AUTHOR AND EDITOR INFORMATION

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• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Background

Amebiasis is a parasitic infection caused by the protozoon Entamoeba histolytica. It is the third leading parasitic cause of death worldwide, surpassed only by malaria and schistosomiasis. On a global basis, amebiasis affects approximately 50 million persons each year, resulting in nearly 100,000 deaths.

Fedor Aleksandrovich Lošch, in St. Petersburg, Russia, first described amebiasis in 1875. He originally named the organism Amoeba coli and documented its pathogenicity in a dog fed with dysenteric stools from a patient. In 1886 in Egypt, Kartulis proved amebae to be the cause of intestinal and hepatic lesions in patients with diarrhea. Later, Councilman and Lafleur, at Johns Hopkins University Hospital, distinguished between bacillary and amebic dysentery in 1891. Walker and Sellards, in the Philippines, described the pathogenic role of amebae in extensive studies in 1913.

The parasite exists in 2 forms: a motile form, called the trophozoite, and a cyst form, responsible for the person-to-person transmission of infection. The trophozoite of E histolytica inhabits the large intestine to produce lesions of amebic colitis. Invasion of the colonic mucosa leads to dissemination of the organism to extracolonic sites, predominantly the liver. Faced with an adverse colonic environment, the trophozoite changes to the cystic form, better adapted to survival.

The trophozoite of E histolytica averages 25 mm, ranging from 10-60 mm (see Image 1). It has a clear ectoplasm and a somewhat granular endoplasm containing several vacuoles. The trophozoite has a single 3- to 5-mm nucleus with fine peripheral chromatin and a central nucleolus. Ingested RBCs may be present within the trophozoite.

The cyst of E histolytica averages 12 mm, ranging from 5-20 mm (see Image 2). It has 1-4 nuclei that are morphologically similar to the nuclei of the trophozoite. The cyst may have iodine-stainable glycogen clumps and chromatoid bodies with smooth rounded edges.

The life cycle of E histolytica is depicted in Image 3. Humans are the only reservoir of E histolytica. Cysts passed in the feces can survive in moist environmental conditions for weeks to months. Upon ingestion of fecally contaminated food or water, the cysts travel to the small intestine, where the trophozoites are released. In 90% of patients, the trophozoites re-encyst and produce asymptomatic infection, which usually resolves spontaneously within 12 months. In the remaining10% of patients who are infected, the parasite causes symptomatic amebiasis. Under unfavorable conditions, the trophozoite reverts to the cyst form, and the life cycle is repeated.

Entamoeba dispar is a nonpathogenic protozoon morphologically identical to E histolytica. The previously reported asymptomatic infections due to the so-called nonpathogenic strains of E histolytica now are recognized to be due to E dispar. These 2 species of Entameba can be distinguished by the monoclonal antibodies. Other morphologically distinct organisms, such as Entamoeba coli and Entamoeba hartmanni, are also nonpathogenic. Infections due to E histolytica cause a spectrum of illnesses, listed below.

• Intestinal disease
• • Asymptomatic infection
  • Symptomatic noninvasive infection
  • Acute proctocolitis (dysentery)
  • Fulminant colitis with perforation
  • Toxic megacolon
  • Chronic nondysenteric colitis
  • Ameboma
  • Perianal ulceration
• Extraintestinal disease
• • Liver abscess
  • Pleuropulmonary disease
  • Peritonitis
  • Pericarditis
  • Brain abscess
  • Genitourinary disease

Pathophysiology

The ingestion of cysts of E histolytica is followed by excystation in the small bowel and invasion of the colon by the trophozoites. The incubation period varies from 2 days to 4 months. Invasive disease begins with the adherence of E histolytica to colonic mucins, epithelial cells, and leukocytes. Adherence of the trophozoite is mediated by a galactose-inhibitable adherence lectin. This lectin is a 260-kd surface protein containing a 170-kd subunit and a 35-kd subunit. The heavier subunit has galactose-binding activity and at least 6 distinct epitopes. These epitopes are different in E dispar.

