Amebic liver abscess is the most frequent extraintestinal manifestation of Entamoeba histolytica infection. This infection is caused by the protozoa E histolytica, which enters the portal venous system from the colon. Amebic liver abscess is an important cause of space-occupying lesions of the liver, mainly in developing countries. Prompt recognition and appropriate treatment of amebic liver abscess lead to improved morbidity and mortality.
E histolytica exists in two forms. The cyst stage is the infective form, and the trophozoite stage causes invasive disease. People who chronically carry E histolytica shed cysts in their feces; these cysts are transmitted primarily by food and water contamination. Rare cases of transmission via oral and anal sex or direct colonic inoculation through colonic irrigation devices have occurred. Cysts are resistant to gastric acid, but the wall is broken down by trypsin in the small intestine. Trophozoites are released and colonize the cecum. To initiate symptomatic infection, E histolytica trophozoites present in the lumen must adhere to the underlying mucosa and penetrate the mucosal layer.
Liver involvement occurs following invasion by E histolytica into mesenteric venules. Amebae then enter the portal circulation and travel to the liver where they typically form one or more abscesses. The E histolytica galactose/N-acetyl-D-galactosamine (Gal/GalNAc) lectin is an adhesion protein complex that sustains tissue invasion.[1] The abscess contains acellular proteinaceous debris, which is thought to be a consequence of induced apoptosis[2] and is surrounded by a rim of amebic trophozoites invading the tissue.
The right lobe of the liver is more commonly affected than the left lobe. This has been attributed to the fact that the right lobe portal laminar blood flow is supplied predominantly by the superior mesenteric vein, whereas the left lobe portal blood flow is supplied by the splenic vein.
Amebic liver abscess is rare and is currently seen almost exclusively in immigrants or travelers to the United States. In 1994, 2,983 cases of amebiasis were reported to the Centers for Disease Control and Prevention (CDC). The disease was removed from the National Notifiable Diseases Surveillance System in 1995. An estimated 4% of patients with amebic colitis develop an amebic liver abscess.
An estimated 10% of the population is infected with Entamoeba dispar. Previously thought to be a nonpathogenic strain of E histolytica, this type of amoeba does not produce clinical symptoms even in the immunocompromised host.
Race-, sex-, and age-related demographics
All races can be affected by amebic liver abscess. Risk factors for infection include travel or residence in endemic areas.
Amebic liver abscess is marked by a 7-12–fold higher incidence in males than in females despite an equal sex distribution of noninvasive colonic amebic disease among adults.[3] However, no sexual preponderance exists among children.
Peak incidence of amebic liver abscess occurs in people in their third, fourth, and fifth decades of life, although it can occur in any age group.
International data
Worldwide, approximately 40-50 million people are infected annually, with the majority of infections occurring in developing countries. The prevalence of infection is higher than 5-10% in endemic areas[4] and sometimes as high as 55%.[5] The highest prevalence is found in developing countries in the tropics, particularly in Mexico, India, Central and South America, and tropical areas of Asia and Africa.
In most cases, rapid clinical improvement is observed in less than 1 week with antiamebic drug therapy alone. Radiological resolution lags behind the resolution of clinical symptoms. The average time to radiological resolution is approximately 12 months, with a range of 3 months to more than 10 years.
Death occurs in approximately 5% of persons having extraintestinal infection, including liver abscess. Rupture into the peritoneal cavity and the pericardium are responsible for most deaths.
Mortality/morbidity
Infection with E histolytica ranks second worldwide among parasitic causes of death, following malaria.
Annually, 40,000-100,000 deaths are caused by infection with E histolytica. Per year, a 10% risk of developing symptomatic invasive amebiasis exists after the acquisition of a pathogenic strain.[6]
Complications
Pleuropulmonary infection is the most common complication. Mechanisms of infection include development of a sympathetic serous effusion; rupture of a liver abscess into the chest cavity, leading to empyema; or a hematogenous spread, resulting in parenchymal infection.
