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Amebiasis

  • Author: Vinod K Dhawan, MD, FACP, FRCPC, FIDSA; Chief Editor: Michael Stuart Bronze, MD  more...
 
Updated: Mar 24, 2016
 

Background

Amebiasis is caused by Entamoeba histolytica (see the image below), a protozoan that is found worldwide (see Etiology).[1, 2, 3, 4] The highest prevalence of amebiasis is in developing countries where barriers between human feces and food and water supplies are inadequate (see Epidemiology).

Trichrome stain of Entamoeba histolytica trophozoi Trichrome stain of Entamoeba histolytica trophozoites in amebiasis. Two diagnostic characteristics are observed. Two trophozoites have ingested erythrocytes, and all 3 have nuclei with small, centrally located karyosomes.

Although most cases of amebiasis are asymptomatic, dysentery and invasive extraintestinal disease can occur. Amebic liver abscess is the most common manifestation of invasive amebiasis, but other organs can also be involved, including pleuropulmonary, cardiac, cerebral, renal, genitourinary, peritoneal, and cutaneous sites. In developed countries, amebiasis primarily affects migrants from and travelers to endemic regions, men who have sex with men, and immunosuppressed or institutionalized individuals.

E histolytica is transmitted via ingestion of the cystic form (infective stage) of the protozoa. Viable in the environment for weeks to months, cysts can be found in fecally contaminated soil, fertilizer, or water or on the contaminated hands of food handlers. Fecal-oral transmission can also occur in the setting of anal sexual practices or direct rectal inoculation through colonic irrigation devices.

Excystation then occurs in the terminal ileum or colon, resulting in trophozoites (invasive form). The trophozoites can penetrate and invade the colonic mucosal barrier, leading to tissue destruction, secretory bloody diarrhea, and colitis resembling inflammatory bowel disease. In addition, the trophozoites can spread hematogenously via the portal circulation to the liver or even to more distant organs (see Pathophysiology).

E histolytica is capable of causing a spectrum of illnesses (see Presentation). Intestinal conditions resulting from E histolytica infection include the following:

  • Asymptomatic infection
  • Symptomatic noninvasive infection
  • Acute proctocolitis (dysentery)
  • Fulminant colitis with perforation
  • Toxic megacolon
  • Chronic nondysenteric colitis
  • Ameboma
  • Perianal ulceration

Extraintestinal conditions resulting from E histolytica infection include the following:

  • Liver abscess
  • Pleuropulmonary disease
  • Peritonitis
  • Pericarditis
  • Brain abscess
  • Genitourinary disease

Laboratory diagnosis of amebiasis is made by demonstrating the organism or by employing immunologic techniques. In addition to standard blood tests, other laboratory studies employed for diagnosis include microscopy, culture, serologic testing, and polymerase chain reaction (PCR) assay (see Workup).

Treatment of amebiasis includes pharmacologic therapy, surgical intervention, and preventive measures, as appropriate (see Treatment). Most individuals with amebiasis may be treated on an outpatient basis, though several clinical scenarios may favor inpatient care.

See Common Intestinal Parasites, a Critical Images slideshow, to help make an accurate diagnosis.

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Pathophysiology

E histolytica is a pseudopod-forming, nonflagellated protozoal parasite that causes proteolysis and tissue lysis (hence the species name) and can induce host-cell apoptosis (see the image below). Humans and perhaps nonhuman primates are the only natural hosts.

Life cycle of Entamoeba histolytica. Life cycle of Entamoeba histolytica.

Ingestion of E histolytica cysts (see the first image below) from the environment is followed by excystation in the terminal ileum or colon to form highly motile trophozoites (see the second image below). Upon colonization of the colonic mucosa, the trophozoite may encyst and is then excreted in the feces, or it may invade the intestinal mucosal barrier and gain access to the bloodstream, whereby it is disseminated to the liver, lung, and other sites. Excreted cysts reach the environment to complete the cycle.


Entamoeba histolytica cyst. Image courtesy of Cen Entamoeba histolytica cyst. Image courtesy of Centers for Disease Control and Prevention.

Entamoeba histolytica trophozoite. Image courtesy Entamoeba histolytica trophozoite. Image courtesy of Centers for Disease Control and Prevention.