After adherence, trophozoites invade the colonic epithelium to produce the ulcerative lesions typical of intestinal amebiasis (see Image 4). The trophozoites of E histolytica lyse the target cells by using lectin to bind to the target cells' membranes and using the parasite's ionophorelike protein to induce a leak of ions (ie, Na⁺, K⁺, Ca⁺) from the target cell cytoplasm. A number of hemolysins, encoded by plasmid (ribosomal deoxyribonucleic acid [rDNA]) and cytotoxic to the intestinal mucosal cells, have been described in E histolytica. An extracellular cysteine kinase causes proteolytic destruction of the tissue, producing flask-shaped ulcers (see Image 5). Phorbol esters and protein kinase C activators augment the cytolytic activity of the parasite.

Spread of amebiasis to the liver occurs via the portal blood. The pathogenic strains evade the complement-mediated lysis in the bloodstream. Trophozoites ascend the portal veins to produce liver abscesses filled with acellular proteinaceous debris. This material has the appearance of anchovy paste. The trophozoites of E histolytica lyse the hepatocytes and the neutrophils. This explains the paucity of inflammatory cells within the liver abscesses. The neutrophil toxins may contribute to hepatocyte necrosis. Triangular areas of hepatic necrosis also may occur due to ischemia caused by portal venous obstruction. The trophozoites of E histolytica may be present along the periphery of these hepatic lesions (see Image 6).

Serum antibodies in patients with amebic liver abscess develop in 7 days and persist for up to 10 years. E dispar infections do not elicit antibody response, unlike asymptomatic E histolytica infections. Mucosal immunoglobulin A (IgA) response to E histolytica occurs during invasive amebiasis. However, no evidence exists 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-d (IFN-d), 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 tumor necrosis factor-alpha (TNF-a), 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-lymphocyte response to E histolytica antigens is depressed by a parasite-induced serum factor.

Frequency

United States

Prevalence rate of amebiasis in the United States is about 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 showing Entamoeba develop symptomatic amebiasis. Increased prevalence of amebiasis in the United States is noted in those who have emigrated from endemic areas, are of lower socioeconomic status, are institutionalized (especially individuals with mental retardation), are male homosexuals, and who live in communal situations.

International

Approximately 10% of the world's population is infected by either E histolytica or E dispar. Amebiasis affects about 50 million persons each year, resulting in approximately 100,000 deaths, all of which are due to E histolytica. Incidence of amebiasis is higher in developing countries. Areas of high prevalence include the Indian subcontinent, southern and western Africa, the Far East, South America, and Central America.

In endemic areas, as many as 25% of patients may be carrying antibodies to E histolytica due to prior infections, which may be largely asymptomatic. Various factors, such as poor education, poverty, overcrowding, contaminated water supply, and unsanitary conditions, contribute to the fecal-oral transmission. An epidemiologic study in Mexico City showed that 9% of the population was infected with E histolytica in the 5- to 10-year period preceding the study.

Travel to endemic areas can predispose individuals to amebiasis. However, amebiasis is an uncommon cause of traveler's diarrhea. The disease usually occurs after a longer stay in endemic areas (eg, > 1 mo).

Mortality/Morbidity

Amebic infections lead to significant morbidity while causing variable mortality as described below.

• Mortality rate in patients with uncomplicated amebic liver abscess is less than 1%.
• Fulminant amebic colitis has a mortality rate of more than 50%.
• Pleuropulmonary amebiasis has a mortality rate of 15-20%.
• Amebic pericarditis has a case fatality rate of 40%.
• Cerebral amebiasis is highly fatal, with a 90% death rate.
• Increased severity of amebiasis is noted in children (especially neonates), women who are pregnant or postpartum, individuals who use corticosteroids, individuals with malignancy, and malnourished individuals.

Sex

Invasive amebiasis, including amebic liver abscess, is much more common in adult males than in females. However, amebic liver abscess is equally common in both sexes among prepubertal children. Acuna-Soto and colleagues have noted that asymptomatic E histolytica infection is distributed equally between sexes. Therefore, the higher proportion of men with invasive amebiasis may be due to a male susceptibility to invasive disease.

