- Author: Vinod K Dhawan, MD, FACP, FRCPC, FIDSA; Chief Editor: Michael Stuart Bronze, MD more...
Laboratory diagnosis of amebiasis is made by demonstrating the organism or by employing immunologic techniques.[48, 49, 50, 51, 52]
Findings from basic blood tests may include the following:
Leukocytosis without eosinophilia (80% of patients)
Elevated alkaline phosphatase level (80%)
Elevated transaminase levels
Mildly elevated bilirubin level
Reduced albumin level
Elevated erythrocyte sedimentation rate (ESR)
Other laboratory studies employed for diagnosis include microscopy, culture, serologic testing, and polymerase chain reaction (PCR) assay.
Microscopic examination of fresh stool smears for trophozoites that contain ingested red blood cells (RBCs) is commonly done (see the image below). The presence of intracytoplasmic RBCs in trophozoites is diagnostic of E histolytica infection, though some studies have demonstrated the same phenomenon with E dispar.
Examination of a single stool sample has a sensitivity of only 33-50%; however, examination of 3 stool samples over no more than 10 days can improve the detection rate to 85-95%. It should be kept in mind that routine microscopy cannot be relied on to distinguish the pathogenic E histolytica from the nonpathogenic E dispar and E moshkovskii.
Stool leukocytes may be found, but in fewer numbers than in shigellosis.
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.
The World Health Organization (WHO) recommends that intestinal amebiasis be diagnosed with an E histolytica -specific test, thus rendering the classic ova-and-parasite stool examination obsolete.
Cultures can be performed either with fecal or rectal biopsy specimens or with liver abscess aspirates. Culture has a success rate of 50-70%, but it is technically difficult. Overall, culture is less sensitive than microscopy.
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. Axenic cultivation, first achieved in 1961, involves growing 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.
Enzyme-linked immunosorbent assay (ELISA) is used to detect antigens from E histolytica in stool samples. Several kits are commercially available.
Antigen-based ELISA kits using monoclonal antibodies against the galactose/N -acetylgalactosamine (GAL/GalNAc)–specific lectin of E histolytica (E histolytica II, TechLab, Blacksburg, VA) yield an overall sensitivity of 71-100% and a specificity of 93-100%. One study showed a much lower sensitivity (14.2%). In patients with amebic liver abscess, serum and liver aspirate antigen detection using the same kit was shown to yield a sensitivity of 96% in serum and 100% in liver aspirate.
Other stool detection kits use monoclonal antibodies against the serine-rich antigen of E histolytica (Optimum S; Merlin Diagnostika, Bornheim-Hersel, Germany) or against other specific antigens (Entamoeba CELISA-PATH, Cellabs, Brookvale, Australia; ProSpecT EIA, Remle Inc, Lenexa, KY).
No specific antigen tests are available for the detection of E dispar and E moshkovskii from clinical samples.
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 1 week. Serologic examination should be repeated 1 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.
ELISA, the assay most commonly used worldwide, measures the presence of serum antilectin antibodies (immunoglobulin G [IgG]). 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 antiamebic antibody response occurs. The sensitivity of ELISA for detection of antibodies to E histolytica in patients with amebic liver abscess is 97.9%, and its specificity is 94.8%. False-negative results can occur within the first 7-10 days after infection.
Immunofluorescent assay (IFA) is also rapid, reliable, and reproducible. In the setting of amebic liver abscess, the sensitivity and specificity of IFA were shown to be 93.6% and 96.7%, respectively.
Indirect hemagglutination assay (IHA) 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 very specific (99.1%), but it is less sensitive than ELISA. It is not useful in differentiating acute infection from previous infection, because high titers may persist for years after successful treatment. False-positive reactions at titers higher than 1:256 are rare. ELISA has replaced IHA in most laboratories.
