AMEBIASIS

Introduction
Background

Amebiasis is caused by Entamoeba histolytica, a protozoan found worldwide. The highest prevalence of amebiasis is in developing countries where barriers between human feces and food and water supplies are inadequate.

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, 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.

Amebic infection was first described by Fedor Losch in 1875 in St. Petersburg, Russia. In 1890, Sir William Osler reported the first North American case of amebiasis, when he observed amebae in stool and abscess fluid from a physician who previously resided in Panama. The species name E histolytica was first coined by Fritz Schaudin in 1903. In 1913, in the Philippines, Walker and Sellards documented the cyst as the infective form of E histolytica. The life cycle was then established by Dobell in 1925.
Pathophysiology

E histolytica is a pseudopod-forming, nonflagellated protozoal parasite that causes proteolysis and tissue lysis (hence its name) and can induce host-cell apoptosis. Humans and perhaps nonhuman primates are the only natural hosts. Ingestion of E histolytica cysts from the environment is followed by excystation in the terminal ileum or colon to form highly motile trophozoites. Upon colonization of the colonic mucosa, the trophozoite may encyst and is then excreted in the feces or may invade the intestinal mucosal barrier and gain access to the blood stream and disseminate to the liver, lung, and other sites. Excreted cysts reach the environment to complete the cycle.

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.1,2 A mucosal immunoglobulin A (IgA) response against this lectin can result in fewer recurrent infections.3 Both lytic and apoptotic pathways have been described. Cytolysis can be undertaken by amoebapores, a family of peptides capable of forming pores in lipid bilayers.1 Furthermore, in animal models of liver abscess, trophozoites induced apoptosis via a non-Fas and non–tumor necrosis factor-α1 receptor pathway.4 The amoebapores, 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.1,5 The cysteine proteinases can also cleave and inactivate the anaphylatoxins C3a and C5a, as well as IgA and immunoglobulin G (IgG).6,7

Epithelial cells also produce various inflammatory mediators, including IL-1B, IL-8, and cyclooxygenase-2, leading to the attraction of neutrophils and macrophages.8,9 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, 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.10 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, suggesting that E histolytica are able to kill hepatocytes without direct contact.1

The genus Entamoeba contains many species, some of which (ie, E histolytica, Entamoeba dispar, Entamoeba moshkovskii, Entamoeba polecki, Entamoeba coli, Entamoeba hartmanni) can reside in the human interstitial lumen. E histolytica is, thus far, the only Entamoeba species definitely associated with disease; the others are considered nonpathogenic.11 More recent studies have recovered E dispar and E moshkovskii from patients with gastrointestinal symptoms, but a causal relationship is undetermined.11

E dispar and E histolytica cannot be differentiated by direct examination, but recent molecular techniques established them as two different species, with E dispar being commensal (including in patients with HIV infection) and E histolytica pathogenic.11 In fact, it is now estimated that many individuals with Entamoeba infections are colonized with E dispar, which appears to be 10 times more common than E histolytica.11 However, in certain regions (eg, Brazil, Egypt), asymptomatic E dispar and E histolytica infections are equally prevalent.1 In Western countries, approximately 20%-30% of men who have sex with men are colonized with E dispar.11
Frequency
United States

The overall prevalence of amebiasis is approximately 4%. However, certain groups are predisposed to amebic colitis, including very young patients, pregnant women, recipients of corticosteroids, and malnourished individuals.1 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. Travelers to endemic areas are at risk for infection; 10% of individuals returning with diarrhea were found to have amebiasis.1 Amebic liver abscess has been reported in travel exposures as short as 4 days (median, 3 mo), whereas amebic colitis is uncommon in short-term travelers.