Bronchopleural fistula may occur in rare instances when patients expectorate a substance that resembles anchovy paste. Trophozoites may be demonstrated in the fluid. Occasionally, this complication may be followed by a spontaneous cure of the amebic liver abscess.
Cardiac involvement results following the rupture of an abscess involving the left lobe of the liver. It usually is associated with very high mortality.
Intraperitoneal rupture occurs in 2-7% of patients. Left lobe abscesses are more likely to progress to rupture because of their later clinical presentation.
Bacterial superinfection can occur.
Rupture into peritoneal organs (eg, stomach) and mediastinum can occur.
Cases of hepatic artery pseudoaneurysm have been reported.
Direct patient and public education at sanitary measures; personal hygiene, including hand washing; and food hygiene.
Educate travelers to endemic areas about the precautions needed. These details are discussed below.
Control of amebiasis can be achieved by exercising proper sanitary measures and avoiding fecally contaminated food and water, including the following:
Regular examination of food handlers and thorough investigation of diarrheal episodes may identify the source of infection in some communities.
Vegetables must be cleaned with a strong detergent soap and soaked in acetic acid or vinegar for approximately 15 minutes to eradicate the cyst forms.
Boiling is the only effective means of eradicating the cysts in water.
Change in sexual practices to avoid fecal-oral contamination is of importance in the male homosexual population.
Travelers to areas with suboptimal sanitation and hygiene should eat only cooked foods or fruits peeled by themselves and should avoid drinking local water, including ice cubes frequently used for cocktails. Notably, many types of bottled water in developing countries are not properly disinfected.
No prophylactic vaccine currently is available for amebiasis, but efforts to better define antigenic candidates and wider use of animal models are encouraging.[7, 8] Note the following:
A serine-rich E histolytica protein (SREHP) has been expressed in avirulent vaccine strains of Salmonella species.
E histolytica galactose/N -acetyl-D-galactosamine (Gal/GalNAc)[9] and synthetic enhanced intranasal lectin-based amebiasis subunits[10] have been extensively studied as attractive candidates for vaccine development.
Gal-inhibitable lectin shows promise in animal studies.[11]
The signs and symptoms of amebic liver abscess often are nonspecific, resembling those of pyogenic liver abscess or other febrile diseases.[12, 13, 14, 15]
Time of onset
Patients with amebic liver abscess usually present acutely (duration of symptoms < 14 d), with the most frequent complaints being fever and abdominal pain. This presentation is characteristic of younger patients.
The subacute presentation is characterized by weight loss and, in less than half the cases, abdominal pain and fever are present.
Abdominal pain
Abdominal pain is the most common element in the history and is present in 90-93% of patients. The pain is usually constant, dull, and aching, and it is most frequently located in the right upper quadrant (54-67%) and may radiate to the right shoulder or scapular area.
The pain increases with coughing, walking, and deep breathing, as well as when patients rest on their right side.
Constitutional symptoms
Fever is present in 87-100% of cases, and rigors are present in 36-69% of cases.
Nausea and vomiting are present in 32-85% of cases, and weight loss is present in 33-64% of cases.
Diarrhea
Diarrhea is present in less than one third of patients at the time of diagnosis. Some patients describe a history of having had dysentery within the previous few months. Bloody diarrhea is present in 7% of cases.
Pulmonary symptoms
Pulmonary symptoms are present in 18-26% of cases. The most frequent symptoms are cough and chest pain, which may represent a sign of secondary pulmonary involvement by abscess rupture in the pleural cavity.
When coughing produces an odorless brown substance similar to anchovy paste, a bronchopleural fistula has developed.[16]
Recent travel to endemic areas
Onset of symptoms usually occurs within 8-12 weeks from the date of travel. In 95% of cases, onset occurs within 5 months of returning from travel to an endemic area. A remote travel history of as many as 12 years has been reported.
Fever is the most common sign and is found in as many as 99% of cases.
Hepatomegaly is present in some cases. The frequency varies widely in different series published, reporting as high as 63% in one series and as low as 18% in another.