Immunoelectrophoresis, counterimmunoelectrophoresis (CIE), and immunodiffusion (ID) use the precipitation property of antigen-antibody complexes in agar. CIE is time-consuming but has a sensitivity of 100% in invasive amebiasis. ID is simple to perform and thus ideal for laboratories that only rarely perform amebic serology; however, it requires a minimum of 24 hours, compared with 2 hours for IHA or ELISA. ID is slightly less sensitive than IHA and ELISA but is equally specific. Complement fixation (CF) is less sensitive than other techniques.
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%.
Polymerase chain reaction assay
A wide variety of PCR-based methods targeting different genes, including a small-subunit rRNA gene (18S rDNA), a 30-kd antigen gene, a serine-rich protein gene, a chitinase gene, a hemolysin gene, and extrachromosomal circular DNA, have been described for the detection and differentiation of E histolytica, E dispar, and E moshkovskii.
Sensitivities can vary according to sampling and the specific target gene used. Field studies that directly compared PCR with stool culture or antigen-detection tests for the diagnosis of E histolytica infection found these methods to be comparably effective. PCR assay can also be used for detection of E histolytica in liver aspirates for the diagnosis of amoebic liver abscess.
PCR-based tests have been strongly endorsed by the WHO. However, application of PCR-based methods in routine diagnosis is still very limited[55, 56, 57] ; the generation of nonspecific DNA fragments from environmental and clinical samples often leads to false-positive results.
Loop-mediated isothermal amplification assay
The loop-mediated isothermal amplification (LAMP) assay has been applied to the detection of E histolytica in cases of hepatic amebiasis. A study that compared this test with PCR testing in 50 patients with clinical suspicion of amebic liver abscess found that LAMP assay detected 5 additional abscesses that were missed by PCR assay. The rapidity, operational simplicity, high specificity and sensitivity, and high yield of LAMP assay suggest that it may prove to be a better diagnostic tool than PCR assay for diagnosis of hepatic amebiasis.
Radiography, Ultrasonography, CT, and MRI
Chest radiography may reveal an elevated right hemidiaphragm and a right-side pleural effusion in patients with amebic liver abscess.
Both ultrasonography and CT scanning are sensitive but nonspecific for amebic liver abscess. Ultrasonography is preferred for the evaluation of amebic liver abscess because of its low cost, rapidity, and lack of adverse effects. CT may be slightly more sensitive than ultrasonography. In cerebral amebiasis, CT shows irregular lesions without a surrounding capsule or enhancement.
On ultrasonograms, amebic liver abscesses usually appear as a solitary homogenous hypoechoic round lesion in the posterosuperior aspect of the right lobe of the liver (70-80% of cases), though 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.
On CT scans with intravenous (IV) 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.
Magnetic resonance imaging (MRI) reveals high signal intensity on T2-weighted images. Perilesional edema and enhancement of rim are noted after injection of gadolinium (86% of cases).
Complete resolution of liver abscess may take as long as 2 years. Repeat imaging is not indicated if the patient is otherwise doing well.
Ultrasound- or CT-guided needle aspiration of the liver should be performed when a diagnosis must be established very rapidly; pyogenic liver abscess can present and appear in similarly to amebic liver abscess.
Liver abscess aspirate is usually an odorless thick yellow-brown liquid classically referred to as “anchovy paste.” This liquid lacks white blood cells (WBCs) as a result of lysis by the parasite. Amebae are visualized in the abscess fluid in a minority of patients with amebic liver abscess (see the image below). Liver aspiration is indicated only if abscesses are large (> 12 cm), abscess rupture is imminent, medical therapy has failed, or abscesses are present in the left lobe.
The 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.
Lower GI Endoscopy
Rectosigmoidoscopy and colonoscopy with biopsy or scraping at the margin of a colonic mucosal ulcer provide valuable materials for diagnostic information in intestinal amebiasis. Tissue can be sent for microscopic evaluation, culture, and PCR assay, where available.
Indications for endoscopy in suspected intestinal amebiasis include the following:
Stool examination findings are negative, but 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
Fulminant colitis is a relative contraindication to colonoscopy, because it increases the risk of intestinal perforation.