Age

Symptomatic intestinal amebiasis occurs in all age groups. Liver abscesses due to amebiasis are 10 times more frequent in adults than in children.

CLINICAL

Section 3 of 11  

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• Clinical
• Differentials
• Workup
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History

• Asymptomatic infections are common following ingestion of the parasite. E dispar does not cause invasive disease or antibody production. As many as 90% of E histolytica infections are also asymptomatic. The infection is self-limited but may be recurrent. Only antigen detection tests can distinguish between E histolytica and E dispar.
• Acute amebic colitis has a gradual onset presenting with a 1- to 2-week history of abdominal pain, diarrhea, and tenesmus. Stool samples, which are watery and contain blood and mucus, have little fecal material. Fever is noted in only a minority of patients. Lower quadrant abdominal tenderness may be noted.
• Fulminant amebic colitis is a rare complication of amebic dysentery. It presents with a rapid onset of severe bloody diarrhea, severe abdominal pain, and high fever. Children younger than 2 years are at increased risk. Intestinal perforation is common.
• Chronic amebic colitis is clinically similar to inflammatory bowel disease. Recurrent episodes of bloody diarrhea and vague abdominal discomfort develop in 90% of patients with chronic amebic colitis who have antibodies to E histolytica. Consider amebiasis in all patients in whom inflammatory bowel disease is suspected before administering steroids. A biopsy of colonic ulcers reveals trophozoites in patients with amebiasis.
• Ameboma is a localized chronic infection of the cecum or ascending colon. It presents as a right lower quadrant abdominal mass, which may be mistaken for carcinoma, tuberculosis, Crohn disease, actinomycosis, or lymphoma. Biopsy findings assist in establishing the correct diagnosis.
• Amebic liver abscess is the most common form of extraintestinal amebiasis. The male-to-female ratio is 10:1. It is rare in children. An estimated 95% of amebic liver abscesses related to travel develop within 5 months.
• • Amebic liver abscess appears with an abrupt onset of high fever; a cough; and dull, aching, constant abdominal pain in the right upper quadrant or epigastrium, usually lasting fewer than 10 days. The pain is constant and may radiate to the right scapula and shoulder. It may become pleuritic and may increase when the patient lies on the right side. In left lobe liver abscess, the pain may be predominantly epigastric and may radiate to the left shoulder. Anorexia, nausea, and vomiting may occur.
  • A small subset of patients with amebic liver abscess has a subacute presentation with vague abdominal discomfort, weight loss, and anemia. Jaundice is unusual. Fewer than 30% have a history of antecedent intestinal amebiasis.
• Pleuropulmonary amebiasis is usually caused by a ruptured right lobe liver abscess. The typical age group is 20-40 years. The male-to-female ratio is 10:1. Approximately 10% of patients with amebic liver abscess develop pleuropulmonary amebiasis, which presents with cough, pleuritic pain, and dyspnea. A hepatobronchial fistula is an unusual problem characterized by the expectoration of sputum resembling anchovy paste. The trophozoites of E histolytica may be found in the sputum sample.
• Amebic peritonitis is generally secondary to a ruptured liver abscess. Left lobe liver abscesses are more likely to rupture. Patients present with fever and rigid distended abdomen. Roughly 2-7% of liver abscesses rupture into the peritoneum.
• Amebic pericarditis is rare but is the most serious complication. It usually is caused by a rupture of the left liver lobe abscess and occurs in 3% of patients with hepatic amebiasis. It presents with chest pain and the features of congestive heart failure.
• Cerebral amebiasis has an abrupt onset and rapid progression to death in 12-72 hours. The patient presents with altered consciousness and focal neurologic signs. CT scan shows irregular lesions without a surrounding capsule or enhancement. A tissue biopsy sample reveals the trophozoites.
• Genitourinary involvement may cause painful genital ulcers or fallopian tube amebiasis.

