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Extraintestinal Entamoeba histolytica amebiasis

Extraintestinal Entamoeba histolytica amebiasis
Literature review current through: Jan 2024.
This topic last updated: Mar 03, 2022.

INTRODUCTION — Extraintestinal amebiasis is usually caused by the protozoan Entamoeba histolytica. Most infections are asymptomatic; clinical manifestations include amebic dysentery and extraintestinal disease. Extraintestinal manifestations include amebic liver abscess and other more rare manifestations such as pulmonary, cardiac, and brain involvement [1].

The extraintestinal manifestations of amebiasis will be reviewed here. Issues related to intestinal infection with E. histolytica are discussed separately, including epidemiology, pathogenesis, clinical manifestations, diagnosis, treatment, and prevention. (See "Intestinal Entamoeba histolytica amebiasis".)

AMEBIC LIVER ABSCESS — Amebic liver abscess is the most common extraintestinal manifestation of amebiasis. It is the fourth leading cause of mortality worldwide due to any parasitic infection and has an estimated 50,000 deaths annually [2,3]. Amebae establish hepatic infection by ascending the portal venous system [4]. Almost all cases are caused by E. histolytica, but liver abscess due to Entamoeba dispar has been reported [5,6].

Epidemiology — Amebic liver abscess (and other extraintestinal disease) is 7 to 10 times more common among adult males than other demographic groups, despite equal sex distribution of colonic amebic disease [7-11]. It is observed most frequently in the fourth and fifth decades of life [12]. The reasons for these observations are not fully understood; suggested mechanisms include hormonal effects and a potential role of alcoholic hepatocellular damage in creating a nidus for portal seeding [8,13].

In developed countries, amebiasis is generally seen in migrants from and travelers to endemic areas. Areas with high rates of amebic infection include India, Africa, Mexico, and parts of Central and South America. Amebiasis is relatively uncommon among short-term travelers, but amebic liver abscesses can occur after travel exposures as short as four days [14]. In one study, 35 percent of travelers with amebic liver abscess had spent less than six weeks in an endemic area [15]. Sexual oral-anal contact may also account for acquisition of infection, so occasionally infection can occur in nonendemic areas among individuals who have never traveled abroad [11,16].

Factors predisposing to progression from intestinal amebiasis to amebic liver abscess are not fully understood. Different genetic strains that are morphologically identical may be more likely to cause a specific manifestation [17]. Conditions that affect cell-mediated immunity increase the chances that E. histolytica infection results in invasive disease with liver involvement. It has been suggested that immunosuppression associated with HIV infection may increase the likelihood of invasive amebiasis, including an amebic liver abscess, but this is potentially confounded by increased rates of oral-anal sexual contact among this population [18-21].

Clinical manifestations — For individuals returning from an endemic area, the clinical presentation typically occurs within 8 to 20 weeks (median 12 weeks). However, a longer interval of many years (even decades) prior to onset of clinical manifestations has been described; one report noted an average interval of 17 months [15,22-26]. Patients with amebic liver abscess usually present with one to two weeks of right upper quadrant pain and fever (38.5 to 39.5°C). Pain may refer to the epigastrium, the right chest, or the right shoulder. The pain is usually dull but may be pleuritic or aching. Other symptoms may include cough, sweating, malaise, weight loss, anorexia, and hiccough. Concurrent diarrhea is present in less than one-third of patients, although some patients report history of dysentery within the previous few months. Jaundice occurs in less than 10 percent of patients [27]. Physical examination reveals hepatomegaly and point tenderness over the liver in approximately 50 percent of cases.

Rupture of liver abscess can occur into any adjoining space or organ; extension into the chest occurs almost four times as often as extension into the peritoneal cavity. In up to 7 percent of cases, the abscess ruptures into the peritoneum, causing peritonitis [28]. Hepatic vein and inferior vena cava thrombosis secondary to amebic liver abscess have also been described [29].