Hepatomegaly with pain upon palpation is one of the most important signs of amebic liver abscess. Point tenderness over the liver, below the ribs, or in the intercostal spaces is a typical finding.
Right upper abdominal quadrant tenderness is present in 55-75% of cases. When the abscess is located in the left lobe (28% of cases), epigastric tenderness is noted.
Pulmonary abnormalities are present in 20-45% of cases, and they consist of dullness on percussion, rales at the right lung base, and nonproductive cough. Breath sounds over the right lung base may be diminished. Pleural rub may be audible.
Jaundice (< 10% of cases) most often occurs in complicated cases with multiple abscesses or a large abscess compressing the biliary tract.
Signs of complications include the following:
Signs of peritoneal irritation, such as rebound tenderness, guarding, and absence of bowel sounds, are present when the abscess ruptures into the peritoneal cavity. Peritonitis occurs in 2-7% of cases.
Pericardial friction rub can be audible when the abscess extends into the pericardium. This sign is associated with a very high mortality.
Signs of pleural effusion are present when the abscess ruptures into the pleural cavity.
Approximately three fourths of patients with an amebic liver abscess have leukocytosis. This most likely will appear if symptoms are acute or complications have developed. However, eosinophilia is rare.
Anemia may be present, but the cause usually is multifactorial.
Chemistry
Hyperbilirubinemia is present in only a small proportion of cases.
In acute liver abscess, the aspartate aminotransferase (AST) levels are high. In chronic liver abscess, the alkaline phosphatase level tends to be elevated and the AST level tends to be within the normal limits. Overall, the alkaline phosphatase level is elevated in about 70% of cases of amebic liver abscess.
Similar complete blood cell (CBC) count and liver test abnormalities are found in patients with pyogenic liver abscesses and are not specific.
Stool Studies
Stool examination
The role of microscopic stool examination is limited. Less than 30-40% of patients with amebic liver abscess have concomitant intestinal amebiasis, and 10% of the population is infected with the nonpathogenic strain of E dispar. Hence, the microscopic examination of the stool for the identification of cysts is of little value. If positive, it may suggest the diagnosis.
Fecal findings suggestive of amebic colitis include a positive test for heme, a paucity of neutrophils, and the presence of Charcot-Leyden crystal protein. The stool examination is still of value if the serologic and antigen identification tests are not available.
Examination of the stool for hematophagous trophozoites of E histolytica must be made on at least three fresh specimens because the trophozoites are very sensitive and may be excreted intermittently. A combination of wet mount, iodine-stained concentrates, and trichrome-stained preparations is used.
Upon examination of the stool, trophozoites may be confused with neutrophils. Cysts must be differentiated morphologically from nonpathogenic Entamoeba hartmanni, Entamoeba coli, and Endolimax nana. Nonpathogenic E dispar cannot be differentiated morphologically and requires fecal antigen detection.
Stool antigen detection
Stool antigen detection facilitates early diagnosis before an antibody response occurs (< 7 d) and differentiates pathogenic from nonpathogenic Entamoeba infection. The primary drawbacks are the requirement for fresh, unpreserved stool specimens[17] and the lack of intestinal amebiasis in as many as 60% of patients with amebic liver abscess.
Stool antigen detection kits based on enzyme immunoassay (EIA) are most common and still quite sensitive compared to polymerase chain reaction (PCR)-based methods.[18]
The PCR stool test shows high sensitivity for detecting E histolytica and for distinguishing nonpathogenic amoebas.[19, 20, 21] However, this test is expensive. Real-time (rapid) PCR is sensitive but not well standardized[22] and is not widely available.
Stool culture
Stool culture for amoeba is sensitive but has limited availability.
Serologic testing
Serologic testing is the most widely used method of diagnosis for amebic liver abscess. In general, the test result should be positive, even in cases when the result of the stool test is negative (only extraintestinal disease).[23]
EIA
EIA has now largely replaced indirect hemagglutination (IHA) testing and counter immunoelectrophoresis (CIE) testing. EIA is relatively simple and easy to perform, rapid, inexpensive, and more sensitive.[24, 25]
The EIA test detects antibodies specific for E histolytica in approximately 95% of patients with extraintestinal amebiasis, in 70% of patients with active intestinal infection, and in 10% of persons who are asymptomatic cyst passers.
