Amebiais

by Sara Jones

Disease Etiology:

Amebiais, pronounced [m-b-sis] is caused by an infection with the parasite

Entamoeba histolytica. [1] Protozoa are unicellular organisms which can only divide in the host
organism. Intestinal amebae with identical morphologic appearances can be one of three
species, E. histolytica or E. dispar or E. moshkovskii.[2] The latter two are non-pathogenic.
Only the E. histolytica which is genetically distinct causes invasive disease. 90% of Entamoeba
infections are due to E. dispar.[1] There are two distinct stages, the cyst stage and the
trophozoite stage. The first stage is not motile but is very resistant to therapy while the latter is
motile and is only active in the host and is sensitive to antibiotic therapy.

Disease Transmission:

Amebiais is spread in humans ingestion of fecally contaminated food or water or through

oral-anal sex, anilingus. [3] The food is usually uncooked food such as salads or vegetables,
although contaminated water may be the source.[4] Poor hand washing is also a factor in
transmission of the disease. Inadequate sanitation and crowding increase the risk of infection.
Developing tropical areas such as Mexico, Central and South America, Asia, and Africa are at
highest risk of infection with amebiasis. The cysts are ingested and undergo encystations in the
small intestine and then divide into trophozoites which invade the colonic mucosa. Trophozoites
are killed in the stomach if ingested, while the cysts are resistant and pass in to the small
intestine unaffected.

Reservoirs
Human beings are the reservoirs for the protozoa, Entamoeba histolytica. 90% of
patients who become infected with Entamoeba histolytica will remain asymptomatic.[6]
Immunosuppression with steroids or due to other reasons increase the risk of invasive disease.
[7] Incubation of the disease may be from 2 days to years, although it usually from within days
to months.

Specific Microbial Characteristics and Virulence Factors:

 The cysts are from 5-15 mm with 1-4 neuclei similar to those in the trophozoite. It has a
spherical cyst wall which is protective of the cyst. They have chromatiod bodies and glycogen
clumps. The cyst wall dissolves in the small intestine into 4 and then 8 trophozoites.[8] The
cysts are resistant to chlorine but are destroyed by drying, deep freezing and by being heated to
50 degrees Celsius for 5 minutes.[4]

The trophozoites are 10-60 mm in diameter and are motile amoeba. The pathogenic
Entamoeba histolytica is characterized by ingested erythrocytes in the trophozoite. It is the
trophozoite which is responsible for the invasive disease in the colon. The lecithin of the
trophozoite, galactose/N-acetylgalactosamine facilitates adherence of the amoeba to the colon
wall. This lecithin is a surface protein which contains 2 main subunits. It is the larger, 170-kd
subunit with the glactose-binding activity. This lecithin also has at least 6 different antigenic
characteristics which differentiate it from E. dispar. [8] Colonic cells without N-terminal
galactose or N-acetylgalactosamine residues are resistant to this adherence. Immune mediated
mucosal immunity to the lecithin, galactose/N-acetylgalactosamine plays a significant role in
preventing the development of invasive disease. Serum IgA anti-lecthin provides host resistance
to disease while anti-lecithin IgG increases the risk of adherence.[10] Once adherence occurs,
cell death occurs due to formation of pores in the target cell lipid bilayers, apoptosis, secretion of
proteases, changing intestinal permeability and also by a contact dependant mechanism.[9]

Specific Tests for Identification:

Microscopy does not distinguish between pathogenic and non-pathogenic Entamoeba

histolytica. Enzyme immunoassay or polymerase chain reaction can be used to detect the
infection. The enzyme immunoassay is readily available as a commercial test and is as accurate
as PCR examination.

Serologic tests do not distinguish new versus past infections and even in patients with
amebic liver abcesses, these tests may be falsely negative initially for the first week when
symptomatic. The indirect hemagglutination assay measures antibody titers for the galactose-
inhibitable adherence lectin It is no more sensitive than the enzyme immunoassay test. Either
one of these two tests takes about 2 hours to perform.[11]

One of the mainstays of diagnosis is checking the stool for ova and parasites. Specimens
must be fresh (within 15 minutes) to show motile trophozoites. If this cannot be done, specimens
are placed in a fixative to prevent degradation.[3]

Signs and Symptoms

While in most, the disease is asymptomatic, symptoms often start with a mild diarrhea
and lower abdominal pain. This may progress to malaise, weight loss and increasing abdominal
pain. The pain may mimic acute appendicitis. The diarrhea will progress to frank dysentery
with bloody mucus like watery diarrhea passing up to 20 times daily as infiltration of the colon
wall increases. As opposed to bacterial enteritis, less than 40% of patients will become febrile
unless fulminate intestinal infection occurs which may cause high fevers, severe abdominal pain
with profuse diarrhea. The patient may develop a toxic megacolon.[7] Patients with chronic
disease may present like those with inflammatory bowel disease or may present with an
asymptomatic abdominal mass which is intraluminal and may be difficult to distinguish from a
carcinoma.[3]. They may have diarrhea every few days alternating with constipation as well as
weakness and weight loss.[12]

Extra-intestinal disease most often presents in the liver. Spread to the liver is through the
portal circulation. Abcesses are solitary in around 2/3rds of cases and 80% of the time, these
abscesses are found in the right lobe of the liver. Jaundice is present in up to 1/3rd of patients and
is usually mild. The liver is usually enlarged and tender. Aspiration rarely shows the
trophozoites or white blood cells. Spread to the liver is more common in males than females for
an unknown reason [3], [4],[7]

Historical Information:

In 1875, Fedor Losch first described amebiasis in St. Petersburg, Russia. 11 years later,
Kartulus, showed that the amoeba were a pathogen for the diarrhea and liver disease in patients
with amebiasis. In 1891, doctors at Johns Hopkins differentiated amoebic from bacterial
dysentery. Over 20 years later, Walker and Sellards, working in the Phillipines were able to
document the pathogenesis of the amebae. There may be up to 100,000 persons worldwide who
die annually from amebic infections[8]

Control/Treatment

Since ingestation of contaminated food products is the most common method of

transmission of the disease, simple measures can decrease ones risk of infectation with amebae.
Hand washing and eating cooked foods as well as drinking bottled water will help, especially in
areas where the disease is endemic. Since chlorine is not effective in killing the cysts, the use of
betadine in washing may be helpful.