Disease may be caused by only a small number of cysts, but the processes of encystation and excystation are poorly understood. The adherence of trophozoites to colonic epithelial cells seems to be mediated by a galactose/N -acetylgalactosamine (GAL/GalNAc)–specific lectin,[4, 5, 6] a 260-kd surface protein containing a 170-kd subunit and a 35-kd subunit. A mucosal immunoglobulin A (IgA) response against this lectin can result in fewer recurrent infections.[7]

Both lytic and apoptotic pathways have been described. Cytolysis can be undertaken by amebapores, a family of peptides capable of forming pores in lipid bilayers.[4] Furthermore, in animal models of liver abscess, trophozoites induced apoptosis via a non-Fas and non–tumor necrosis factor (TNF)-α1 receptor pathway.[8] The amebapores, at sublytic concentrations, can also induce apoptosis.

Cysteine proteinases have been directly implicated in invasion and inflammation of the gut and may amplify interleukin (IL)-1–mediated inflammation by mimicking the action of human IL-1–converting enzyme, cleaving IL-1 precursor to its active form.[4, 9] The cysteine proteinases can also cleave and inactivate the anaphylatoxins C3a and C5a, as well as IgA and immunoglobulin G (IgG).[10, 11]

E histolytica possesses about 100 putative transmembrane kinases (TMKs), which are commonly divided into 9 subgroups. Of these, EhTMKB1-9 is expressed in proliferating trophozoites and induced by serum. In an animal model, it was found to be involved in phagocytosis and to play a role as a virulence factor in amebic colitis.[12] These findings suggest that TMKs such as EhTMKB1-9 may be attractive targets for future drug development.

Epithelial cells also produce various inflammatory mediators, including IL-1β, IL-8, and cyclooxygenase (COX)-2, leading to the attraction of neutrophils and macrophages.[13, 14] Corticosteroid therapy is known to worsen the clinical outcome, possibly because of its blunting effect on this innate immune response.

Additional host defenses, including the complement system, could be inhibited directly by the trophozoites, as is suggested by the finding that a region of the GAL/GalNAc–specific lectin showed antigenic crossreactivity with CD59, a membrane inhibitor of the C5b-9 attack complex in human red blood cells.[15]

Spread of amebiasis to the liver occurs via the portal blood. The pathogenic strains evade the complement-mediated lysis in the bloodstream. Trophozoites that reach the liver create unique abscesses with well-circumscribed regions of dead hepatocytes surrounded by few inflammatory cells and trophozoites and unaffected hepatocytes. These findings suggest that E histolytica organisms are able to kill hepatocytes without direct contact.[4]

Serum antibodies in patients with amebic liver abscess develop in 7 days and persist for as long as 10 years. A mucosal IgA response to E histolytica occurs during invasive amebiasis; however, no evidence suggests that invasive amebiasis is increased in incidence or severity in patients with IgA deficiency.

Cell-mediated immunity is important in limiting the disease and preventing recurrences. Antigen-specific blastogenic responses occur, leading to production of lymphokines, including interferon-delta, which activates the killing of E histolytica trophozoites by the macrophages. This killing depends on contact, oxidative pathways, nonoxidative pathways, and nitric oxide (NO).

Lymphokines, such as TNF-α, are capable of activating the amebicidal activity of neutrophils. Incubation of CD8+ lymphocytes with E histolytica antigens in vitro elicits cytotoxic T-cell activity against the trophozoites. During acute invasive amebiasis, T-cell response to E histolytica antigens is depressed by a parasite-induced serum factor.

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Etiology

Amebiasis is a parasitic infection caused by the protozoal organism E histolytica, which can give rise both to intestinal disease (eg, colitis) and to various extraintestinal manifestations, including liver abscess (most common) and pleuropulmonary, cardiac, and cerebral dissemination.

The genus Entamoeba contains many species, some of which (ie, E histolytica, Entamoeba dispar, Entamoeba moshkovskii, Entamoeba polecki, Entamoeba coli, and Entamoeba hartmanni) can reside in the human interstitial lumen. Of these, E histolytica is the only one definitely associated with disease; the others are considered nonpathogenic.[16] Studies have recovered E dispar and E moshkovskii from patients with gastrointestinal (GI) symptoms, but whether these species cause these symptoms remains to be determined.[16]

Although E dispar and E histolytica cannot be differentiated by means of direct examination, molecular techniques have demonstrated that they are indeed 2 different species, with E dispar being commensal (as in patients with HIV infection) and E histolytica pathogenic.[16]

It is currently believed that many individuals with Entamoeba infections are actually colonized with E dispar, which appears to be 10 times more common than E histolytica[16] ; however, in certain regions (eg, Brazil and Egypt), asymptomatic E dispar and E histolytica infections are equally prevalent.[4] In Western countries, approximately 20%-30% of men who have sex with men are colonized with E dispar.[16]

E histolytica is transmitted primarily through the fecal-oral route. Infective cysts can be found in fecally contaminated food and water supplies and contaminated hands of food handlers. Sexual transmission is possible, especially in the setting of oral-anal practices (anilingus). Poor nutrition, through its effect on immunity, has been found to be a risk factor for amebiasis.[17]

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Epidemiology

United States statistics

The overall prevalence of amebiasis in the United States is approximately 4%. E dispar infection, which is always asymptomatic, is 10 times more common than E histolytica infection. Moreover, only 10% of E histolytica infections cause invasive disease. Therefore, only 1% of persons with stool microscopy findings that reveal Entamoeba develop symptomatic amebiasis.