Physical

• Patients with acute amebic colitis may have lower quadrant abdominal tenderness. Fever is noted in only a minority of patients. Dehydration is uncommon. Occult blood is nearly always present in stools.
• Amebic liver abscess may present with fever and tender hepatomegaly. Right lower intercostal tenderness may be elicited, particularly posteriorly. Breath sounds may be diminished at the right lung base, and rales may be heard. A small subset of patients has a subacute presentation with hepatomegaly, weight loss, and anemia. Jaundice is unusual.
• Pleuropulmonary amebiasis may produce findings of right-sided pleural effusions, empyema, basilar atelectasis, pneumonia, and lung abscess.
• Patients with amebic peritonitis present with fever and a tender, rigid, and distended abdomen.
• Amebic pericarditis presents with features of congestive heart failure. A pericardial friction rub may be audible.
• Cerebral amebiasis presents with altered consciousness and focal neurologic signs. CT scan shows irregular lesions without a surrounding capsule or enhancement.
• Genital ulcers due to amebiasis have a punched-out appearance and profuse discharge.

Causes

Amebiasis is a parasitic infection caused by the protozoon E histolytica.

DIFFERENTIALS

Section 4 of 11  

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• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Other Problems to be Considered

Infectious

• Campylobacter
• Shigella
• Salmonella
• Yersinia
• Enteroinvasive Escherichia coli
• Enterohemorrhagic Escherichia coli

Noninfectious

• Inflammatory bowel disease
• Ischemic colitis
• Diverticulitis
• Arteriovenous malformation

WORKUP

Section 5 of 11  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Lab Studies

• Stool
• • Light microscopy: Perform stool examination in patients in whom intestinal amebiasis is suspected. This may aid in the workup, but does not make a specific diagnosis because one cannot distinguish between E histolytica and E dispar using a microscope.
  • Enzyme immunoassay (EIA): This is the best test for making the specific diagnosis of E histolytica in the clinical setting. One type of EIA is commercially available from TechLab of Virginia.
  • Other stool tests
    • Occult blood is almost always present in invasive disease.
    • Fecal leukocytes may be absent.
• Serum tests
• • Antibody tests
    • Antibody detection is most useful in patients with extraintestinal disease, ie, amebic liver abscess, when organisms are generally not found on stool examination. Several methods are commercially available for antibody detection.
      • Indirect hemagglutination antibody (IHA) test detects antibody specific for E histolytica. The antigen used in IHA consists of a crude extract of axenically cultured organisms. Antibody titers of more than 1:256 to the 170-kd subunit of the galactose-inhibitable adherence lectin are noted in approximately 95% of patients with extraintestinal amebiasis, 70% of patients with active intestinal infection, and 10% of asymptomatic individuals. IHA is not useful in differentiating acute from previous infection because high titers may persist for years after successful treatment. False-positive reactions at titers higher than 1:256 are rare.
      • EIA is as sensitive and specific as the IHA test and has replaced IHA in most laboratories.
      • Immunodiffusion (ID) is simple to perform, making it ideal for the laboratory that has only an occasional request for amebic serology. However, it requires a minimum of 24 hours to complete, as compared to 2 hours for the IHA or EIA test. ID is slightly less sensitive than IHA and EIA, but is equally specific.
    • Although detection of immunoglobulin M (IgM) antibodies specific for E histolytica has been reported, sensitivity in patients with current invasive disease is only about 64%.

Imaging Studies

• Chest radiography may reveal elevated right hemidiaphragm and a right-sided pleural effusion in patients with amebic liver abscess.
• Ultrasonography is preferred for the evaluation of amebic liver abscess because of its low cost, rapidity, and lack of adverse effects. A single lesion is usually seen in the posterosuperior aspect of the right lobe of the liver. Multiple abscesses may occur in some patients.
• CT may be slightly more sensitive than ultrasonography. In cerebral amebiasis, CT shows irregular lesions without a surrounding capsule or enhancement.
• MRI reveals high signal intensity on T2-weighted images. Perilesional edema and enhancement of rim are noted after injection of gadolinium (86%).
• Complete resolution of liver abscess may take up to 2 years. Repeat imaging is not indicated if the patient is otherwise doing well.