International

Entamoeba species infect approximately 10% of the world's population. The prevalence of Entamoeba infection is as high as 50% in areas of Central and South America, Africa, and Asia. In Egypt, 38% of individuals presenting with acute diarrhea to an outpatient clinic were found to have amebic colitis.1 E histolytica seroprevalence studies in Mexico revealed that more than 8% of the population were positive.12 Asymptomatic E histolytica infections seem to be region-dependent, as high as 11% in Brazil. Since the introduction of molecular techniques, it is estimated that 500 million individuals with Entamoeba infection are colonized by E dispar.11
Mortality/Morbidity

* Amebiasis is second only to malaria in terms of protozoa-associated mortality. The combined prevalence of amebic colitis and amebic liver abscess is estimated at 40-50 million cases annually worldwide, resulting in 40,000-100,000 deaths.11,1,13
* Asymptomatic intestinal amebiasis occurs in 90% of infected individuals. However, only 4%-10% of individuals with asymptomatic amebiasis who were monitored for one year eventually developed colitis or extraintestinal disease.11
* Case fatality rates associated with amebic colitis range from 1.9%-9.1%. Amebic colitis evolves to fulminant necrotizing colitis or rupture in approximately 0.5% of cases; in such cases, the mortality rate jumps to greater than 40%.14
* The mortality rate due to amebic liver abscess has fallen to 1-3% in the last century following the introduction of effective medical treatment. Nevertheless, amebic liver abscess is complicated by sudden intraperitoneal rupture in 2-7% of patients, leading to a higher mortality rate.1

Race

* In Japan and Taiwan, HIV seropositivity is a risk factor for invasive extraintestinal amebiasis.15 This has not been observed elsewhere.

Sex

* Amebic colitis affects both sexes equally.1
* 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 sexual disparity is unknown, although hormonal effects may be implicated, as the prevalence of amebic liver abscess is also increased among postmenopausal women. Alcohol may also been an important risk factor. The sexual distribution is equal in children.1

Age

Very young children seem to be predisposed to fulminant colitis.
Clinical
History

* Amebic colitis
o The most common presentation of amebic colitis is gradual onset of bloody diarrhea, abdominal pain, and tenderness spanning several weeks’ duration.
o Rectal bleeding without diarrhea can occur, especially in children.
o Only approximately 10-30% of patients with amebic colitis develop fever.
o Weight loss and anorexia may occur.
o Fulminant or necrotizing colitis usually manifests as severe bloody diarrhea and widespread abdominal pain with evidence of peritonitis and fever.
o Predisposing factors for fulminant colitis include poor nutrition, pregnancy, corticosteroid use, and very young age.
* Amebic liver abscess
o The most typical presentation of amebic liver abscess is fever, right upper quadrant pain, and tenderness of less than 10 days’ duration.
o Unlike amebic colitis, amebic liver abscess is associated with fever in 85-90% of cases.
o A more subacute presentation can be seen, with concomitant weight loss and anorexia.
o Cough can occur. Jaundice is unusual.
o Acute abdominal symptoms and signs should prompt rapid investigation for intraperitoneal rupture.
o Sixty to 70% of patients with amebic liver abscess do not have concomitant colitis, although a history of dysentery within the previous year may be obtained.
o Amebic liver abscess may manifest years after travel to or residency in an endemic area.
o A history of alcohol abuse is common, but a clear causal relationship is unclear.
* Pleuropulmonary amebiasis: Cough, pleuritic chest pain, and respiratory distress may be clues to rupture through the diaphragm, a rare but serious complication of amebic liver abscess.
* Cerebral amebiasis
o Occurring in 0.6% of amebic liver abscess cases, abrupt onset of nausea, vomiting, headache, and mental status change should prompt rapid investigation for CNS involvement.
o Progression can be very rapid.