Occasionally, patients have a more chronic presentation with months of fever, weight loss, and abdominal pain with or without hepatomegaly. Recurrent episodes of infection over many years (despite adequate treatment) has also been described [30].

In a study comparing the presentations of HIV-infected and HIV-uninfected patients with amebic liver abscess, no differences in clinical manifestations or radiographic findings between the two groups were observed [31].

Patients with amebic liver abscess often have a leukocytosis (>10,000/mm3) without eosinophilia. Liver function testing demonstrates an elevated alkaline phosphatase (80 percent of cases), and hepatic transaminases may also be elevated. Other common nonspecific findings include an abnormal chest radiograph and proteinuria. (See 'Imaging' below.)

Uncommonly, patients with amebic hepatic abscesses may also have localized colonic infection resulting in a mass of granulation tissue forming an ameboma, which may mimic colon cancer [32,33]. Patients with amebomas usually are found to have a tender palpable mass. (See "Intestinal Entamoeba histolytica amebiasis", section on 'Clinical manifestations'.)

Other complications include hepatic vein and inferior vena cava thrombosis; these have been attributed to mechanical compression and inflammation associated with a large abscess [34].

Patients with secondary cardiac or pulmonary involvement may present with symptoms primarily due to these complications. (See 'Other extraintestinal sites' below.)

Diagnosis — Amebic liver abscess should be suspected in the setting of fever and right upper quadrant pain together with relevant epidemiology (resident in, migration from, or travel to an endemic area). In such circumstances, the diagnosis may be supported by radiographic imaging of the liver. In the setting of suggestive findings on imaging studies, confirmatory serologic or antigenic testing should be pursued, perhaps supplemented with stool microscopy or antigenic testing of stool, with or without evaluation for the parasite in liver abscess fluid. However, simultaneous liver abscess and amebic colitis is uncommon, so stool microscopy and polymerase chain reaction (PCR) are usually negative in the setting of liver abscess [10].

Imaging — Radiographic imaging of the liver can be pursued with ultrasound, computed tomography (CT), or magnetic resonance imaging (MRI). Ultrasonography usually demonstrates a cystic intrahepatic cavity. Amebic liver abscesses are most commonly found in the posterior part of the right lobe; 70 to 80 percent are solitary subcapsular lesions, although multiple lesions can be present [10,35]. Localization in the left lobe predisposes to extension into the pericardial sac. (See 'Cardiac infection' below.)

On ultrasound, the abscess appears as a round, well-defined hypoechoic mass (image 1) [36]. On CT scan, it appears as a low-density mass with a peripheral enhancing rim. On MRI, the abscess appears as low-signal intensity on T1-weighted images and high-signal intensity on T2-weighted images. After healing, the periphery of the abscess may calcify as a thin, round ring [36].

On gallium citrate and technetium-labeled sulfur colloid radionuclide liver scans, amebic abscesses are "cold" (with a bright rim in some cases), whereas pyogenic abscesses are "hot." Radiographic findings must be interpreted in the appropriate clinical context with consideration of the differential diagnoses, including pyogenic abscess and malignancy.

Serial imaging is generally not helpful since lesions may appear to increase in size or number on ultrasound following initiation of treatment, even with appropriate therapy and clinical improvement [37]. Treated lesions may become anechoic, calcified, or may persist as cystic-appearing lesions. Complete radiologic resolution may take two years or more. Therefore, persistent abnormalities on ultrasound imaging should not prompt retreatment or additional testing in a patient who is clinically well.

A chest radiograph abnormality will be observed in approximately 50 percent of patients with an amebic liver abscess, most commonly elevation of the right hemidiaphragm [38]. This finding does not necessarily signal pulmonary involvement in the infection.

Serology and antigen detection — Most commercial serologic tests are based on immunoglobulin (Ig)G enzyme-linked immunosorbent assay (ELISA). Approximately 99 percent of patients with amebic liver abscess develop detectable antibodies, but serologic testing may be negative in the first seven days [22,28,35]. Serum antibodies are detectable in 92 to 97 percent of patients at the time of presentation.