Other Tests

• Leukocytosis may be noted, but eosinophilia is not a feature of amebiasis.
• Mild anemia may be noted.
• The erythrocyte sedimentation rate is generally elevated.
• Cholesterol may be elevated.
• Liver function tests reveal elevated alkaline phosphatase in 80% of patients, elevated transaminases, and reduced albumin.
• Urinalysis may reveal proteinuria.

Procedures

• Rectosigmoidoscopy and colonoscopy may provide useful diagnostic information in intestinal amebiasis. Consider rectosigmoidoscopy and colonoscopy before using steroids in patients in whom inflammatory bowel disease is suspected. Small mucosal ulcers covered with yellowish exudates are observed. The intervening mucosa appears normal (see Image 4). Biopsy results and a scraping of ulcer edge may show trophozoites. Indications for endoscopy in suspected intestinal amebiasis include the following:
• • Stool examination is negative, but the serum antibody test is positive.
  • Stool examination is negative, but immediate diagnosis is required.
  • Stool examination and the antibody test are negative, but a high suspicion exists.
  • Evaluation of chronic intestinal syndromes or mass lesions is desired.
• Aspiration of liver is indicated only for large abscesses (>12 cm), imminent abscess rupture, failure of medical therapy, or presence of left lobe abscesses.

Histologic Findings

Infection of the human colon by E histolytica produces focal ulceration of the intestinal mucosa. Histopathological examination reveals numerous E histolytica trophozoites. Due to the lysis of cells by E histolytica, acute inflammatory cells seldom are found in the biopsy material (see Image 5, Image 7).

TREATMENT

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Medical Care

Asymptomatic infections are not treated in endemic areas. Treat E histolytica infections in patients with AIDS even if infection is asymptomatic. E dispar infections in patients with AIDS are self-limited (average duration 11 wk). Several agents are available for the treatment of various forms of amebiasis. The recommended dose and the duration of therapy are described under the individual agents discussed in Medication.

• Asymptomatic intestinal infection may be treated with iodoquinol, paromomycin, or diloxanide furoate.
• Recommended drugs for treatment of symptomatic intestinal disease and for hepatic abscess are metronidazole and tinidazole. Since these drugs may not eliminate the intraluminal cysts, immediately follow this therapy with treatment with iodoquinol, paromomycin, or diloxanide furoate.

Surgical Care

Surgical intervention may be necessary in the management of amebiasis in a few select situations.

• Toxic megacolon may occur and requires total colectomy.
• Surgical decompression may be necessary for amebic brain abscess.
• Rupture of amebic liver abscess into the pericardium may require surgical drainage.
• Conservatively manage intestinal perforation due to amebiasis.

Consultations

• Infectious disease specialist
• Surgeon

Diet

No special diet is recommended.

MEDICATION

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Drug Category: Antibiotics

Activity against anaerobic bacteria and protozoa is exhibited by several agents. Metronidazole is considered the drug of choice for symptomatic, invasive disease. Paromomycin is the drug of choice for noninvasive disease. Because parasites persist in the intestine of 40-60% of patients treated with metronidazole, follow it with Paromomycin to cure luminal infection. Do not give the 2 medications at the same time because the diarrhea that often results from paromomycin might be confused with continuing active intestinal disease from the parasite.