Certain groups are predisposed to amebic colitis, including very young patients, pregnant women, recipients of corticosteroids, and malnourished individuals.[4] In 1993, a total of 2970 cases of amebiasis were reported to the Centers for Disease Control and Prevention (CDC); 33% of cases were reported in Hispanic immigrants and 17% in immigrants from Asia or the Pacific Islands.

An increased prevalence of amebiasis is noted in institutionalized persons (especially those with mental retardation), male homosexuals, and persons living in communal settings.

Travelers to endemic areas are at risk for infection. Amebic liver abscess has been reported in travel exposures as short as 4 days (median, 3 months), whereas amebic colitis is uncommon in short-term travelers. In one study, 10% of individuals returning with diarrhea were found to have amebiasis.[4] In another, the rate of acute amebic diarrhea ranged from 1.5% in travelers returning from Southeast Asia to 3.6% in those returning from Central America, with an overall rate of 2.7%.[18]

The US national death certificate data from 1990 to 2007 identified 134 deaths from amebiasis. A declining trend of deaths was noted and over 40% occurred in residents of California and Texas with US-born persons accounting for the majority of amebiasis deaths.[19]

International statistics

Worldwide, approximately 50 million cases of invasive E histolytica disease occur each year, resulting in as many as 100,000 deaths. This represents the tip of the iceberg because only 10%-20% of infected individuals become symptomatic.[20, 21, 22] The incidence of amebiasis is higher in developing countries.[23]

Earlier estimates of E histolytica infection, based on examination of stool for ova and parasites, are inaccurate, because this test cannot differentiate E histolytica from E dispar and E moshkovskii. In developing countries, the prevalence of E histolytica, as determined by enzyme-linked immunosorbent assay (ELISA) or polymerase chain reaction (PCR) assay of stool from asymptomatic persons, ranges from 1% to 21%. On the basis of current techniques, it is estimated that 500 million people with Entamoeba infection are colonized by E dispar.[16]

The prevalence of Entamoeba infection is as high as 50% in areas of Central and South America, Africa, and Asia.[24] E histolytica seroprevalence studies in Mexico revealed that more than 8% of the population were positive.[25] In endemic areas, as many as 25% of patients may be carrying antibodies to E histolytica as a result of prior infections, which may be largely asymptomatic. The prevalence of asymptomatic E histolytica infections seem to be region-dependent; in Brazil, for example, it may be as high as 11%.

In Egypt, 38% of individuals presenting with acute diarrhea to an outpatient clinic were found to have amebic colitis.[4] A study in Bangladesh indicated that preschool children experienced 0.09 episodes of E histolytica -associated diarrhea and 0.03 episodes of amebic dysentery each year. In Hue City, Vietnam, the annual incidence of amebic liver abscess was reported to be 21 cases per 100,000 inhabitants.[26]

An epidemiologic study in Mexico City reported that 9% of the population was infected with E histolytica in the 5-year to 10-year period preceding the study. Various factors, such as poor education, poverty, overcrowding, contaminated water supply, and unsanitary conditions, contributed to fecal-oral transmission.

Several studies have evaluated the association of amebiasis with AIDS.[27, 28, 29, 30, 31, 32] The impact of the AIDS pandemic on the prevalence of invasive amebiasis remains controversial. Some reports suggest that invasive amebiasis is not increased among patients with HIV infection[33] ; however, others suggest that amebic liver abscess is an emerging parasite infection in individuals with HIV infection in disease-endemic areas, as well as in non–disease-endemic areas.[34, 34]

Of 31 patients with amebic liver abscess at Seoul National University Hospital from 1990 to 2005, 10 (32%) were HIV-positive.[35] In a case-control study of persons seeking voluntary counseling and testing for HIV infection, homosexual activity, fecal-oral contamination, lower educational achievement, and older age were associated with increased risk of amebiasis.[36]

Age-related demographics

Symptomatic intestinal amebiasis occurs in all age groups. Liver abscesses due to amebiasis are 10 times more frequent in adults than in children. Very young children seem to be predisposed to fulminant colitis.

