eMedicine Specialties > Pediatrics: General Medicine > Parasitology

Amebiasis

Vinod K Dhawan, MD, FACP, FRCP(C), Professor, Department of Clinical Medicine, University of California at Los Angeles; Professor of Medicine, Charles R Drew University of Medicine and Science; Chief, Division of Infectious Diseases, MLK-Harbor Hospital
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

Updated: Aug 11, 2008

Introduction

Background

Amebiasis is a parasitic infection caused by the protozoon Entamoeba histolytica. Amebiasis 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. In 1891, Councilman and Lafleur, at Johns Hopkins University Hospital, distinguished between bacillary and amebic dysentery. In 1913 in the Philippines, Walker and Sellards described the pathogenic role of amebae in extensive studies.

The parasite has 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 Media file 1). It has a clear ectoplasm and a somewhat granular endoplasm that contains several vacuoles. The trophozoite has a single 3-mm 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 Media file 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 Media file 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 spontaneously resolves within 12 months. In the remaining 10% 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 are now recognized to be due to E dispar. These 2 species of Entameba can be distinguished by the monoclonal antibodies. Specific and sensitive means to detect E histolytica in stool are now available and include antigen detection and polymerase chain reaction (PCR). Other morphologically distinct organisms, such as Entamoeba coli and Entamoeba hartmanni, are also nonpathogenic. Infections due to E histolytica cause a spectrum of illnesses, as follows:

• 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

Amebiasis is acquired by the fecal-oral route through consumption of fecally contaminated food or water. Direct oral-anal contact (anilingus) can also lead to fecal exposure to E histolytica. The ingestion of E histolytica cysts 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 that contains 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 Media file 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. Numerous hemolysins, encoded by plasmid (ribosomal DNA [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 Media file 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 may also 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 Media file 6).

Serum antibodies in patients with amebic liver abscess develop in 7 days and persist for as long as 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 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-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

In the United States, amebiasis is most commonly seen in immigrants from developing countries and travelers to those areas. In one study, 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%.¹ Additionally, increased prevalence of amebiasis in the United States is noted in institutionalized persons (especially with mental retardation), male homosexuals, and those who live in communal settings.

The prevalence rate 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.

International

Worldwide, approximately 50 million cases of invasive E histolytica disease occur each year, with as many as 100,000 deaths. This represents the tip of the iceberg because only 10%-20% of infected individuals become symptomatic.

Earlier estimates of E histolytica infection based on examination of stool for ova and parasites, are inaccurate because this test can not differentiate E histolytica from E dispar and Entamoeba moshkovskii, which are morphologically identical but nonpathogenic organisms. Prevalence rates of E histolytica, as determined by enzyme-linked immunosorbent assay (ELISA) or PCR tests on stool from asymptomatic persons in developing countries range from 1-21%.

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. 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. The annual incidence of amebic liver abscess was reported to be 21 cases per 100,000 inhabitants in Hue City, Vietnam.² 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, contribute to the fecal-oral transmission.

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.⁴ 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

History

• The incubation period is commonly 2-4 weeks but ranges from a few days to years. Amebiasis is more severe in very young patients, in elderly patients, and in patients receiving corticosteroids. The clinical spectrum of amebiasis ranges from asymptomatic infection to fulminant colitis and peritonitis to extraintestinal amebiasis, most commonly amebic liver abscess. The clinical expression of amebiasis may be related to geography. For instance, amebic colitis is the predominant presentation in Egypt, whereas amebic liver abscesses predominate in South Africa.
• 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.
• Amebic colitis is gradual in onset, with symptoms presenting over 1-2 weeks, distinguishing it from bacterial dysentery. Diarrhea is the most common symptom. Patients with amebic colitis typically present with cramping abdominal pain, watery or bloody diarrhea, and weight loss. Fever is noted in 10% of patients. 
• Fulminant amebic colitis is a rare complication of amebic dysentery (<0.5%). 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. Patients may develop toxic megacolon, which is typically associated with the use of corticosteroids. Mortality rates with fulminant amebic colitis may exceed 40%. 
• 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. Amebic colitis should be ruled out prior to treatment of suspected inflammatory bowel disease because corticosteroid therapy worsens amebiasis.
• A less common form of intestinal disease, ameboma, results from formation of annular colonic granulation in response to the infecting amebae, resulting in a large local lesion of the bowel. 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.
• It results from spread of the organisms from the intestinal submucosa to the liver via the portal system. However, approximately 40% of patients who have amebic liver abscess do not have a history of prior bowel symptoms. 
• Amebic liver abscess occurs in as many as 5% of patients with symptomatic intestinal amebiasis and is 10 times as frequent in men as in women. 
• Approximately 80% of patients with amebic liver abscess present within 2-4 weeks of infection. An estimated 95% of amebic liver abscesses related to travel develop within 5 months.
• Amebic liver abscess presents with fever and a constant, dull, upper right abdominal or epigastrium pain. Involvement of the diaphragmatic surface of the liver may lead to right-sided pleuritic pain or referred shoulder pain. Associated GI symptoms occur in 10-35% of patients and include nausea, vomiting, abdominal distention, diarrhea, and constipation. 
• A small subset of patients with amebic liver abscess has a subacute presentation with vague abdominal discomfort, weight loss, and anemia. Jaundice is unusual. 
• Pleuropulmonary amebiasis is most commonly the result of contiguous spread from a liver abscess rupturing through the right hemidiaphragm. However, a case of amebic lung abscess acquired through hematogenous spread has been reported. 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 is usually 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.
• Amebic abscesses resulting from hematogenous spread have occasionally been described in the brain 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 scanning reveals 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 scanning reveals 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.