On endoscopic examination, small mucosal ulcers covered with yellowish exudates are observed. The mucosal lining between the ulcers appears normal. The mucosa resembles that seen in inflammatory bowel disease (IBD). Biopsy results and a scraping of ulcer edge may reveal trophozoites. Ameboma (a carcinomalike annular lesion) can also be seen, usually in the cecum and ascending colon.[4, 59]
Rectosigmoidoscopy and colonoscopy should be considered before steroids are used in patients with suspected IBD. In a multivariate analysis, the best combination of findings for predicting amebic colitis was the combination of cecal lesions, multiple lesions, and exudates.
The intestinal biopsy specimen should be taken from the edge of ulcers and evaluated for motile trophozoites.
Histopathologic findings may include nonspecific mucosal thickening, multiple discrete ulcers separated by regions of normal-appearing colonic mucosa, diffusely inflamed and edematous mucosa, necrosis, or wall perforation (see the image below).
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 (see the images below).
Different chemical stains can be used (see the image below), including periodic acid−Schiff stain, which makes E histolytica appear magenta in color.
Pritt BS, Clark CG. Amebiasis. Mayo Clin Proc. 2008 Oct. 83(10):1154-9; quiz 1159-60. [Medline].
Grecu F, Bulgariu T, Blanaru O, Dragomir C, Lunca C, Stratan I, et al. Invasive amebiasis. Chirurgia (Bucur). 2006 Sep-Oct. 101(5):539-42. [Medline].
Haque R, Huston CD, Hughes M, Houpt E, Petri WA Jr. Amebiasis. N Engl J Med. 2003 Apr 17. 348(16):1565-73. [Medline].
Stanley SL Jr. Amoebiasis. Lancet. 2003 Mar 22. 361(9362):1025-34. [Medline].
Ravdin JI, Stanley P, Murphy CF, Petri WA Jr. Characterization of cell surface carbohydrate receptors for Entamoeba histolytica adherence lectin. Infect Immun. 1989 Jul. 57(7):2179-86. [Medline]. [Full Text].
Haque R, Mondal D, Duggal P, Kabir M, Roy S, Farr BM, et al. Entamoeba histolytica infection in children and protection from subsequent amebiasis. Infect Immun. 2006 Feb. 74(2):904-9. [Medline]. [Full Text].
Seydel KB, Stanley SL Jr. Entamoeba histolytica induces host cell death in amebic liver abscess by a non-Fas-dependent, non-tumor necrosis factor alpha-dependent pathway of apoptosis. Infect Immun. 1998 Jun. 66(6):2980-3. [Medline]. [Full Text].
Kelsall BL, Ravdin JI. Degradation of human IgA by Entamoeba histolytica. J Infect Dis. 1993 Nov. 168(5):1319-22. [Medline].
Reed SL, Keene WE, McKerrow JH, Gigli I. Cleavage of C3 by a neutral cysteine proteinase of Entamoeba histolytica. J Immunol. 1989 Jul 1. 143(1):189-95. [Medline].
Abhyankar MM, Shrimal S, Gilchrist CA, Bhattacharya A, Petri WA Jr. The Entamoeba histolytica serum-inducible transmembrane kinase EhTMKB1-9 is involved in intestinal amebiasis. Int J Parasitol Drugs Drug Resist. 2012 Dec. 2:243-248. [Medline]. [Full Text].
Seydel KB, Li E, Swanson PE, Stanley SL Jr. Human intestinal epithelial cells produce proinflammatory cytokines in response to infection in a SCID mouse-human intestinal xenograft model of amebiasis. Infect Immun. 1997 May. 65(5):1631-9. [Medline]. [Full Text].
Braga LL, Ninomiya H, McCoy JJ, Eacker S, Wiedmer T, Pham C, et al. Inhibition of the complement membrane attack complex by the galactose-specific adhesion of Entamoeba histolytica. J Clin Invest. 1992 Sep. 90(3):1131-7. [Medline]. [Full Text].
Fotedar R, Stark D, Beebe N, Marriott D, Ellis J, Harkness J. Laboratory diagnostic techniques for Entamoeba species. Clin Microbiol Rev. 2007 Jul. 20(3):511-32, table of contents. [Medline]. [Full Text].