Physical

* Amebic colitis
o Fever (10-30%)
o Weight loss (40%)
o Diffuse abdominal tenderness (12-85%)
o Heme-positive stools (70-100%)
o Abdominal pain, distension, and rebound tenderness likely in fulminant colitis
* Amebic liver abscess
o Fever (85-90%)
o Right upper quadrant abdominal tenderness (84-90%)
o Weight loss (33-50%)
o Hepatomegaly (30-50%)
o Jaundice (6-10%)

Causes

* Amebiasis is an infection caused by the protozoal organism E histolytica, which can cause colitis and other extraintestinal manifestations, including liver abscess (most common) and pleuropulmonary, cardiac, and cerebral dissemination.
* 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.Differential Diagnoses
Abdominal Abscess
Inflammatory Bowel Disease
Arteriovenous Malformations
Perforated abdominal viscus
Campylobacter Infections
Pericarditis
Cholecystitis
Peritonitis
Colitis, Ischemic
Pyogenic Hepatic Abscesses
Diverticulitis
Right lower lobe pneumonia
Echinococcosis
Salmonellosis
Escherichia Coli Infections
Shigellosis
Hepatitis A

Hepatitis, Viral

Hepatocellular Adenoma

Workup
Laboratory Studies

* Microscopy11
o Microscopic stool examination for trophozoites from a single stool sample in amebic colitis is only 33-50% sensitive. Examination of 3 stool samples over no more than 10 days can improve the detection rate to 85-95%.

Trichrome stain of Entamoeba histolytica...
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.

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Trichrome stain of Entamoeba histolytica...

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.

o Stool leukocytes may be found, but in fewer numbers than in shigellosis.
o Stool examination findings in patients with amebic liver abscess are usually negative. Repeated stool sampling in patients with proven amebic liver abscess is positive in 8-40% of cases. Identification of the parasite in a liver abscess aspirate is only 20% sensitive.
o The presence of intracytoplasmic red blood cells in trophozoites is diagnostic of E histolytica infection, although recent studies demonstrated the same phenomenon with E dispar.
o The World Health Organization (WHO) recommends that intestinal amebiasis be diagnosed with an E histolytica -specific test, thus rendering the classic stool ova and parasite examination obsolete.
* Culture11
o Xenic cultivation, first introduced in 1925, is defined as the growth of the parasite in the presence of an undefined flora. This technique is still in use today using modified Locke-egg media.
o Axenic cultivation, first achieved in 1961, involves growth of the parasite in the absence of any other metabolizing cells. Only a few strains of E dispar have been reported to be viable in axenic cultures.
o Cultures can be performed using fecal or rectal biopsy specimens and liver abscess aspirates. The success rate is between 50% and 70%, but the technique is technically difficult. Overall, it is less sensitive than microscopy.
* Antigen detection11
o Enzyme-linked immunosorbent assay (ELISA) is used to detect antigens from E histolytica in stool samples. Several kits are commercially available.
o Antigen-based ELISA kits using monoclonal antibodies against the GAL/GalNAc–specific lectin of E histolytica (E histolytica II, TechLab, Blacksburg, VA) yield an overall sensitivity of 71%-100% and specificity of 93%-100%. One study showed a much lower sensitivity (14.2%).
o In patients with amebic liver abscess, serum and liver aspirate antigen detection using the same kit was shown to yield a sensitivity of 96% and 100%, respectively.
o Other stool detection kits use monoclonal antibodies against the serine-rich antigen of E histolytica (Optimum S kit, Merlin Diagniostika, Bornheim-Hersel, Germany) or against other specific antigens (Entamoeba CELISA-PATH, Cellabs, Brookvale, Australia; ProSpecT EIA, Remle Inc, Lenexa, KY).
o No specific antigen tests are available for the detection of E dispar and E moshkovskii from clinical samples.
* Serology11
o Multiple serologic assays are available for the diagnosis of amebiasis.
o ELISA is the most used assay throughout the world and is used to measure the presence of serum antilectin antibodies (IgG). The sensitivity for detection of antibodies to E histolytica in patients with amebic liver abscess is 97.9%, whereas the specificity is 94.8%. False-negative results can occur within the first 7-10 days following infection.
o Immunofluorescent assay (IFA) is also rapid, reliable, and reproducible. In the setting of amebic liver abscess, the sensitivity and specificity of IFA was shown to be 93.6% and 96.7%, respectively.
o Indirect hemagglutination (IHA) is very specific (99.1%) but is less sensitive than ELISA.
o Immunoelectrophoresis, counter-immunoelectrophoresis (CIE), and immunodiffusion tests use the precipitation property of antigen-antibody complexes in agar. CIE is time-consuming but has shown a sensitivity of 100% in invasive amebiasis.
o Complement fixation (CF) is less sensitive than other techniques.
o The seropositivity prevalence is very high in endemic areas, limiting antibody-based testing for diagnosing currently active disease, since antibodies can persist for years after infection.
* Polymerase chain reaction11
o E histolytica can be identified in various types of clinical specimens, including feces, tissues, and liver abscess aspirates.
o A wide variety of polymerase chain reaction (PCR) methods targeting different genes, including a small-subunit rRNA gene (18S rDNA), 30-kDa antigen gene, serine-rich protein gene, chitinase gene, hemolysin gene, and extrachromosomal circular DNA, have been described for the detection and differentiation of E histolytica, E dispar, and E moshkovskii.
o Sensitivities can vary according to sampling and the specific target gene used. Performed on feces, PCR yields a sensitivity that is similar to that of stool antigen-based assay.
o PCR-based tests have been strongly endorsed by the WHO.
o Application of PCR-based methods in routine diagnosis is still very limited, as the generation of nonspecific DNA fragments from environmental and clinical samples often leads to false-positive results
* Nonspecific laboratory tests
o Amebic liver abscess
+ Leukocytosis without eosinophilia (80%)
+ Elevated alkaline phosphatase (80%)
+ Mildly elevated transaminases
+ Mild anemia
+ Elevated erythrocyte sedimentation rate