The EIA serology findings revert to negative in 6-12 months following eradication of infection. Even in highly endemic areas, fewer than 10% of patients who are asymptomatic have positive amebic serology findings.
Initial negative test results may appear in as many as 10% of patients with amebic liver abscess. Under these circumstances, order repeat serology testing in 1 week. This test result will usually be positive.
Serum antigen detection
E histolytica galactose lectin antigen is detectable by enzyme-linked immunosorbent assay (ELISA) in at least 75% of serum samples obtained from patients with amebic liver abscess. Studies reported an antigen seropositivity of 96% with a reversal rate of 82% after 1 week of treatment with metronidazole. This test may be useful for patients who present acutely, before an antibody response occurs. The sample needs to be obtained before starting the treatment, as the treatment leads to rapid antigen loss. This test can be used for rapid diagnosis in highly endemic areas, where serology can be misleading, but it is not widely available.[17]
Rapid antigen and antibody tests are currently being evaluated and seem very promising.[26]
None of the imaging tests can definitively differentiate between a pyogenic liver abscess, an amebic abscess, and malignant disease. Clinical, epidemiologic, and serologic correlation is needed for diagnosis.
Ultrasonography
Ultrasonography is the preferable initial diagnostic test. It is rapid, inexpensive, and is only slightly less sensitive than computed tomography (CT) scanning (75-80% sensitivity vs 88-95% for CT scan).
Ultrasonography simultaneously evaluates the gallbladder and avoids radiation exposure.
As opposed to scanning with technetium-99m, ultrasonography often can distinguish an abscess from a tumor or other solid focal lesion. The lesions tend to be round or oval, with well-defined margins, and are hypoechoic.
CT scanning
CT scanning is sensitive but the findings are not specific. The abscess typically appears low density with smooth margins and a contrast-enhancing peripheral rim.
The use of injected contrast may differentiate hepatic abscesses from vascular tumors. See the images below.
View Image
CT scan of the abdomen with IV and oral contrast is shown. Note the thick-walled cavity with low attenuation center and contrast-enhanced periphery.
View Image
CT scan of the abdomen with contrast showing a large amebic abscess with multiloculated appearance and atypical left liver lobe location. CT scan cann....
Magnetic resonance imaging (MRI)
MRI is sensitive, but the findings are not specific. This imaging modality provides information comparable with less expensive imaging procedures.
Nuclear imaging studies
Technetium-99m liver scanning is useful for differentiating an amebic liver abscess from a pyogenic abscess; however, it is not used as a first-line test.
Because amebic liver abscesses do not contain leukocytes, they appear as cold lesions on hepatic nuclear scanning, with a typical hot halo or a rim of radioactivity surrounding the abscess. In contrast, pyogenic liver abscesses contain leukocytes and, therefore, typically appear as hot lesions on nuclear scanning.
Gallium scanning is helpful in differentiating a pyogenic abscess (similar to technetium-99m nuclear hepatic scanning) but requires delayed images, which makes the test less helpful.
Other imaging studies
Hepatic angiography is only useful to differentiate liver abscesses from vascular lesions.
Plain chest or abdominal films may show elevation and limitation of motion of the right diaphragm, basilar atelectasis, and right pleural effusion or gas within the abscess cavity.
Aspiration of the abscess content is indicated only if rupture of the abscess is thought to be imminent, differentiation between amebic abscess and pyogenic abscess is critical, or there is no response to antiprotozoal therapy in 5-7 days (see Surgical Care).[27] Note the following:
Aspiration may be performed under computed tomography (CT) scan or sonographic guidance.
Send the collected specimen for Gram stain and cultures.
Amebae rarely are recovered from the aspirate (15%) and, often, they are present only in the peripheral parts of the abscess, invading and destroying adjacent tissue.