In endemic areas, up to 35 percent of uninfected individuals have anti-amebic antibodies due to previous infection with E. histolytica [39]. Therefore, negative serology is helpful for exclusion of disease, but positive serology cannot distinguish between acute and previous infection [14].

New serologic tests based on recombinant E. histolytica antigens have been developed. In one study of two different antigens among 20 patients with known amebic liver abscesses, patients lost seroreactivity with the recombinant antigens more rapidly than with conventional serologic tests; such assays may be especially useful in endemic areas. [40]. In another study, the combined diagnostic efficacy of indirect ELISAs using crude soluble antigen and excretory-secretory antigen for serodiagnosis of amebic liver abscess was improved by using both assays (as compared with either single assay) [41]. Lateral flow rapid dipstick tests based on IgG-4 assays are also in development [42].

Drainage — Needle aspiration under ultrasound or CT guidance or insertion of a pigtail catheter are not routinely required but may be warranted if the cyst is >10 cm in diameter, appears to be at imminent risk of rupture (particularly for lesions in the left lobe), if there is clinical deterioration or lack of response to empiric therapy, or if exclusion of alternative diagnoses is needed [43]. In some cases, aspiration may be therapeutic as well as diagnostic [44,45]. For cases that have required catheter drainage, practices vary with regards to indications for removal. Size of the residual abscess (eg, <3 cm) or fulfillment of the following four criteria have been proposed: improvement in abdominal pain, no fever for 48 hours, drainage output <10 mL per 24 hours for two consecutive days, and improvement in leukocyte count [46].  

Amebic liver abscesses contain acellular, proteinaceous debris, and a brown fluid likened to "anchovy paste," consisting predominantly of necrotic hepatocytes. Trophozoites are seen on microscopy of the aspirate in fewer than 20 percent of cases and are often present only in the peripheral parts of the abscess, invading and destroying adjacent tissue [47]. This is in contrast to aspirates from pyogenic liver abscesses in which bacterial organisms and polymorphonuclear cells are usually readily apparent by Gram stain. (See "Pyogenic liver abscess".)

Antigen testing and/or PCR on aspirated material may also be helpful in establishing the diagnosis [12,22,48-51]. Multiple commercial and in-house tests have been reported, with sensitivities generally ranging from 75 to 100 percent [49,52,53], with PCR being more sensitive than antigen-based assays [54]. In one study comparing nested-multiplex PCR, Taqman (18S rRNA), and SYBR Green real-time PCR (16S-like rRNA) assays to detect E. histolytica from liver abscess pus and stool samples, the highest positivity rate was observed with Taqman and the lowest rate was observed with conventional nested-multiplex PCR [55]. One study has also shown that cell-free circulating E. histolytica DNA can be detected by quantitative PCR; 17 out of 19 patients with amebic liver abscess had positive serum quantitative PCR results [56].

Rarely, amebic hepatic abscesses can become secondarily infected with enteric bacteria, so aspirated fluid should also be sent for bacterial culture.

Differential diagnosis — The differential diagnosis of amebic liver abscess includes:

Pyogenic liver abscess – The clinical presentations of amebic liver abscess and pyogenic liver abscess are compared in the table (table 1). The diagnosis of pyogenic liver abscess is established by aspiration and culture of the abscess material. In the setting of clinical suspicion for amebic abscess together with confirmatory serologic or antigenic testing (with or without stool testing), aspiration is not usually required to rule out pyogenic liver abscess. (See "Pyogenic liver abscess".)

Echinococcal disease – Both Echinococcus and amebic liver abscess present with liver lesions; symptoms of Echinococcus are unusual before the cyst reaches 10 cm. Echinococcus may be distinguished from amebic liver abscess based on imaging and serology. Aspiration is reserved for situations in which other diagnostic methods are inconclusive. (See "Echinococcosis: Clinical manifestations and diagnosis".)