Drug Name	Tinidazole (Fasigyn, Tindamax)
Description	5-nitroimidazole derivative with selective antimicrobial activity against anaerobic bacteria and protozoa. The mechanism by which tinidazole exhibits activity against Giardia and Entamoeba species is not known.
Adult Dose	Intestinal amebiasis: 600 mg bid or 800 mg tid PO for 5 d; alternatively, 2 g PO qd for 3 d with food Hepatic amebic abscess: 2 g PO qd for 3-5 d with food
Pediatric Dose	<3 years: Not established >3 years: Intestinal amebiasis: 50 mg/kg/d PO for 3 d with food; not to exceed 2 g/dose Amebic liver abscess: 50 mg/kg/d PO for 3-5 d with food; not to exceed 2 g/dose, limited data exist for pediatric patients treated > 3 d (monitor closely)
Contraindications	Documented hypersensitivity; first trimester of pregnancy
Interactions	Limited data exist; interaction information based on experience with other nitroimidazole derivatives (ie, metronidazole); may prolong PT when coadministered with warfarin; avoid alcoholic beverages and preparations containing ethanol or propylene glycol during and 3 d following administration (may cause disulfiramlike reaction); may increase serum levels of lithium, phenytoin, cyclosporine, tacrolimus, and fluorouracil; CYP450 inducers (eg, phenobarbital, rifampin, phenytoin) may increase elimination; CYP450 inhibitors (eg, cimetidine, ketoconazole) may decrease elimination; concurrent administration with cholestyramine may decrease oral bioavailability; oxytetracycline may antagonize effect
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Carcinogenicity has been observed in mice and rats treated chronically with metronidazole (another nitroimidazole), although not observed with tinidazole, use cautiously; seizures and peripheral neuropathy have been reported; caution with history of blood dyscrasia; may cause metallic/bitter taste, nausea, anorexia, vomiting, weakness, fatigue, dizziness, or headache; if administered on day of hemodialysis, administer additional dose equivalent to one half of recommended dose following dialysis

Drug Name	Paromomycin (Humatin)
Description	Amebicidal aminoglycoside antibiotic that is poorly absorbed. Active only against intraluminal form of amebiasis. Used to eradicate cysts of E histolytica following treatment with metronidazole or tinidazole for an invasive disease.
Adult Dose	25-35 mg/kg/d PO divided q8h for 7 d
Pediatric Dose	Administer as in adults
Contraindications	Documented hypersensitivity; intestinal obstruction
Interactions	Nephrotoxic potential may increase with concurrent administration of other aminoglycosides, penicillins, cephalosporins, amphotericin B, or loop diuretics
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Due to narrow therapeutic index and toxic hazards associated with extended administration, do not use for long-term therapy; caution in renal failure, hypocalcemia, myasthenia gravis, and conditions that depress neuromuscular transmission; adjust dose in renal impairment

Drug Category: Anthelmintics

Parasite biochemical pathways are different from the human host; thus, toxicity is directed to the parasite, egg, or larvae.

Drug Name	Iodoquinol (Yodoxin)
Description	Halogenated hydroxyquinoline. Luminal amebicide; acts primarily in bowel lumen since it is poorly absorbed. Best tolerated when given with meals. Since active only against intraluminal form of amebiasis, used to eradicate cysts of E histolytica after treatment of invasive disease.
Adult Dose	650 mg PO tid for 20 d
Pediatric Dose	30-40 mg/kg/d PO divided tid for 20 d; not to exceed 2 g/d
Contraindications	Documented hypersensitivity; iodine intolerance; impaired renal or liver function
Interactions	None reported
Pregnancy	C - Safety for use during pregnancy has not been established.
Precautions	Occasional adverse effects include skin rash, acne, thyroid gland enlargement, nausea, diarrhea, cramps, and pruritus; rare adverse effects include optic neuritis, optic atrophy, loss of vision, peripheral neuropathy with prolonged use, and iodine sensitivity

FOLLOW-UP

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Deterrence/Prevention

• Improved sanitation and clean water supply decrease incidence of amebiasis. The amount of chlorine normally used to purify water is inadequate in killing the cysts. Drinking water can be rendered safe by boiling, 0.22 µm filtration, or iodination with tetraglycine hydroperiodide. Bottled water may be used for drinking when traveling to endemic areas.
• Eating only cooked food or self-peeled fruits in endemic areas minimizes risk. Avoid eating raw fruits and salads, which are difficult to sterilize.
• Disease transmission can be reduced by early treatment of carriers in nonendemic areas.
• Vaccination for amebiasis currently is being investigated. One potential vaccine candidate is the galactose-inhibitable adherence lectin of E histolytica.

