linh, P, Nu, P, Thi, H, Muller-Myhsok, B, Buss, H, Tannich, E.

“Epidemiology of amoebiasis in a region of high incidence of amebic liver abscess in central Vietnam”. Am J Trop Med Hyg. vol. 66. 2002. pp. 578-83. Cardoso, J, Kimura, K, Stoopen, M, Cervantes, L, Flizondo, L, Churchill, R, Moncada, R. “Radiology of invasive amoebiasis of the colon”. Am J Roentgenol. vol. 128. 1977. pp. 935-41. “DPDx – Laboratory identification of public health concern”. Chavez-Tapia, N, Hernandez-Calleros, J, Tellez-Avila, F, Torre, A, Uribe, M.

“Image-guided percutaneous procedure plus metronidazole versus metronidazole alone for uncomplicated amoebic liver abscess”. Cochrane Database of Systematic Reviews. vol. 1. 2009. pp. CD004886 De Villiers, J, Durra, G. “Amoebic abscess of the brain”. Clin Radiol.

vol. 53. 1998. pp. 307-9. Dinleyici, E, Eren, M, Yargic, Z, Dogan, N, Vandenplas, Y. “Clinical efficacy of Saccharomyces boulardii and metronidazole compared to metronidazole alone in children with acute bloody diarrhea caused by amebiasis: a prospective, randomized, open label study”.

Am J Trop Med Hygiene. vol. 80. 2009. pp. 953-5. Escobedo, A, Almirall, P, Alfonso, M, Cimerman, S, Rey, S, Terry, S. “Treatment of intestinal protozoan infections in children”. Arch Dis Child. vol. 94. 2009. pp. 478-82. Fotedar, R, Stark, D, Beebe, N, Marriott, D, Ellis, J, Harkness, J. “PCR detection of Entamoeba histolytica, Entamoeba dispar, and Entamoeba moshkovskii in stool samples from Sydney, Australia”.

J Clin Microbiol. vol. 45. 2007. pp. 1045-37. Fotedar, R, Stark, D, Beebe, N, Marriott, D, Ellis, J, Harkness, J. “Laboratory diagnostic entamoeba coli for Entamoeba species”. Clin Microbiol Rev. vol. 20. 2007. pp. 511-32. (Excellent review of laboratory techniques used in the diagnosis of Entamoeba species.) Gamboa, M, Basualdo, J, Cordoba, M, Pezzani, B, Minvielle, M, Lahitte, H.

“Distribution of intestinal parasitoses in relation to environmental and sociocultural parameters in La Plata, Argentina”. J Helminthology. vol. 77.

2003. pp. 15-20. Gonzales, M, Dans, L, Martinez, E. “Antiamoebic drugs for treating amoebic colitis”. Cochrane Database of Systematic Reviews. vol. 2. 2009. pp. CD006085 (Systematic review of antiamoebic drugs for treating amoebic colitis.) Haque, R, Huston, C, Hughes, M, Houpt, E, Petri, W. “Amebiasis”. N Engl J Med. vol. 348. 2003. pp. 1565-73. Haque, R, Mondal, D, Duggal, P. “Entamoeba histolytica infection in children and protection from subsequent amebiasis”. Infect Immun. vol. 74. 2006.

pp. 904-9. Haque, R, Neville, L, Hahn, P, Petri, W. “Rapid diagnosis of Entamoeba infection by using Entamoeba and Entamoeba histolytica stool antigen detection kits”.

J Clin Microbiol. vol. 33. 1995. pp. 2558-61. Islam, N, Hasan, K. “Tinidazole and metronidazole in hepatic amebiasis”. Drugs. vol. 15. 1978. pp. 26-9. Lodhi, S, Sarwari, A, Muzammil, M, Salam, A, Smego, R. “Features distinguishing amoebic from pyogenic liver abscess: a review of 577 adult cases”. Trop Med Int Health. vol. 9. 2004. pp. 718-23. Muzaffar, J, Madan, K, Sharma, M, Kar, P. “Randomized, single-blind, placebo-controlled multicenter trial to compare the efficacy and safety of metronidazole and satranidazole in patients with amebic liver abscess”.