Malignancy – Patients with hepatocellular carcinoma usually have no symptoms other than those related to chronic liver disease, whereas patients with amebic liver abscess usually present with right upper quadrant pain and fever. These diagnoses are distinguished based on imaging and tissue biopsy. (See "Clinical features and diagnosis of hepatocellular carcinoma".)

The differential diagnosis of solid and cystic liver lesions is discussed further separately. (See "Approach to the adult patient with an incidental solid liver lesion" and "Diagnosis and management of cystic lesions of the liver".)

Treatment

Clinical approach — For circumstances in which amebic liver abscess is suspected based on epidemiology, clinical manifestations, and radiographic findings, it is reasonable to initiate empiric treatment pending further diagnostic evaluation (including confirmatory antigenic or serologic testing and evaluation for the parasite in stool and liver abscess pus).

In general, treatment of amebic liver abscess consists of a tissue agent and a luminal agent (to eliminate intraluminal cysts). In cases of uncomplicated amebic liver abscess, there has been no benefit observed with drainage in addition to medical therapy [43]. Aspiration or catheter drainage may be warranted for patients with either a large left-lobe abscess, a lack of clinical response within five days of appropriate antimicrobial therapy, and in cases of uncertainty about the diagnosis [8]. Percutaneous catheter drainage may be favorable compared with aspiration. In a randomized controlled trial of 543 patients in India with amebic liver abscess, percutaneous catheter drainage was associated with faster clinical and radiologic recovery but similar long-term outcomes compared with percutaneous needle aspiration [57].

Tissue agents — Patients with an amebic liver abscess should be treated with metronidazole (500 to 750 mg orally three times daily for 7 to 10 days) or tinidazole (2 g once daily for 5 days) [58-60]. The cure rate with this therapy is >90 percent. Shorter duration of metronidazole is not generally recommended [59]. Metronidazole is well absorbed from the gastrointestinal tract; intravenous therapy offers no significant advantage as long as the patient can take oral medications and has no major defect in small bowel absorption. (See "Intestinal Entamoeba histolytica amebiasis", section on 'Symptomatic infection'.)

Alternatives to metronidazole or tinidazole include ornidazole and nitazoxanide [59,60]. Nitazoxanide (500 mg twice daily for 10 days) has been shown to be effective in a small case series [61].

In the setting of slow response to metronidazole or relapse following therapy, therapeutic aspiration, percutaneous catheter drainage, and/or a prolonged course of metronidazole may be warranted.

Luminal agents — Following therapy for invasive amebiasis, treatment with a luminal agent to eliminate intraluminal cysts is warranted, even if stool microscopy is negative. Intraluminal infection can be treated with one of the following regimens: paromomycin (25 to 30 mg/kg per day orally in three divided doses for 7 days), diiodohydroxyquin (650 mg orally three times daily for 20 days for adults and 30 to 40 mg/kg per day in three divided doses for 20 days for children), or diloxanide furoate (500 mg orally three times daily for 10 days for adults and 20 mg/kg per day in three divided doses for 10 days for children). (See "Intestinal Entamoeba histolytica amebiasis", section on 'Symptomatic infection'.)

Pregnancy — Amebic liver abscess can cause significant morbidity and potential mortality during pregnancy.

For pregnant women with amebic liver abscess, we favor treatment with metronidazole [62]. Use of metronidazole in pregnancy is controversial; it crosses the placenta and rapidly enters the fetal circulation. There are no well-controlled studies demonstrating safety of metronidazole in pregnancy; therefore, it should be used only in the setting of severe illness (eg, if the risks to the mother associated with deferring treatment outweigh potential harm to the fetus).

Chloroquine (600 mg base daily for two days, followed by 300 mg base daily for three weeks) is an acceptable alternative agent to metronidazole for treatment of amebic liver abscess in pregnant women [63-66].