Imaging Studies

* Both ultrasonography and CT scanning are sensitive but nonspecific for amebic liver abscess. Lesions are usually solitary and located in the right hepatic lobe (70-80%), although multiple abscesses are possible.
* On sonograms, amebic liver abscesses usually appear as a homogenous hypoechoic round lesion.
* On CT scans with intravenous contrast, amebic liver abscess can appear as a rounded, low-attenuation lesion with an enhancing rim. Furthermore, the abscess may be homogenous or septated, with or without observable fluid levels.

Procedures

* Liver aspiration
o Ultrasound- or CT-guided needle aspiration should be performed when a diagnosis must be established very rapidly, since pyogenic liver abscess can present and appear in a similar fashion.
o Liver abscess aspirate is usually an odorless thick yellow-brown liquid classically referred to as "anchovy paste."
o Aspirate can be sent for microscopy, culture, antigen detection, and PCR, where available. A Gram stain should also be performed if a pyogenic etiology is suspected clinically.
* Colonoscopy
o Colonoscopy can be performed for biopsy in the setting of negative findings on stools studies, including antigen testing. Tissue can be sent for microscopic evaluation, culture, and PCR, where available.
o Fulminant colitis is a relative contraindication to colonoscopy since the risk of intestinal perforation is increased.
o A friable and diffusely ulcerated mucosa resembling inflammatory bowel disease can be observed.
o A carcinomalike annular lesion called ameboma can also be seen, usually in the cecum and ascending colon.1,16

Histological Findings

* The intestinal biopsy specimen should be taken from the edge of ulcers and evaluated for motile trophozoites.
* Histopathological findings can comprise of mucosal thickening, multiple discrete ulcers separated by regions of normal-appearing colonic mucosa, diffusely inflamed and edematous mucosa, necrosis, or wall perforation.
* Amebic invasion through the mucosa and into submucosal tissues is the hallmark of amebic colitis.
* Lateral extension through the submucosal tissues gives rise to the classic flask-shaped ulcer of amebic colitis.
* Different chemical stains can be used, including periodic acid-Schiff stain, which makes E histolytica appear magenta in color.