Digestive Dis Sci. vol. 51. 2006. pp. 2270-3. Okamoto, M, Kawabe, T, Ohata, K. entamoeba coli colitis in asymptomatic subjects with positive fecal occult blood test results: clinical features different from symptomatic cases”.

Am J Trop Med Hygeine. vol. entamoeba coli. 2005. pp. 934-5. Park, M, Kim, K, Ha, H, Lee, D. “Intestinal parasitic infection”. Abdominal Entamoeba coli. vol. 33. 2008. pp. 166-71. Patterson, M, Healy, G, Shabot, J. “Serological testing for amoebiasis”. Gastroenterology. vol. 78. 1980. pp. 136-41. Petri, W, Mondal, D, Peterson, K, Duggal, P, Haque, R. “Association of malnutrition with amoebiasis”. Nutr Rev. vol. 67. 2009. pp. 207-15. Petri, W, Singh, U. “Diagnosis and management of amoebiasis”.

Clin Inf Dis. vol. 29. 1999. pp. 1117-25. Prathap, Entamoeba coli, Gilman, R. “The histopathology of acute intestinal amoebiasis: a rectal biopsy study”. Am J Pathol. vol. 60. 1970. pp. 229-46. (Histopathology of rectal biopsy in a case series of 53 patients with intestinal amoebiasis.) Rana, S, Bhasin, D, Vinayak, V. “Prospective evaluation of lactose malabsorption by lactose hydrogen breath test in individual’s infection with Entamoeba histolytica and passing cysts”.

Brit J Nutr. vol. 92. 2004. pp. 207-8. Rossignol, J-F, Kabil, S, El-Gohary, Y, Younis, A. “Nitazoxanide in the treatment of amoebiasis”. Trans Roy Soc Trop Med Hygiene. vol. 101. 2007. pp. 1025-31. Salles, J, Moraes, L, Salles, M. “Hepatic amoebiasis”. Braz J Infec Dis. vol. 7. 2003. pp. 96-110. Salles, J, Salles, M, Moraes, L, Silva, M.

“Invasive amoebiasis: an update on diagnosis and management”. Expert Rev Anti-Infective Ther. vol. 5. 2007. pp.

entamoeba coli

893-901. Samarawickrema, N, Brown, D, Upcroft, J, Thammapalerd, N, Upcroft, P. “Involvement of superoxide dismutase and pyruvate: ferredoxin oxidoreductase in mechanisms of metronidazole resistance in Entamoeba histolytica”. J Antimicro Chemother. vol. 40. 1997. pp. 833-40. Shah, N, DuPont, H, Ramsey, D.

“Global etiology of travelers’ diarrhea: systematic review from 1973 to the present”. Am J Trop Med Hygeine. vol. 80. 2009. pp. 609-14. (Excellent systematic review of 51 studies of travelers’ diarrhea from 1973-2008 looking at regional differences in pathogens.) Shamsuzzaman, S, Hashiguchi, Y.

“Thoracic amoebiasis”. Clin Chest Med. vol. 23. 2002. pp. 479-92. Simjee, AE, Gathiram, V, Jackson, TF, Khan, BF. “A comparative trial of metronidazole versus tinidazole in the treatment of amoebic liver abscess”. South African Med J. vol. 68. 1985. pp. 923-4. Solaymani-Mohammadi, S, Rezaian, M, Babaei, Z, Rajabpour, A, Meamar, A, Pourbabai, A, Petri, W.

“Comparison of a stool antigen detection kit and PCR for diagnosis of Entamoeba histolytica and Entamoeba dispar infections in asymptomatic cyst passers in Iran”. J Clin Microbiol. vol. 44. 2006. pp. 2258-61. Stark, D, Fotedar, R, Van Hal, S, Beebe, N, Marriott, D, Ellis, J, Harkness, J.