Differential Diagnoses

Other Problems to Be Considered

Intestinal amebiasis should be distinguished from the following conditions:

• Infectious conditions
  • Campylobacter
  • Shigella
  • Salmonella
  • Yersinia
  • Enteroinvasive Escherichia coli
  • Enterohemorrhagic E coli
• Noninfectious conditions
  • Inflammatory bowel disease
  • Ischemic colitis
  • Diverticulitis
  • Arteriovenous malformation

Amebic liver abscess should be distinguished from the following conditions:

• Pyogenic liver abscess
• Necrotic hepatoma
• Echinococcal cyst  

The likelihood of a liver abscess to be amebic rather than pyogenic is increased by the history of residence in or recent travel to endemic areas, male sex, increased age (>50 y), presence of a single lesion in the right lobe of the liver, and the absence of jaundice, biliary disease, or diabetes mellitus.

Workup

Laboratory Studies

• Stool  
  • Light microscopy: Examination of a fresh stool smear for trophozoites that contain ingested RBCs is rather insensitive. Routine microscopy cannot distinguish the E dispar and E moshkovskii (nonpathogenic amebae) from E histolytica.  
  • An enzyme immunoassay kit to specifically detect E histolytica in fresh stool specimens is commercially available.  
  • PCR-based diagnostic tests have been developed but are not widely available. Field studies that directly compared PCR with stool culture or antigen-detection tests for the diagnosis of E histolytica infection suggest that these methods are equally comparable.
  • Other stool tests
    • The stool samples are always heme positive.
    • Fecal leukocytes may be absent.
• Serum tests
  • Antibody tests: Serum antibodies against amebae are present in 70-90% of individuals with symptomatic intestinal E histolytica infection.  Antiamebic antibodies are present in as many as 99% of individuals with liver abscess who have been symptomatic for longer than a week. Serologic examination should be repeated a week later in those with negative test on presentation. However, serologic tests do not distinguish new from past infection because the seropositivity persists for years after an acute infection. 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, compared with 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%.
  • The galactose lectin antigen is present in the serum of 75% of subjects with amebic liver abscess and may be particularly useful in patients presenting acutely, before an IgG serum anti-amebic antibody response occurs.

Imaging Studies

• Chest radiography may reveal an 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. In an ultrasonographic evaluation of 212 patients, 34 (16%) had multiple abscesses, 75 (35%) had an abscess in the left lobe, and the remaining 103 (49%) had a solitary abscess in the right lobe.  
• 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 as long as 2 years. Repeat imaging is not indicated if the patient is otherwise doing well.

Other Tests

• Leukocytosis without eosinophilia is observed in 80% of cases.
• Mild anemia may be noted.
• Liver function tests reveal elevated alkaline phosphatase levels (in 80% of patients), elevated transaminase levels, mild elevation of serum bilirubin level, and reduced albumin levels.
• The erythrocyte sedimentation rate is elevated.