The WHO recommends treating all patients with proven Entamoeba histolytica
infections. In places with limited resources and positive stool samples, they recommend only
treating symptomatic patients to limit the development of resistant strains of Entamoeba
histolytica. Prophylaxis is never recommended.

Asymptomatic Entamoeba histolytica infections should be treated with intraluminal

amebicides such as paromomycin which has the advantage of not being absorbed by the
intestine. Symptomatic cases are best treated with a tissue amebicide such as metronidazole in a
5-10 day course of therapy. After the metronidazole regimen is completed, it should be followed
with ain intraluminal amebicide to make sure that there are no resivoirs of disease left in the
intestines. A new medication, nitizoxanide has shown a lot of interest because it will eradicate
other protozoa, in addition to the Entamoeba histolytica in a 3 day course of therapy.[2],[3],[4],
[5]

Prevention/ Vaccines

Currently there is no vaccine available for amebiasis in humans. However, in 2007 a

vaccine was developed which was tested in gerbils and confirmed immunity. The vaccine was
designed to induce an immune response to the surface lecithin responsible for adherence of the
ameboe to the intestinal wall.[13]

Local and global cases/outbreaks

Approximately 1% of the US population has an amebic infection. Worldwide, estimates of

infection are as high as 50,000,000 people annually. Outbreaks are common in endemic areas of
the world, especially associated with the occurrence of natural disasters which affect the ability
to provide clean water and which affect hygene.
Entamoeba histolytica Trophozoite: Courtesy of CDC

Entamoeba histolytica Cyst: Courtesy of CDC

Gross disease in the colon due to Entamoeba histolytica

[5] http://emedicine.medscape.com/article/996092-media

References

[1]Center for Disease Control. Division of Parasitic Disease. Amebiais. last reviewed
September 3, 2008
.http://www.cdc.gov/ncidod/dpd/parasites/Amebiasis/factsht_Amebiasis.htm#what 03/14/10

[2] Petri, WA, Singh, U. Enteric Amebiasis. In: Tropical Infectious Diseases: Principles,
pathogens, and practice. Second edition, Guerrant, R, Walker, DH, Weller, PF (eds). Elsevier,
Philadelphia 2006. p. 967.

[3] Mayo Clinic Proceedings Amebiais Bobbi S. Pritt, MD and

C. Graham Clark, PhD, Mayo Clinic Proceedings October 2008 vol. 83 no. 10 1154-1160
http://www.mayoclinicproceedings.com/content/83/10/1154.full 03/14/10

[4] Journal of the Royal Society of Medicine, Amoebiasis: a review James Harris; JRSM 75:
190-197, 1982 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1437583/pdf/jrsocmed00251-
0056.pdf 03/14/10

[5] Emedicine, from WebMD Amebiasis Vinod K Dhawan, MD and Thomas R Naparst, MD,
Updated August 11, 2008 http://emedicine.medscape.com/article/996092-media

03/14/10

[6] Gathiram V, Jackson TF. A longitudinal study of asymptomatic carriers of pathogenic

zymodemes of Entamoeba histolytica. S Afr Med J. 1987 Nov 21;72(10):669-72 Pubmed
http://www.ncbi.nlm.nih.gov/pubmed/2891197?dopt=Abstract 03/14/10

[7] Harrisons Practice Amebiasis Last updated: February 22, 2010

http://www.harrisonspractice.com/practice/ub/view/Harrisons%20Practice/141104/all/Amebiasis
03/14/10
[8] Emedicine, from WebMD Amebiasis Vinod K Dhawan, MD and Thomas R Naparst, MD,
Updated August 11, 2008 http://emedicine.medscape.com/article/996092-overview

03/14/10

[9] Update for Patients; Intestinal Entamoeba histolytica amebiasis Karin Leder, MBBS,
FRACP, PhD, MPH, DTMH and Peter F Weller, MD, FACP; Updated 2010
http://www.utdol.com/patients/content/topic.do?topicKey=~xgxgkbDEMr.rOv 03/14/10

[10] Haque, R, Duggal, P, Ali, IM, et al. Innate and acquired resistance to amebiasis in
Bangladeshi children. J Infect Dis 2002; 186:547. http://www.jstor.org/pss/30084484 03/14/10

[11] Emedicine, from WebMD Amebiasis Vinod K Dhawan, MD and Thomas R Naparst, MD,
Updated August 11, 2008 http://emedicine.medscape.com/article/996092-diagnosis
03/14/10

[12] CDC Yellow Book for Travelers Amebiasis Sharon Roy, Barbara L. Herwaldt,
Stephanie P. Johnston Last updated July 27, 2009
http://wwwnc.cdc.gov/travel/yellowbook/2010/chapter-5/amebiasis.aspx 03/14/10

[13] Catherine P. A. Ivory and Kris Chadee; Intranasal Immunization with Gal-Inhibitable
Lectin plus an Adjuvant of CpG Oligodeoxynucleotides Protects againstEntamoeba
histolytica Challenge Infection and Immunity, October 2007, 75: 4917-4922
http://iai.asm.org/cgi/content/abstract/75/10/4917 03/14/10