Trichrome stain of Entamoeba histolytica...
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.

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Trichrome stain of Entamoeba histolytica...

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 an Entamoeba histolytica300 cm3).1

Consultations

* Infectious disease specialist
* General surgeon
* Gastrointestinal specialist

Medication

* Asymptomatic amebiasis should be treated with a luminal agent (iodoquinol, paromomycin, diloxanide furoate) to eradicate infection. This recommendation is based on two arguments: First, invasive disease may develop; second, shedding of E histolytica cysts in the environment is a public health concern.1
* Asymptomatic E dispar infections should not be treated, but education should be pursued since it is a marker of fecal-oral contamination.1
* Amebic colitis is first treated with a nitroimidazole derivative (metronidazole being the only one available in the United States), followed by a luminal agent to eradicate colonization.1
* Amebic liver abscess can be cured without drainage and even by one dose of metronidazole. Clinical defervescence should occur during the first 3-4 days of treatment. Metronidazole failure may be an indication for surgical intervention. Treatment with a luminal agent should also follow.1
* Disseminated amebiasis should be treated with metronidazole, which can cross the brain-blood barrier.
* Empirical antibacterial agents should be used concomitantly if perforated viscus is a concern.

Amebicides

Parasite biochemical pathways are sufficiently different from the human host to allow selective interference by chemotherapeutic agents in relatively small doses.

Iodoquinol (Yodoxin)

Amebicidal against E histolytica. Considered effective against trophozoite and cyst forms.

* Dosing
* Interactions
* Contraindications
* Precautions

Adult

650 mg PO tid for 20 d
Pediatric

10-13 mg/kg PO tid for 20 d

* Dosing
* Interactions
* Contraindications
* Precautions

None reported

* Dosing
* Interactions
* Contraindications
* Precautions

Documented hypersensitivity; hepatic dysfunction

* Dosing
* Interactions
* Contraindications
* 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 thyroid disease; protein-bound serum iodine levels may increase during treatment with iodoquinol, interfering with certain thyroid function tests

Paromomycin (Humatin)

Amebicidal and antibacterial aminoglycoside obtained from a strain of Streptomyces rimosus, active in intestinal amebiasis against trophozoite and cyst forms of E histolytica. Recommended for the treatment of Diphyllobothrium latum, Taenia saginata, Taenia solium, Dipylidium caninum, and Hymenolepis nana.

* Dosing
* Interactions
* Contraindications
* Precautions

Adult

25-35 mg/kg/d PO divided tid for 7 d
Pediatric

Administer as in adults

* Dosing
* Interactions
* Contraindications
* Precautions

Nephrotoxic potential may increase with concurrent administration of other aminoglycosides, penicillins, cephalosporins, amphotericin B, and loop diuretics; may decrease serum concentrations of digoxin

* Dosing
* Interactions
* Contraindications
* Precautions

Documented hypersensitivity; intestinal obstruction

* Dosing
* Interactions
* Contraindications
* 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

Because of narrow therapeutic index and toxic hazards associated with extended administration, not for long-term therapy; caution in renal failure, hypocalcemia, myasthenia gravis, and conditions that depress neuromuscular transmission; adjust dose in renal impairment; may cause abdominal cramping, nausea, emesis, and diarrhea; malabsorption, ototoxicity, and nephrotoxicity can occur if administered in high doses or in ulcerative colitis

Diloxanide (Entamide, Furamide)

Dichloroacetamide derivative. Amebicidal against trophozoite and cyst forms of E histolytica. Not available in United States.