Procedures

• Rectosigmoidoscopy and colonoscopy with biopsy or scraping at margin of colonic mucosal ulcer provides valuable materials for diagnostic information in intestinal amebiasis. Small mucosal ulcers covered with yellowish exudates are observed. The mucosal lining between ulcers appears normal (see Media file 4). Rectosigmoidoscopy and colonoscopy should be considered before using steroids in patients in whom inflammatory bowel disease is suspected. Biopsy results and a scraping of ulcer edge may reveal trophozoites. Indications for endoscopy in suspected intestinal amebiasis include the following:
  • Stool examination findings are negative, but the serum antibody test findings are positive.
  • Stool examination findings are negative, but immediate diagnosis is required.
  • Stool examination and antibody test results are negative, but amebiasis is strongly suspected.
  • Evaluation of chronic intestinal syndromes or mass lesions is desired.
• Aspiration of the liver abscess is occasionally required to rule out a pyogenic abscess. Aspiration amebic liver abscess yields an anchovy-pastelike material that lacks WBCs due to lysis by the parasite. Amebae are visualized in the abscess fluid in a minority of patients with amebic liver abscess. 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

• Histopathologic findings include nonspecific mucosal thickening and focal ulcerations with or without amebae in a diffusely inflamed mucosal layer. 
• Classic flask-shaped ulcers may be seen with ulceration extending through the mucosa and muscularis mucosa into the submucosa (see Media file 5, Media file 7). 
• Staining with periodic acid–Schiff or immunoperoxidase and antilectin antibodies aid in the visualization of amebae.

Treatment

Medical Care

Asymptomatic infections are not treated in endemic areas. However, in nonendemic areas asymptomatic infection should be treated because of its potential to progress to invasive disease. Luminal agents that are minimally absorbed by the GI tract (eg, paromomycin, iodoquinol, diloxanide furoate) are best suited for such therapy.Metronidazole is the mainstay of therapy for invasive amebiasis. Tinidazole has been recently approved by the US Food and Drug Administration (FDA) for intestinal or extraintestinal amebiasis. Other nitroimidazoles with longer half-lives (ie, secnidazole, ornidazole) are currently unavailable in the United States . Nitroimidazole therapy leads to clinical response in approximately 90% of patients with mild-to-moderate amebic colitis. Chloroquine has also been used for patients with hepatic amebiasis. Dehydroemetine (available from the Centers for Disease Control and Prevention [CDC] Drug Services [404-639-3670]) has been successfully used but is not preferred due to its potential myocardial toxicity. For more information, see CDC Drug Service.

Intraluminal parasites are not affected by nitroimidazole therapy. Therefore, nitroimidazole therapy should be followed by treatment with a luminal agent such as paromomycin or diloxanide furoate to prevent a relapse. The recommended dose and the duration of therapy are described under the individual agents discussed in Medication.

Broad-spectrum antibiotics may be added to treat bacterial superinfection in a case of fulminant amebic colitis and suspected perforation. Bacterial coinfection of amebic liver abscess has occasionally been observed (both before and as a complication of drainage), and adding antibiotics to the treatment regimen is reasonable in the absence of a prompt response to nitroimidazole therapy.

Surgical Care

Surgical intervention is required for acute abdomen due to perforated amebic colitis, massive GI bleeding, or toxic megacolon. Toxic megacolon is rare and is typically associated with the use of corticosteroids. Surgical attempts to correct amebic bowel perforation or peritonitis should be avoided, although some patients may benefit from peritoneal lavage.

Unlike pyogenic liver abscess, amebic liver abscess generally responds to medical therapy alone and drainage is seldom necessary. When necessary, imaging-guided percutaneous treatment (needle aspiration or catheter drainage) has replaced surgical intervention as the procedure of choice for reducing the size of an abscess. The indications for drainage of amebic liver abscess include the following:

• Presence of left-lobe abscess (>10 cm in diameter)
• Impending rupture and abscess that does not respond to medical therapy within 3-5 days

Consultations

• Infectious disease specialist
• Gastroenterologist
• Surgeon

Diet

No special diet is recommended.

Medication

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.

Metronidazole (Flagyl, Protostat)

Kills trophozoites of E histolytica in intestine and tissue. Does not eradicate cysts from intestines.

Dosing

Adult

Intestinal amebiasis:
PO: 500-750 mg PO tid for 5-10 d; alternatively, 2 g PO qd for 3 d or a single dose of 50 mg/kg
IV: 500 mg IV q6h for 5-10 d
Amebic liver abscess: 500 mg IV q6h for 10 d

Pediatric

35-50 mg/kg/d PO/IV divided q8h for 10 d

Interactions

Metronidazole potentiates effect of warfarin; elimination is accelerated by simultaneous use of phenytoin and phenobarbital; clearance is decreased by cimetidine

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Avoid during first trimester of pregnancy; frequent adverse effects include nausea, anorexia, headache, and metallic taste; occasional adverse effects include vomiting, diarrhea, insomnia, weakness, dry mouth, stomatitis, vertigo, tinnitus, paresthesia, rash, dark urine, urethral burning, disulfiramlike reaction with alcohol, and candidiasis; rare adverse effects include seizures, pseudomembranous colitis, ataxia, leukopenia, peripheral neuropathy, pancreatitis, and encephalopathy

Tinidazole (Fasigyn, Tindamax)

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.