Amebic liver abscesses only rarely yield positive bacterial cultures following secondary bacterial infection of the abscess cavity.
Detecting E histolytica antigen in the aspirate is possible and is accomplished as previously described for stool specimens. It is highly specific. The sensitivity was only 20% using enzyme-linked immunosorbent assay (ELISA), but newer polymerase chain reaction (PCR)-based assays have a sensitivity of 83% and a specificity of 100%.[28, 29] However, currently, PCR-based detection is not widely available.
Many possible complications are associated with aspiration of the abscess, of which the most common are infection and bleeding. Other complications include amebic peritonitis or inadvertent puncture of an echinococcal cyst.
The liver involvement in amebiasis consists of necrotic abscesses and periportal inflammation. The abscess contains acellular proteinaceous debris and is surrounded by a rim of amebic trophozoites invading tissue. The abscess contains a chocolate-colored fluid that resembles anchovy paste and consists predominantly of necrotic hepatocytes. Triangular areas of hepatic necrosis, possibly due to ischemia from amebic obstruction of the portal vessels, have been observed. E histolytica can also induce hepatocyte and neutrophilic apoptosis. Some authors postulate that amebic liver abscess probably results from the coalescence of small microabscesses. Periportal fibrosis may be present, but whether this represents prior trophozoite invasion or a host reaction to amebic antigens or toxins is not known.
Most uncomplicated amebic liver abscesses can be treated successfully with conservative management,[30] such as with amebicidal drug therapy alone. Use tissue amebicides to eradicate the invasive trophozoite forms in the liver. After completion of treatment with tissue amebicides, administer luminal amebicides for eradication of the asymptomatic colonization state. Failure to use luminal agents can lead to relapse of infection in approximately 10% of patients.
In general, metronidazole, tinidazole, emetine, and dehydroemetine are active in invaded tissues; chloroquine is active only in the liver; tetracycline acts on the bowel wall; and diloxanide furoate, paromomycin, and iodoquinol are luminal agents only. The details on tissue and luminal amebicidal agents are discussed in Medication.
Metronidazole
Metronidazole remains the drug of choice for amebic liver abscess. Metronidazole enters the protozoa by passive diffusion and is converted to reactive cytotoxic nitroradicals by reduced ferredoxin or flavodoxin. Tinidazole, another nitroimidazole closely related to metronidazole, was approved for the treatment of amebic liver abscess and invasive amebiasis. Tinidazole is well tolerated by patients. Tinidazole may be administered once daily and appears to be at least as effective as metronidazole, with a clinical cure rate of more than 90%.
Metronidazole, 750 mg 3 times a day orally for 10 days, was reported to be curative in 90% of patients with amebic liver abscess. The drug also is available for intravenous administration for those patients who are unable to take the medication by the oral route.
Resolution of symptoms is fairly rapid and is observed within 3 days in most patients in the United States. In endemic areas outside the United States, it takes relatively longer to resolve the symptoms because the abscesses are quite large or multiple by the time patients seek medical attention.
In vivo E histolytica resistance to metronidazole has not been reported. Nevertheless, in vitro studies have shown an association between metronidazole resistance and decreased expression of ferredoxin 1 and flavodoxin and increased expression of iron-containing superoxide dismutase and peroxiredoxin in E histolytica.
Usual adverse effects of metronidazole include nausea, headache, and metallic taste. Abdominal cramps, vomiting, diarrhea, and dizziness also may occur. Dark urine caused by a metabolite of the drug may be observed.
Other items to consider
Other considerations include the following:
No randomized controlled trials exist that demonstrate the benefits of combination therapy over monotherapy.
Outside the United States, other closely related amebicidal agents, such as secnidazole or ornidazole, can be substituted in appropriate dosages. These drugs are not available in the United States.
Chloroquine phosphate may be substituted or added in the event of failure of resolution of clinical symptoms with metronidazole or another nitroimidazole within 5 days, or intolerance to metronidazole or a nitroimidazole. Chloroquine has the disadvantage of being associated with higher relapse rates than nitroimidazoles. Adverse effects include gastrointestinal upset, headache, dizziness, and blurred vision. Retinopathy does not occur at the dose used for amebic liver abscess.