Freedman DO, Weld LH, Kozarsky PE, Fisk T, Robins R, von Sonnenburg F, et al. Spectrum of disease and relation to place of exposure among ill returned travelers. N Engl J Med. 2006 Jan 12. 354(2):119-30. [Medline].
Valenzuela O, Morán P, Gómez A, Cordova K, Corrales N, Cardoza J, et al. Epidemiology of amoebic liver abscess in Mexico: the case of Sonora. Ann Trop Med Parasitol. 2007 Sep. 101(6):533-8. [Medline].
van Hal SJ, Stark DJ, Fotedar R, Marriott D, Ellis JT, Harkness JL. Amoebiasis: current status in Australia. Med J Aust. 2007 Apr 16. 186(8):412-6. [Medline].
Ximénez C, Morán P, Rojas L, Valadez A, Gómez A. Reassessment of the epidemiology of amebiasis: state of the art. Infect Genet Evol. 2009 Dec. 9(6):1023-32. [Medline].
Stauffer W, Abd-Alla M, Ravdin JI. Prevalence and incidence of Entamoeba histolytica infection in South Africa and Egypt. Arch Med Res. 2006 Feb. 37(2):266-9. [Medline].
Tengku SA, Norhayati M. Public health and clinical importance of amoebiasis in Malaysia: a review. Trop Biomed. 2011 Aug. 28(2):194-222. [Medline].
Caballero-Salcedo A, Viveros-Rogel M, Salvatierra B, Tapia-Conyer R, Sepulveda-Amor J, Gutierrez G, et al. Seroepidemiology of amebiasis in Mexico. Am J Trop Med Hyg. 1994 Apr. 50(4):412-9. [Medline].
Blessmann J, Van Linh P, Nu PA, Thi HD, Muller-Myhsok B, Buss H, et al. Epidemiology of amebiasis in a region of high incidence of amebic liver abscess in central Vietnam. Am J Trop Med Hyg. 2002 May. 66(5):578-83. [Medline].
Bowley DM, Loveland J, Omar T, Pitcher GJ. Human immunodeficiency virus infection and amebiasis. Pediatr Infect Dis J. 2006 Dec. 25(12):1192-3. [Medline].
Brindicci G, Picciarelli C, Fumarola L, Carbonara S, Stano F, Ciracì E, et al. Amoebic hepatic abscesses in an HIV-positive patient. AIDS Patient Care STDS. 2006 Sep. 20(9):606-11. [Medline].
Chen Y, Zhang Y, Yang B, Qi T, Lu H, Cheng X, et al. Seroprevalence of Entamoeba histolytica infection in HIV-infected patients in China. Am J Trop Med Hyg. 2007 Nov. 77(5):825-8. [Medline]. [Full Text].
Hsu MS, Hsieh SM, Chen MY, Hung CC, Chang SC. Association between amebic liver abscess and human immunodeficiency virus infection in Taiwanese subjects. BMC Infect Dis. 2008 Apr 16. 8:48. [Medline]. [Full Text].
Karp CL, Auwaerter PG. Coinfection with HIV and tropical infectious diseases. I. Protozoal pathogens. Clin Infect Dis. 2007 Nov 1. 45(9):1208-13. [Medline].
Infection by human immunodeficiency virus-1 is not a risk factor for amebiasis. Am J Trop Med Hyg. 2006 Nov. 75(5):1023. [Medline].
Hung CC, Ji DD, Sun HY, Lee YT, Hsu SY, Chang SY, et al. Increased risk for Entamoeba histolytica infection and invasive amebiasis in HIV seropositive men who have sex with men in Taiwan. PLoS Negl Trop Dis. 2008 Feb 27. 2(2):e175. [Medline]. [Full Text].
Muzaffar J, Madan K, Sharma MP, Kar P. Randomized, single-blind, placebo-controlled multicenter trial to compare the efficacy and safety of metronidazole and satranidazole in patients with amebic liver abscess. Dig Dis Sci. 2006 Dec. 51(12):2270-3. [Medline].