Sex-related demographics

Amebic colitis affects both sexes equally.[4] However, invasive amebiasis is much more common in adult males than in females. In particular, amebic liver abscess is 7-12 times more common in men than in women, with a predominance among men aged 18-50 years. The reason for this disparity is unknown, though hormonal effects may be implicated, as the prevalence of amebic liver abscess is also increased among postmenopausal women. Alcohol may also be an important risk factor.

Among prepubertal children, amebic liver abscess is equally common in both sexes.[4] Acuna-Soto et al noted that asymptomatic E histolytica infection is distributed equally between sexes.[37] Therefore, the higher proportion of adult males with invasive amebiasis may be due to a male susceptibility to invasive disease.

Race-related demographics

In Japan and Taiwan, HIV seropositivity is a risk factor for invasive extraintestinal amebiasis.[34] This association has not been observed elsewhere. Among HIV-positive patients, homosexual intercourse, and not immunosuppressed status, seems to be a risk factor for amebic colitis.[38]

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Prognosis

Amebic infections can lead to significant morbidity while causing variable mortality. In terms of protozoan-associated mortality, amebiasis is second only to malaria. The severity of amebiasis is increased in the following groups:

  • Children, especially neonates
  • Pregnant and postpartum women
  • Those using corticosteroids
  • Those with malignancies
  • Malnourished individuals

Intestinal infections due to amebiasis generally respond well to appropriate therapy, though it should be kept in mind that previous infection and treatment will not protect against future colonization or recurrent invasive amebiasis.

Asymptomatic intestinal amebiasis occurs in 90% of infected individuals. However, only 4%-10% of individuals with asymptomatic amebiasis who were monitored for 1 year eventually developed colitis or extraintestinal disease.[16]

With the introduction of effective medical treatment, mortality has fallen below 1% for patients with uncomplicated amebic liver abscess. However, amebic liver abscess can be complicated by sudden intraperitoneal rupture in 2-7% of patients, and this complication leads to a higher mortality.[4]

Case-fatality rates associated with amebic colitis range from 1.9% to 9.1%. Amebic colitis evolves to fulminant necrotizing colitis or rupture in approximately 0.5% of cases; in such cases, mortality may exceeds 40%[39] or even, according to some reports, 50%.

Pleuropulmonary amebiasis has a 15-20% mortality rate. Amebic pericarditis has a case-fatality rate of 40%. Cerebral amebiasis carries a very high mortality (90%).

A study of 134 deaths in the United States from 1990 to 2007 found that mortality was highest in men, Hispanics, Asian/Pacific Islanders, and people aged 75 years or older.[19] An association with HIV infection was also observed. Although deaths declined during the course of the study, more than 40% occurred in California and Texas. US-born persons accounted for the majority of amebiasis deaths; however, all of the fatalities in Asian/Pacific Islanders and 60% of the deaths in Hispanics were in foreign-born individuals.

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Patient Education

Individuals traveling to endemic areas should be advised on practices that minimize the risk of amebiasis, such as the following:

  • Avoid drinking contaminated water; use bottled water while traveling if possible
  • If local water is to be drunk, purify it by (a) boiling it for more than 1 minute, (b) using 0.22 µm filtration, or (c) iodinating it with tetraglycine hydroperiodide
  • Avoid eating raw fruits and salads, which are difficult to sterilize; eat only cooked food or self-peeled fruits if possible
  • Wash uncooked vegetables and soak them in acetic acid or vinegar for 10-15 minutes
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Contributor Information and Disclosures
Author

Vinod K Dhawan, MD, FACP, FRCPC, FIDSA Professor, Department of Clinical Medicine, University of California, Los Angeles, David Geffen School of Medicine; Chief, Division of Infectious Diseases, Rancho Los Amigos National Rehabilitation Center

Vinod K Dhawan, MD, FACP, FRCPC, FIDSA is a member of the following medical societies: American College of Physicians, American Medical Association, American Society for Microbiology, Infectious Diseases Society of America, Royal College of Physicians and Surgeons of Canada

Disclosure: Received honoraria from Pfizer Inc for speaking and teaching.