Emetine or dehydroemetine has a direct lethal action on the trophozoites of E histolytica. These agents are very toxic and, therefore, should be used only as a second-line therapy. Their toxicity includes cardiac arrhythmias, precordial pain, muscle weakness, vomiting, and diarrhea. Dehydroemetine is less toxic than emetine.
Administer a luminal amebicidal agent to eradicate the intestinal carriage after the amebic liver abscess has been treated with one of the tissue amebicides noted below. Failure to use luminal agents can lead to relapse of infection in approximately 10% of patients. Luminal agents with proven efficacy include diloxanide furoate, iodoquinol, and paromomycin. Note the following:
Diloxanide furoate is free of major adverse effects. The most common adverse effect is flatulence and occasional gastrointestinal upset.
Iodoquinol (diiodohydroxyquin) rarely causes abdominal pain, diarrhea, or rash. A structurally related diiodohydroxyquin caused subacute myelopticoneuropathy and is obsolete now.
Although paromomycin may occasionally cause nausea, abdominal cramps, or diarrhea, it is the preferred luminal amebicidal.
The details on the luminal amebicides are discussed in Medication.
Consultations
Consult with an interventional radiologist for imaging-guided aspiration of the abscess.
Consult with a general surgeon for open surgical drainage of the abscess under rare circumstances (see Surgical Care).
Diet and activity
No specific diet change or modification is required. However, discuss food hygiene with patients because amebiasis is associated with suboptimal personal or food hygiene (see Patient Education).
No restriction of activity is needed, except during the first few days of acute illness with pain.
If emetine or dehydroemetine is used, the patient should remain sedentary for approximately 4 weeks after completing therapy because of their toxicity.
Consider therapeutic aspiration of amebic liver abscess in the following situations: (1) high risk of abscess rupture, as defined by cavity size greater than 5 cm; (2) left lobe liver abscess, which is associated with higher mortality and frequency of peritoneal leak or rupture into the pericardium; (3) failure to observe a clinical medical response to therapy within 5-7 days; and (4) cannot differentiate from a pyogenic liver abscess.
The following are predictive of the need for aspiration: (1) age older than 55 years, (2) abscess greater than 5 cm in diameter,[31] and (3) failure of medical therapy after 7 days.[32] In endemic areas, because of the late presentation and the existence of multiple abscesses, as many as 50% of patients may require aspiration.[33] However, routine needle aspiration offers only minimal benefit over medical care alone for uncomplicated amebic liver abscess and, unless one of the above indications exists, should be avoided.[34] Prompt medical care decreases the need for aspiration.[35]
Imaging-guided needle aspiration and catheter drainage are the procedures of choice. Generally, surgical drainage is not necessary and should be avoided; however, consider open surgical drainage when the abscess is inaccessible to needle drainage or a response to therapy has not occurred in 5-7 days.
Simple needle aspiration is less invasive, is less expensive, and has the advantage of being able to drain multiple abscesses in the same session. Simple needle aspiration avoids problems related to catheter care (see Procedures).
Although catheter drainage may be more effective than needle aspiration, in a study by Rajak et al,[36] the average time for clinical improvement, mean hospital stay, and time to resolution were similar among the patients who were successfully treated in the two treatment groups.
Follow-up ultrasonography or computed tomography scanning is unnecessary after resolution of symptoms and signs because the radiological resolution may take several months to years. See Prognosis.
Luminal amebicides fail to eradicate the luminal forms of E histolytica in approximately 10-15% of patients treated with these agents; therefore, a follow-up stool examination is recommended after completion of therapy. A second course of a luminal amebicide is required in a few weeks if the first course fails to eradicate the intestinal carriage.
Clinical Context:
Oral synthetic antiprotozoal and antibacterial agent. Effectively eradicates amebic tissue infections, including liver abscess, but is only partially effective against luminal forms. Luminal amebicide also must be used to eradicate bowel luminal infection. Only effective against trophozoites and not cyst forms.