Hung CC, Wu PY, Chang SY, Ji DD, Sun HY, Liu WC, et al. Amebiasis among persons who sought voluntary counseling and testing for human immunodeficiency virus infection: a case-control study. Am J Trop Med Hyg. 2011 Jan. 84(1):65-9. [Medline]. [Full Text].
Acuna-Soto R, Maguire JH, Wirth DF. Gender distribution in asymptomatic and invasive amebiasis. Am J Gastroenterol. 2000 May. 95(5):1277-83. [Medline].
Nagata N, Shimbo T, Akiyama J, Nakashima R, Nishimura S, Yada T. Risk factors for intestinal invasive amebiasis in Japan, 2003-2009. Emerg Infect Dis. 2012 May. 18(5):717-24. [Medline].
Aristizábal H, Acevedo J, Botero M. Fulminant amebic colitis. World J Surg. 1991 Mar-Apr. 15(2):216-21. [Medline].
Andrade JE, Mederos R, Rivero H, Sendzischew MA, Soaita M, Robinson MJ, et al. Amebiasis presenting as acute appendicitis. South Med J. 2007 Nov. 100(11):1140-2. [Medline].
Hardin RE, Ferzli GS, Zenilman ME, Gadangi PK, Bowne WB. Invasive amebiasis and ameboma formation presenting as a rectal mass: An uncommon case of malignant masquerade at a western medical center. World J Gastroenterol. 2007 Nov 14. 13(42):5659-61. [Medline].
Loulergue P, Mir O. Pleural empyema secondary to amebic liver abscess. Int J Infect Dis. 2009 May. 13(3):e135-6. [Medline].
Otan E, Akbulut S, Kayaalp C. Amebic acute appendicitis: systematic review of 174 cases. World J Surg. 2013 Sep. 37(9):2061-73. [Medline].
Sodhi KS, Ojili V, Sakhuja V, Khandelwal N. Hepatic and inferior vena caval thrombosis: vascular complication of amebic liver abscess. J Emerg Med. 2008 Feb. 34(2):155-7. [Medline].
Abd-Alla MD, Jackson TF, Gathiram V, el-Hawey AM, Ravdin JI. Differentiation of pathogenic Entamoeba histolytica infections from nonpathogenic infections by detection of galactose-inhibitable adherence protein antigen in sera and feces. J Clin Microbiol. 1993 Nov. 31(11):2845-50. [Medline]. [Full Text].
Haque R, Mollah NU, Ali IK, Alam K, Eubanks A, Lyerly D, et al. Diagnosis of amebic liver abscess and intestinal infection with the TechLab Entamoeba histolytica II antigen detection and antibody tests. J Clin Microbiol. 2000 Sep. 38(9):3235-9. [Medline]. [Full Text].
Helmy MM, Rashed LA, Abdel-Fattah HS. Detection and differentiation of Entamoeba histolytica and Entamoeba dispar isolates in clinical samples by PCR. J Egypt Soc Parasitol. 2007 Apr. 37(1):257-74. [Medline].
Shamsuzzaman SM, Haque R, Hasin SK, Hashiguchi Y. Evaluation of indirect fluorescent antibody test and enzyme-linked immunosorbent assay for diagnosis of hepatic amebiasis in Bangladesh. J Parasitol. 2000 Jun. 86(3):611-5. [Medline].
Ahmad N, Khan M, Hoque MI, Haque R, Mondol D. Detection of Entamoeba histolytica DNA from liver abscess aspirate using polymerase chain reaction (PCR): a diagnostic tool for amoebic liver abscess. Bangladesh Med Res Counc Bull. 2007 Apr. 33(1):13-20. [Medline].
Fotedar R, Stark D, Beebe N, Marriott D, Ellis J, Harkness J. PCR detection of Entamoeba histolytica, Entamoeba dispar, and Entamoeba moshkovskii in stool samples from Sydney, Australia. J Clin Microbiol. 2007 Mar. 45(3):1035-7. [Medline]. [Full Text].