Dosing

Adult

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

<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)

Interactions

Limited data available; 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 PO bioavailability; oxytetracycline may antagonize effect

Contraindications

Documented hypersensitivity; first trimester of pregnancy

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

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

Paromomycin (Humatin)

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.

Dosing

Adult

25-35 mg/kg/d PO divided q8h for 7 d

Pediatric

Administer as in adults

Interactions

Nephrotoxic potential may increase with concurrent administration of other aminoglycosides, penicillins, cephalosporins, amphotericin B, or loop diuretics

Contraindications

Documented hypersensitivity; intestinal obstruction

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

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

Anthelmintics

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

Iodoquinol (Yodoxin)

Halogenated hydroxyquinoline. Luminal amebicide; acts primarily in bowel lumen because it is poorly absorbed. Best tolerated when given with meals. Because it is active only against intraluminal form of amebiasis, it is used to eradicate cysts of E histolytica after treatment of invasive disease.

Dosing

Adult

650 mg PO tid for 20 d

Pediatric

30-40 mg/kg/d PO divided tid for 20 d; not to exceed 2 g/d

Interactions

None reported

Contraindications

Documented hypersensitivity; iodine intolerance; impaired renal or liver function

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

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

Chloroquine phosphate (Aralen)

Inhibits growth by concentrating within acid vesicles of parasite, which increases internal pH of organism. Also inhibits hemoglobin utilization and metabolism of parasite. In vitro studies with trophozoites of E histolytica demonstrate that chloroquine possesses amebicidal activity comparable to that of emetine. Highly effective in treatment of amebic liver abscess when administered with emetine or dehydroemetine. Like emetine and dehydroemetine, it is not effective against luminal forms. Irreversible retinal damage does not occur with dose and duration used for treatment of hepatic amebiasis.

Dosing

Adult

Hepatic amebiasis:
500 mg salt (300-mg base) PO bid for 2 d, followed by 250 mg salt (150-mg base) bid for 2-3 wk

Pediatric

Hepatic amebiasis: 10 mg (as base)/kg/d PO divided bid for 2-3 wk

Interactions

Cimetidine may increase serum levels of chloroquine (possibly other 4-aminoquinolones); magnesium trisilicate may decrease absorption of 4-aminoquinolones

Contraindications

Documented hypersensitivity; psoriasis, retinal and visual field changes attributable to 4-aminoquinolones

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in hepatic disease, G-6-PD deficiency, psoriasis, porphyria; not recommended for long-term use in children; perform periodic ophthalmologic examinations; test for muscle weakness; retinopathy, tinnitus, nerve deafness, skin eruption, headache, anorexia, nausea, vomiting, and diarrhea may occur

Dehydroemetine (Mebadin)

Preferred over emetine because it is less toxic. Eradicates amebic tissue infections, including liver abscess, but does not act on luminal forms. Luminal amebicide also must be used to eradicate the bowel luminal infection. Only effective against the trophozoite forms and not the cyst form. Available in United States only from the Parasitic Disease Drug Service, CDC (Atlanta, GA 30333, [404-639-3670]). For more information, see CDC Drug Service.

Dosing

Adult

1-1.5 mg/kg SC/IM qd for 8-10 d; not to exceed 90 mg/kg/d

Pediatric

1-1.5 mg/kg/d SC/IM divided bid for 8-10 d; not to exceed 90 mg/kg/d

Interactions

None reported

Contraindications

Documented hypersensitivity; cardiac disease, renal disease, recent history of polyneuritis

Precautions

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Caution in women who are pregnant and small children; hospitalize when administered because of the potential of serious cardiotoxicity and neuromuscular toxicity; monitor pulse and blood pressure at least tid; perform ECG prior to first injection, on day 5, day 10, and then weekly for 2 wk after last injection; discontinue if resting pulse >110 beats per min, marked hypotension, precordial pain, marked neuromuscular symptoms, T-wave depression, arrhythmias, or proteinuria occur

Diloxanide furoate (Furamid, Entamizole, Furamide)

Luminal amebicide; acts primarily in bowel lumen because it is poorly absorbed. Used to eradicate cysts of E histolytica after treatment of invasive disease. Not available in the United States.