Clinical Context:
Nitroimidazole derivative used for susceptible protozoal infections. Eradicates amebic tissue infections, including liver abscess, but it is only partially effective against luminal forms. Luminal amebicide must also be used to eradicate bowel luminal infection. Only effective against trophozoites and not cyst forms.
Clinical Context:
Preferred agent because it is less toxic than emetine. 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 US only from the Parasitic Disease Drug Service, Centers for Disease Control and Prevention (Atlanta, GA 30333; telephone: 404-639-3356).
Clinical Context:
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. Not available in US.
Clinical Context:
Diiodohydroxyquin. Amebicidal against E histolytica and is considered effective against trophozoite and cyst forms. Used to eradicate concurrent intestinal amebiasis in order to prevent recurrence of hepatic amebiasis.
Clinical Context:
Dichloroacetamide derivative. Amebicidal against trophozoite and cyst forms of E histolytica. Available in US only from the Parasitic Disease Drug Service, Centers for Disease Control and Prevention (Atlanta, GA 30333; telephone: 404-639-3356).
Clinical Context:
Amebicidal and antibacterial aminoglycoside active in intestinal amebiasis. Not significantly absorbed from GI tract. Amebicidal against luminal forms.
Clinical Context:
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 the 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 the dose and duration used for the treatment of hepatic amebiasis.
Daniel Matei Brailita, MD, Infectious Disease Specialist, Mary Lanning Healthcare and Central Nebraska Infectious Diseases
Disclosure: Nothing to disclose.
Coauthor(s)
Ambrish Ojha, MBBS,
Disclosure: Nothing to disclose.
Ildiko Lingvay, MD, MPH, MSc, Assistant Professor, Department of Internal Medicine, Division of Endocrinology, Diabetes, and Metabolism, University of Texas Southwestern Medical Center at Dallas
Disclosure: Received consulting fee from GI Dynamics for consulting; Received honoraria from NovoNordisk, Inc for board membership.
KoKo Aung, MD, MPH, FACP, Professor of Internal Medicine and Associate Academic Dean, Vice President, Texas Tech University Health Sciences Center at El Paso, Paul L Foster School of Medicine
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Chief Editor
BS Anand, MD, Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine
Disclosure: Nothing to disclose.
Additional Contributors
Robert J Fingerote, MD, MSc, FRCPC, Consultant, Clinical Evaluation Division, Biologic and Gene Therapies, Directorate Health Canada; Consulting Staff, Department of Medicine, Division of Gastroenterology, York Central Hospital, Ontario
Disclosure: Nothing to disclose.
Acknowledgements
Harvey Kantor, MD Chief, Professor, Department of Internal Medicine, Division of Infectious Diseases, Texas Tech University Health Science Center
Harvey Kantor, MD is a member of the following medical societies: American College of Physicians, American Medical Association, American Society for Microbiology, Illinois State Medical Society, Infectious Diseases Society of America, New York Academy of Sciences, Royal Society of Medicine, and Sigma Xi
Ravdin JI, Stauffer W. Entamoeba histolytica (amebiasis). Mandell Gl, Bennett J, Dolin R, eds. Principles and Practice of Infectious Diseases. 6th ed. Philadelphia, PA: Elsevier; 2005. Vol 2: Part III, sect H, 3097-4111.
CT scan of the abdomen with IV and oral contrast is shown. Note the thick-walled cavity with low attenuation center and contrast-enhanced periphery.
CT scan of the abdomen with contrast showing a large amebic abscess with multiloculated appearance and atypical left liver lobe location. CT scan cannot differentiate amebic liver abscess from pyogenic liver abscess.
CT scan of the abdomen with IV and oral contrast is shown. Note the thick-walled cavity with low attenuation center and contrast-enhanced periphery.
CT scan of the abdomen with contrast showing a large amebic abscess with multiloculated appearance and atypical left liver lobe location. CT scan cannot differentiate amebic liver abscess from pyogenic liver abscess.
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