Khairnar K, Parija SC. A novel nested multiplex polymerase chain reaction (PCR) assay for differential detection of Entamoeba histolytica, E. moshkovskii and E. dispar DNA in stool samples. BMC Microbiol. 2007 May 24. 7:47. [Medline]. [Full Text].
Stark D, van Hal S, Fotedar R, Butcher A, Marriott D, Ellis J, et al. Comparison of stool antigen detection kits to PCR for diagnosis of amebiasis. J Clin Microbiol. 2008 May. 46(5):1678-81. [Medline]. [Full Text].
Singh P, Mirdha BR, Ahuja V, Singh S. Loop-mediated isothermal amplification (LAMP) assay for rapid detection of Entamoeba histolytica in amoebic liver abscess. World J Microbiol Biotechnol. 2013 Jan. 29(1):27-32. [Medline].
Misra SP, Misra V, Dwivedi M. Ileocecal masses in patients with amebic liver abscess: etiology and management. World J Gastroenterol. 2006 Mar 28. 12(12):1933-6. [Medline].
Nagata N, Shimbo T, Akiyama J, Nakashima R, Niikura R, Nishimura S, et al. Predictive value of endoscopic findings in the diagnosis of active intestinal amebiasis. Endoscopy. 2012 Apr. 44(4):425-8. [Medline].
Gonzales ML, Dans LF, Martinez EG. Antiamoebic drugs for treating amoebic colitis. Cochrane Database Syst Rev. 2009 Apr 15. CD006085. [Medline].
Petri WA Jr, Singh U. Diagnosis and management of amebiasis. Clin Infect Dis. 1999 Nov. 29(5):1117-25. [Medline].
Salles JM, Salles MJ, Moraes LA, Silva MC. Invasive amebiasis: an update on diagnosis and management. Expert Rev Anti Infect Ther. 2007 Oct. 5(5):893-901. [Medline].
Kimura M, Nakamura T, Nawa Y. Experience with intravenous metronidazole to treat moderate-to-severe amebiasis in Japan. Am J Trop Med Hyg. 2007 Aug. 77(2):381-5. [Medline].
Moon TD, Oberhelman RA. Antiparasitic therapy in children. Pediatr Clin North Am. 2005 Jun. 52(3):917-48, viii. [Medline].
Bammigatti C, Ramasubramanian NS, Kadhiravan T, Das AK. Percutaneous needle aspiration in uncomplicated amebic liver abscess: a randomized trial. Trop Doct. 2013 Jan. 43(1):19-22. [Medline].
Athié-Gutiérrez C, Rodea-Rosas H, Guízar-Bermúdez C, Alcántara A, Montalvo-Javé EE. Evolution of surgical treatment of amebiasis-associated colon perforation. J Gastrointest Surg. 2010 Jan. 14(1):82-7. [Medline].
Jha AK, Das G, Maitra S, Sengupta TK, Sen S. Management of large amoebic liver abscess--a comparative study of needle aspiration and catheter drainage. J Indian Med Assoc. 2012 Jan. 110(1):13-5. [Medline].
Chaudhry OA, Petri WA Jr. Vaccine prospects for amebiasis. Expert Rev Vaccines. 2005 Oct. 4(5):657-68. [Medline].
Snow MJ, Stanley SL Jr. Recent progress in vaccines for amebiasis. Arch Med Res. 2006 Feb. 37(2):280-7. [Medline].
Stanley SL Jr. Vaccines for amoebiasis: barriers and opportunities. Parasitology. 2006. 133 Suppl:S81-6. [Medline].
Quach J, St-Pierre J, Chadee K. The future for vaccine development against Entamoeba histolytica. Hum Vaccin Immunother. 2014 Feb 6. 10(6):[Medline].
Kikuchi T, Koga M, Shimizu S, Miura T, Maruyama H, Kimura M. Efficacy and safety of paromomycin for treating amebiasis in Japan. Parasitol Int. 2013 Dec. 62(6):497-501. [Medline].