Subsequently, pregnant women should receive treatment with paromomycin to eliminate intraluminal cysts. However, paromomycin should be avoided in the setting of severe amebic colitis in pregnancy, since there may be breakdown of the intestinal barrier with risk for systemic absorption.

Prognosis — Uncomplicated amebic liver abscess has a mortality rate of <1 percent if diagnosed and treated early. In one study of 135 patients with amebic liver abscess in India with overall mortality rate of 17 percent, independent risk factors for increased mortality included bilirubin level >3.5 mg/dL, serum albumin <2.0 g/dL, large volume of the abscess cavity, multiple abscesses, and encephalopathy [67].

OTHER EXTRAINTESTINAL SITES — Rarely, amebic disease involves other sites outside the liver. Lung disease, cardiac involvement, brain abscess, perinephric or splenic abscess, vaginal or uterine involvement, rectovaginal fistulae, and cutaneous disease can all occur [68].

Pleuropulmonary infection — Pleuropulmonary involvement following E. histolytica infection is relatively rare. Risk factors for development of pulmonary amebiasis include malnutrition, chronic alcoholism, and atrial septal defect with left-to-right shunt [69].

Pleural manifestations may include development of a sympathetic serous effusion. Liver abscess rupture into the pleural space results in an amebic empyema; rupture into the lung can lead to consolidation, abscess formation, or a hepatobronchial fistula [70,71]. Other mechanisms of pleural involvement include lymphatic spread from the liver through the diaphragm or hematogenous embolic spread from the liver or colon [69,71]. Hematogenous spread is an unusual disorder and should be suspected when there is pulmonary amebiasis in the absence of hepatic disease or in noncontiguous pulmonary and hepatic disease.

Clinical manifestations — Clinical manifestations include pain, cough, hemoptysis, and dyspnea [72]. The pain may be pleuritic or localized to the right upper quadrant. Cough can be nonproductive but more often is associated with expectoration of material ranging from small amounts of sputum to large amounts of amebic pus. If a hepatobronchial fistula develops, the patient may expectorate necrotic material that can include liver abscess contents; such material may have a reddish brown or "anchovy sauce" appearance.

The liver may not be palpably enlarged if the original abscess is high up in the right lobe or if it has been decompressed by rupture. Pulmonary consolidation is common in the right lower and middle lobes. A case of pulmonary amebiasis presenting as superior vena cava syndrome has also been reported [73].

Diagnosis — The diagnosis of amebic pleuropulmonary disease can be established by the same tests used to diagnose hepatic amebic abscesses. Amebic serology is positive in over 90 percent. (See 'Diagnosis' above.)

Treatment — In general, amebic pleural effusions should be aspirated. Drained pleural effusions resolve rapidly with drainage and antimicrobial therapy, which consists of metronidazole (750 mg orally three times daily for 7 to 10 days) or tinidazole (2 g once daily for 5 days) [74]. Most patients respond to a single course of treatment with resolution of symptoms before the end of therapy. In rare cases, a second course of metronidazole or tinidazole is need because of failure to achieve complete resolution after the initial regimen. Relapses are rare.

Treatment with a luminal agent to eliminate intraluminal cysts is also warranted. (See 'Luminal agents' above.)

Cardiac infection — Cardiac involvement in amebic disease is rarer than pleuropulmonary disease. When it occurs, it usually results from rupture of a liver abscess into the pericardium, particularly in the setting of abscesses involving the left lobe of the liver [75]. This can result in severe chest pain, pericardial effusion, acute pericarditis, myocarditis, pericardial abscess, congestive cardiac failure, pericardial tamponade, or constrictive pericarditis, with high associated mortality. Clinically, cardiac involvement may present suddenly as a purulent pericarditis with cardiac tamponade or more slowly with gradual progression of pericardial effusion [76]. Polymerase chain reaction testing on pericardial fluid may be positive for E. histolytica [77].