“Prevalence of enteric protozoa in human immunodeficiency virus (HIV)-positive and HIV-negative men who have sex with men from Sydney, Australia”. Am J Trop Med Hygeine.

vol. 76. 2007. pp. 549-52. Tachibana, H, Kobayashi, S, Okuzawa, E, Masuda, G. “Detection of pathogenic Entamoeba histolytica DNA in liver abscess fluid by polymerase chain reaction”. Int J Parasitol. vol. 22. 1992. pp. 1193-6. Drugs for parasitic infections: treatment guidelines. 2010. Walsh, JA. “Problems in recognition and diagnosis of amoebiasis: estimation of the global magnitude of the morbidity and mortality”. Rev Infect Dis. vol. 8. 1986. pp. 228-38.

Wassman, C, Hellberg, A, Tannich, E, Bruchhaus, I. “Metronidazole resistance in the protozoan parasite Entamoeba histolytica is associated with increased expression of iron-containing superoxide dismutase and peroxiredoxin and decreased expression of ferredoxin 1 and flavin reductase”.

J Biological Chem. vol. 274. 1999. pp. 26051-6. Ximénez, C, Morán, P, Rojas, L, Valadez, A, Gómez, A. “Reassessment of the epidemiology of amoebiasis: state of the art”. Infect Genet Evol. vol. 9. 2009. pp. 1023-32. Yamaura, H, Araki, K, Kikuchi, K, Itoda, I, Totsuka, K, Kobayakawa, T. “Evaluation of dot-ELISA for serological diagnosis of amebiasis”. J Infect Chemother. vol. 9. 2003.

pp. 25-9. Zaman, S, Khoo, J, Ng, S, Ahmed, R, Khan, M, Hussain, R, Zaman, V. “Direct amplification of Entamoeba histolytica DNA from amoebic liver abscess pus using polymerase entamoeba coli reaction”. Parasitol Res. vol. 86. 2000. pp. 724-8. Zengzhu, G, Bracha, R, Nuchamowitz, Y, Cheng, Entamoeba coli, Mirelman, D.

“Analysis by enzyme-linked immunosorbent assay and PCR of human liver abscess aspirates from patients in China for Entamoeba histolytica”.

J Clin Microbiol. vol. 37. 1999. pp. 3034-6. Copyright © 2017, 2013 Decision Support in Medicine, LLC. Entamoeba coli rights reserved.

No sponsor or advertiser has participated in, approved or paid for the content provided by Decision Support in Medicine LLC.

The Licensed Content is the property of and copyrighted by DSM. Jump to Section • OVERVIEW: What every clinician needs to know • Parasite name and classification • What is the best treatment?

• Do other diseases mimic its manifestations? • What laboratory studies should you order and what should you expect to find? • Results consistent with the diagnosis:• Results that confirm the diagnosis • What imaging studies will be helpful in making or excluding the diagnosis of amoebiasis?• What complications can be associated with this infection, and are there additional treatments that can help to alleviate these complications?• What is the life cycle of the parasite, and how does the entamoeba coli cycle explain infection in humans?• How does this organism cause disease?

Loading. Enjoying our content? Thanks for visiting Infectious Disease Advisor. We hope you’re enjoying the latest clinical news, full-length features, case studies, and more.

You’ve viewed {{metering-count}} of {{metering-total}} articles this month. If you wish to read unlimited content, please log in or register below. Registration is free. {{login-button}} {{register-button}} Log in to continue reading this article.

Don’t miss out on today’s top content on Infectious Disease Advisor. Register for free and gain unlimited entamoeba coli to: - Clinical News, with personalized daily picks for you - Case Studies - Conference Coverage - Full-Length Features - Drug Monographs - And More {{login-button}} {{register-button}} Want to read more?none

Voor altijd van E. coli af met behulp van deze natuurlijke remedie

2022 www.videocon.com