Coauthor(s)

Kerry O Cleveland, MD Professor of Medicine, University of Tennessee College of Medicine; Consulting Staff, Department of Internal Medicine, Division of Infectious Diseases, Methodist Healthcare of Memphis

Kerry O Cleveland, MD is a member of the following medical societies: American College of Physicians, Society for Healthcare Epidemiology of America, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

J Robert Cantey, MD Professor, Department of Medicine, Division of Infectious Diseases, Medical University of South Carolina

J Robert Cantey, MD is a member of the following medical societies: Alpha Omega Alpha, American Society for Microbiology, International Society of Travel Medicine, Southern Society for Clinical Investigation, Musculoskeletal Infection Society, American Society for Clinical Investigation, Infectious Diseases Society of America, Phi Beta Kappa

Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, Oklahoma State Medical Association, Southern Society for Clinical Investigation, Association of Professors of Medicine, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Acknowledgements

Michael Stuart Bronze, MD Professor, Stewart G Wolf Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Medical Association, Association of Professors of Medicine, Infectious Diseases Society of America, Oklahoma State Medical Association, and Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

Vinod K Dhawan, MD, FACP, FRCP(C), FIDSA Professor, Department of Clinical Medicine, University of California, Los Angeles, David Geffen School of Medicine; Chief, Division of Infectious Diseases, Rancho Los Amigos National Rehabilitation Center

Vinod K Dhawan, MD, FACP, FRCP(C), FIDSA is a member of the following medical societies: American College of Physicians, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, and Royal College of Physicians and Surgeons of Canada

Disclosure: Pfizer Inc Honoraria Speaking and teaching

Maria A Horga, MD Assistant Professor, Department of Pediatric Infectious Diseases, Bristol-Myers Squibb

Disclosure: Nothing to disclose.

Alexandre Lacasse, MD, MSc Internal Medicine Faculty, Assistant Director, Medicine Clinic, Infectious Disease Consultant, St Mary's Health Center

Alexandre Lacasse, MD, MSc is a member of the following medical societies: American College of Physicians, American Medical Association, Association of Program Directors in Internal Medicine, Infectious Diseases Society of America, and Society for Healthcare Epidemiology of America

Disclosure: Nothing to disclose.

Klaus-Dieter Lessnau, MD, FCCP Clinical Associate Professor of Medicine, New York University School of Medicine; Medical Director, Pulmonary Physiology Laboratory; Director of Research in Pulmonary Medicine, Department of Medicine, Section of Pulmonary Medicine, Lenox Hill Hospital

Klaus-Dieter Lessnau, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Medical Association, American Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Thomas R Naparst, MD Clinical Instructor in Emergency Medicine, New York University School of Medicine; Consulting Staff, Department of Emergency Medicine, New York Downtown Hospital

Thomas R Naparst, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Michael D Nissen, MBBS, FRACP, FRCPA Associate Professor in Biomolecular, Biomedical Science & Health, Griffith University; Director of Infectious Diseases and Unit Head of Queensland Paediatric Infectious Laboratory, Sir Albert Sakzewski Viral Research Centre, Royal Children's Hospital

Michael D Nissen, MBBS, FRACP, FRCPA is a member of the following medical societies: American Academy of Pediatrics, American Society for Microbiology, Pediatric Infectious Diseases Society, Royal Australasian College of Physicians, and Royal College of Pathologists of Australasia

Disclosure: Nothing to disclose.

Russell W Steele, MD Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association

Disclosure: Nothing to disclose.

Robert Swords, MD Fellow, Department of Medicine, Division of Infectious Diseases, Medical University of South Carolina

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Martin Weisse, MD Program Director, Associate Professor, Department of Pediatrics, West Virginia University

Martin Weisse, MD is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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Trichrome stain of Entamoeba histolytica trophozoites in amebiasis. Two diagnostic characteristics are observed. Two trophozoites have ingested erythrocytes, and all 3 have nuclei with small, centrally located karyosomes.
Trichrome stain of Entamoeba histolytica cyst in amebiasis. Each cyst has 4 nuclei with characteristically centrally located karyosomes. Cysts measure 12-15 mm.
Entamoeba histolytica trophozoite. Image courtesy of Centers for Disease Control and Prevention.
Entamoeba histolytica cyst. Image courtesy of Centers for Disease Control and Prevention.
Life cycle of Entamoeba histolytica.
Gross pathology of intestinal ulcers due to amebiasis. Image courtesy of Centers for Disease Control and Prevention.
Histopathology of typical flask-shaped ulcer of intestinal amebiasis. Image courtesy of Centers for Disease Control and Prevention.
Entamoeba histolytica in liver aspirate, trichrome stain. Image courtesy of Centers for Disease Control and Prevention.
Histopathology of amebiasis. Image courtesy of Centers for Disease Control and Prevention.
 
 
 
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