Dosing

Adult

500 mg PO tid for 10 d

Pediatric

20 mg/kg/d PO divided tid for 10 d; not to exceed 1500 mg/d

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Flatulence is common; nausea, vomiting, or diarrhea occasionally may be noted; rarely, diplopia, dizziness, or pruritus occurs

Follow-up

Deterrence/Prevention

• Improved sanitation is critical to preventing orofecal transmission of organisms such as E histolytica. Travelers to developing countries should be advised to avoid consumption of unsafe food and water and sexual practices that may lead to fecal-oral transmission. Eating only cooked food or self-peeled fruits in endemic areas minimizes the risk. Travelers should avoid eating raw fruits and salads, which are difficult to sterilize. 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.
• Disease transmission can be reduced by early treatment of carriers in nonendemic areas.
• Development of a vaccine for invasive amebiasis is still in its infancy.^5,6,7  Many components of the ameba are immunogenic and may serve as targets for a future vaccine, including the galactose and N-acetyl-D-galactosamine lectin, the serine-rich E histolytica protein, cysteine proteinases, lipophosphoglycans, amebapores, and the 29-kDa protein. Progress in vaccine development has been facilitated by new animal models that allow better testing of potential vaccine candidates and by the application of recombinant technology to vaccine design. Oral vaccines using amebic antigens that are coadministered with some form of cholera toxin or expressed in attenuated strains of Salmonella or Vibrio cholera have been developed and tested in animals for mucosal immunogenicity.

Complications

• Bowel perforation
• GI 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
• The 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

Medicolegal 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 GI endoscopy in all patients in whom inflammatory bowel disease is suspected before treating with steroids.

Multimedia

Media file 1: Entamoeba histolytica trophozoite. Courtesy of Centers for Disease Control and Prevention.

Media file 2: Entamoeba histolytica cyst. Courtesy of Centers for Disease Control and Prevention.

Media file 3: Life cycle of Entameba histolytica.

Media file 4: Gross pathology of intestinal ulcers due to amebiasis. Courtesy of Centers for Disease Control and Prevention.

Media file 5: Histopathology of typical flask-shaped ulcer of intestinal amebiasis. Courtesy of Centers for Disease Control and Prevention.

Media file 6: Entamoeba histolytica in liver aspirate, trichrome stain. Courtesy of Centers for Disease Control and Prevention.

Media file 7: Histopathology of amebiasis. Courtesy of Centers for Disease Control and Prevention.

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Keywords

amebiasis, intestinal amebiasis, Entamoeba histolytica, E histolytica, Amoeba coli, A coli, amebic colitis, Entamoeba dispar, E dispar, dysentery, amebic dysentery, acute amebic colitis, fulminant amebic colitis, chronic amebic colitis, ameboma, amebic liver abscess, pleuropulmonary amebiasis, amebic peritonitis, amebic pericarditis, cerebral amebiasis, proctocolitis, dysentery, colitis, megacolon, ameboma, peritonitis, pericarditis, brain abscess, toxic megacolon, peritonitis, hepatic necrosis, portal venous obstruction, HIV, AIDS, diarrhea, bacterial dysentery, inflammatory bowel disease, carcinoma, tuberculosis, Crohn disease, actinomycosis, lymphoma, jaundice, fallopian tube amebiasis, ulcers, empyema, basilar atelectasis, pneumonia, lung abscess, heart failure

Contributor Information and Disclosures

Author

Vinod K Dhawan, MD, FACP, FRCP(C), Professor, Department of Clinical Medicine, University of California at Los Angeles; Professor of Medicine, Charles R Drew University of Medicine and Science; Chief, Division of Infectious Diseases, MLK-Harbor Hospital
Vinod K Dhawan, MD, FACP, FRCP(C) 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 None None

Coauthor(s)

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.

Medical Editor

Michael D Nissen, MBBS, BMedSc, 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, BMedSc, 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.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

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.

CME Editor

Robert W Tolan Jr, MD, Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine
Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility
Disclosure: GlaxoSmithKline Honoraria Speaking and teaching; MedImmune Honoraria Consulting; MedImmune Honoraria Speaking and teaching; Merck Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching; sanofi pasteur Grant/research funds Unrestricted research grant; sanofi pasteur  Consulting; sanofi pasteur Honoraria Speaking and teaching; Tap Honoraria Speaking and teaching

Chief Editor

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: None None None

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author Maria A Horga, MD, to the development and writing of this article.

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