* Dosing
* Interactions
* Contraindications
* Precautions

Adult

500 mg PO tid for 10 d
Pediatric

<2 years: Not recommended >2 years: 20 mg/kg PO divided tid for 10 d

* Dosing
* Interactions
* Contraindications
* Precautions

None reported

* Dosing
* Interactions
* Contraindications
* Precautions

Documented hypersensitivity

* Dosing
* Interactions
* Contraindications
* 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

GI adverse effects (eg, flatulence, abdominal cramps, nausea, emesis, diarrhea) may occur

Metronidazole (Flagyl)

Active against various anaerobic bacteria and protozoa. Appears to be absorbed into cells. Intermediate metabolized compounds are formed and bind DNA and inhibit protein synthesis, causing cell death. Antimicrobial effect may be due to production of free radicals.
Indicated for invasive amebiasis.

* Dosing
* Interactions
* Contraindications
* Precautions

Adult

500-750 mg PO tid for 10 d
Pediatric

35-50 mg/kg PO divided tid for 10 d

* Dosing
* Interactions
* Contraindications
* Precautions

Cimetidine may increase toxicity of metronidazole; may increase effects of anticoagulants; may increase toxicity of lithium and phenytoin; ingestion of ethanol during therapy may induce a disulfiramlike reaction with abdominal cramps, nausea, and emesis

* Dosing
* Interactions
* Contraindications
* Precautions

Documented hypersensitivity

* Dosing
* Interactions
* Contraindications
* Precautions

Pregnancy

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

Adjust dose in hepatic disease; monitor for seizures and development of peripheral neuropathy; alcoholic beverages should be avoided during administration and for 3 d after

Tinidazole (Fasigyn)

5-Nitroimidazole derivative used for susceptible protozoal infections. Indicated to treat intestinal amebiasis and amebic liver abscess caused by E histolytica in adults and children aged 3 y and older.

* Dosing
* Interactions
* Contraindications
* Precautions

Adult

Intestinal amebiasis: 600 mg PO bid 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 Follow-up
Further Inpatient Care

* Patients with suspected fulminant colitis, liver abscess intractable to medical treatment, or suspected amebic liver abscess rupture should be admitted to the hospital for further evaluation.

Further Outpatient Care

* Follow-up stool examination after therapy completion is recommended to ensure intestinal eradication.

Deterrence/Prevention

* Amebiasis is prevented by eradicating fecal contamination of food and water through improved sanitation, hygiene, and water treatment.
* Amebic cysts are not killed by soap or low concentrations of chlorine or iodine; therefore, water in endemic areas should be boiled for more than 1 minute and vegetables should be washed with a detergent soap and soaked in acetic acid or vinegar for 10-15 minutes before consumption.
* Avoiding sexual practices that involve fecal-oral contact may reduce the risk of sexual transmission of infective cysts.
* Screen family members or close contacts of an index case, since reinfection is possible.
* Effective recombinant antigen-based vaccines in animals prevent amebic liver abscess and generate mucosal antiamebic antibodies. In humans, natural E histolytica infection does not seem to result in long-term immunity, as individuals with a previous amebic liver abscess are as susceptible to a new infection as other members of the population.1

Complications

* Amebic colitis
o Fulminant or necrotizing colitis
o Toxic megacolon
o Ameboma
o Rectovaginal fistula
* Amebic liver abscess
o Intraperitoneal, intrathoracic, or intrapericardial rupture, with or without secondary bacterial infection
o Direct extension to pleura or pericardium
o Dissemination and formation of brain abscess

Prognosis

* Following treatment, invasive amebiasis carries a good prognosis.
* Fulminant colitis and amebic liver abscess rupture are associated with higher mortality rates.
* Prior infection and treatment do not protect against future colonization or recurrent invasive amebiasis.

Patient Education

* Individuals traveling to endemic areas should be advised on the proper food and water handling.
o Uncooked vegetables should be washed and soaked in acetic acid or vinegar for 10-15 minutes.
o Local water should be boiled for more than 1 minute.

Miscellaneous
Medicolegal Pitfalls

* Failure to recognize symptoms and signs of peritonitis or perforated viscus can delay surgical evaluation.
* Failure to perform follow-up stool examination may facilitate persistent colonization with a continued risk for invasive disease.