Complications

• Bowel perforation
• Gastrointestinal bleeding
• Stricture formation
• Fistula formation
• Intussusception
• Secondary bacterial infection of amebic liver abscess (uncommon)
• Peritonitis
• Pericarditis
• Empyema
• Brain abscess

Prognosis

• Intestinal infections due to amebiasis generally respond well to appropriate therapy. The severity of amebiasis is increased in the following individuals:
• • Children, especially neonates
  • Pregnant and postpartum women
  • Those using corticosteroids
  • Those with malignancies
  • Malnourished individuals
• Mortality rate in patients with uncomplicated amebic liver abscess is less than 1%.
• Fulminant amebic colitis has a mortality rate of more than 50%.
• Pleuropulmonary amebiasis has a 15-20% mortality rate.
• Amebic pericarditis has a case fatality rate of 40%.
• Cerebral amebiasis is highly fatal with a 90% death rate.

Patient Education

• Educate patients about the prevention of amebiasis during travel to endemic areas. This includes avoiding drinking contaminated water and avoiding eating raw fruits and salads, which are difficult to sterilize. Bottled water may be used during such travel. Eating only cooked food or self-peeled fruits in endemic areas minimizes risk.

MISCELLANEOUS

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Medical/Legal Pitfalls

• Failure to suspect and treat amebiasis in a returning traveler may cause legal liability.
• Intestinal amebiasis may be mistakenly treated as chronic ulcerative colitis.

Special Concerns

• Intestinal amebiasis may be mistakenly treated as inflammatory bowel disease. Perform lower gastrointestinal endoscopy in all patients in whom inflammatory bowel disease is suspected before treating with steroids.

MULTIMEDIA

Section 10 of 11  

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• Follow-up
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• Multimedia
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Media file 1:  Entamoeba histolytica trophozoite. Courtesy of Centers for Disease Control and Prevention.
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Media file 2:  Entamoeba histolytica cyst. Courtesy of Centers for Disease Control and Prevention.
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Media file 3:  Life cycle of Entameba histolytica.
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Media file 4:  Gross pathology of intestinal ulcers due to amebiasis. Courtesy of Centers for Disease Control and Prevention.
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Media file 5:  Histopathology of typical flask-shaped ulcer of intestinal amebiasis. Courtesy of Centers for Disease Control and Prevention.
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Media file 6:  Entamoeba histolytica in liver aspirate, trichrome stain. Courtesy of Centers for Disease Control and Prevention.
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Media file 7:  Histopathology of amebiasis. Courtesy of Centers for Disease Control and Prevention.
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REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
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• Follow-up
• Miscellaneous
• Multimedia
• References

• Abd-Alla MD, Jackson TF, Reddy S, Ravdin JI. Diagnosis of invasive amebiasis by enzyme-linked immunosorbent assay of saliva to detect amebic lectin antigen and anti-lectin immunoglobulin G antibodies. J Clin Microbiol. Jun 2000;38(6):2344-7. [Medline].
• Adams EB, MacLeod IN. Invasive amebiasis. I. Amebic dysentery and its complications. Medicine (Baltimore). Jul 1977;56(4):315-23. [Medline].
• Adams EB, MacLeod IN. Invasive amebiasis. II. Amebic liver abscess and its complications. Medicine (Baltimore). Jul 1977;56(4):325-34. [Medline].
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• Chavez-Rueda K, Agundis-Mata C, Zenteno E, et al. Diagnostic tests using idiotype expression in amebiasis [In Process Citation]. Arch Med Res. Jul-Aug 2000;31(4 Suppl):S25-7. [Medline].
• Conter RL, Pitt HA, Tompkins RK, Longmire WP Jr. Differentiation of pyogenic from amebic hepatic abscesses. Surg Gynecol Obstet. Feb 1986;162(2):114-20. [Medline].
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Article Last Updated: Mar 30, 2006