Brain abscess — Cerebral amebiasis results from hematogenous spread of infection. It is characterized by abrupt onset of symptoms and rapid progression to death if untreated. Findings on computed tomography (CT) scan may consist of irregular foci without a capsule or surrounding enhancement [78,79]. Central nervous system (CNS) abscesses due to E. histolytica are distinct from CNS lesions caused by free-living amebae. (See "Free-living amebas and Prototheca".)

For circumstances in which amebic brain abscess is suspected based on epidemiology, clinical manifestations, and radiographic findings, metronidazole should be started immediately; surgical intervention for decompression and/or tissue biopsy may be required. (See "Pathogenesis, clinical manifestations, and diagnosis of brain abscess".)

Cutaneous infection — Cutaneous amebiasis can affect any body region. It may be the only manifestation of infection or may occur in the setting of other organ involvement. Cutaneous disease in the perineal region is a rare manifestation of amebiasis and may manifest as painful perianal/perineal ulceration [80]. This clinical entity most likely results from direct inoculation from stool and is most common in infants wearing diapers [81]. Perineal cutaneous amebiasis also occurs as a sexually transmitted infection in endemic areas, including among individuals who practice insertive anal intercourse [82,83].

SUMMARY AND RECOMMENDATIONS

Introduction − Extraintestinal manifestations of Entamoeba histolytica include amebic liver abscess and more rare manifestations such as pulmonary, cardiac, and brain involvement. Amebae establish hepatic infection by ascending the portal venous system. (See 'Introduction' above.)

Epidemiology − In developed countries, amebiasis is generally seen in migrants from and travelers to endemic areas. Amebic liver abscess (and other extraintestinal disease) is more common among adult males than other demographic groups. (See 'Epidemiology' above.)

Clinical manifestations

Liver abscess − Patients with amebic liver abscess typically present with one to two weeks of right upper quadrant pain and fever. Concurrent diarrhea is present in less than one-third of patients, although some patients report history of dysentery within the previous few months. Physical examination frequently reveals hepatomegaly and point tenderness over the liver. (See 'Clinical manifestations' above.)

Pleuropulmonary infection − Pleural space involvement of E. histolytica can occur in the setting of liver abscess rupture into the pleural space, resulting in an amebic empyema. Rupture into the lung can lead to consolidation, abscess formation, and/or hepatobronchial fistula. Clinical manifestations include pain, cough, hemoptysis, and dyspnea. Cough may be productive of necrotic material that can include liver abscess contents.

Diagnosis − In the setting of relevant epidemiology and suggestive symptoms, the diagnosis of amebic liver abscess is generally established by radiographic imaging and confirmed with serologic or antigenic testing, perhaps supplemented with stool microscopy or antigenic testing of stool, with or without evaluation for the parasite in liver abscess fluid. (See 'Diagnosis' above.)

Treatment and management

Liver abscess − In general, treatment of extraintestinal amebic disease is managed with a tissue agent and a luminal agent (to eliminate intraluminal cysts). For patients with amebic liver abscess, we suggest t metronidazole or tinidazole rather than other agents (Grade 2C). For such patients, we also suggest subsequent treatment with paromomycin (Grade 2C), in order to eliminate intraluminal cysts. Dosing is outlined above. (See 'Treatment' above.)

Abscess drainage − Needle aspiration of amebic liver abscess is not routinely required but may be warranted if the cyst appears to be at imminent risk of rupture (particularly for lesions in the left lobe), if there is clinical deterioration or lack of response to empiric therapy, or if exclusion of alternative diagnoses is needed. (See 'Drainage' above.)

Pleuropulmonary infection − Treatment of amebic pleural effusions should consist of aspiration and antimicrobial therapy. We suggest treatment of pulmonary infection with metronidazole or tinidazole (Grade 2C). We suggest subsequent treatment with paromomycin to eliminate intraluminal cysts (Grade 2C). (See 'Treatment' above.)

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Topic 5728 Version 29.0

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