· What is Amebiasis?
Amebiasis is a disease caused by Entamoeba histolytica, a unicellular
eukaryotic parasite. E. histolytica belongs to thegenus Entamoeba,
along with 5 other parasites: E. coli, E. hartamanni, E.
dispar, E. gingivalis, and E. polecki. However, only E. histolytica
· Who can get Amebiasis?
Humans, and possibly some non-human primates, are the only natural hosts which can contain Amebiasis and contribute to transmission. However, many types of mammals, including dogs and cats, can contain E. histolytica, although none shed cysts with their feces. Therefore, the organism does NOT survive outside of their body, and the mammals do not contribute to transmission. There are NO VECTORS.
· How many people have Amebiasis?
Until recently, scientists were not able to visually distinguish between E. histolytica and E. dispar, leading them to grossly overestimate the prevalence of Amebiasis. The true estimated prevalence of E. histolytica is close to 1% worldwide. Entamoeba histolytica is the second leading cause of mortality due to parasitic disease in humans. (The first being malaria). Amebiasis is the cause of an estimated 50,000-100,000 deaths each year.
· What is the geographic distribution?
Amebiasis is located worldwide. However, it is primarily in developing countries, particularly in areas of crowing and poor sanitation. Areas such as the tropics, subtropics, and the arctic have higher prevalence rates than intemperate climates. Within industrialized countries, high-risk groups include immigrants, travelers, institutionalized individuals, and homosexual males.
· What is the lifecycle?
There are two forms of E. histolytica:
1) Cysts (infective), only exist outside the host. They are round and usually10-15 micrometers in diameter. They are non-motile and surrounded by a wall that includes chitin to help survive the acid in the stomach:
2) Trophozoites (noninfective), exist inside the host and in fresh feces. They are highly motile amoebas, and reproduce by binary fission:
The lifecycle of Amebiasis is very simple, with the human ingesting infective cysts. Inthe human, the cysts become feeding trophozoites and reproduce asexually. The trophozoites form cysts again and get passed in the feces, where they are eventually ingested again.
There are, however, two types of infection: pathogenic (symptomatic) and nonpathogenic (asymptomatic). The diagram below clearly explains the progression of each type (see accompanying text below figure).
Infective cysts are ingested through water or food contaminated with infected feces. The cysts travel through the digestive track until the small intestine. There, excystation occurs, forming a motile trophozoite. It then travels to the large intestine and colon.
Here the infection can follow either of two phases: pathogenic and non-pathogenic.
In the pathogenic phase, the virulent trophozoite invades the gut, intestinal lumen, and sometimes the mucosa. Here they kill epithelial cells, neutrophils, and lymphocytes. In the process, they destroy tissues and cells, and produce colitis.
Occasionally they manage to enter the capillaries, where they can be transported to the liver, lungs, or the brain. Once in those organs, the parasite can cause abscesses. The abscesses may subsequently burst, releasing many trophozoites which can re-enter the lumen.
After feeding, the trophozoites extrude all ingested material and binary fission occurs. They “round up” and form cysts, where they areresistant to the environment. The cysts pass through the digestive system and are contained in the feces. In feces, they can live anywhere from2-5 weeks, waiting for a new host.
In the non-pathogenic phase, the trophozoites feed on bacteria and detritus from the outer lining of the gut. They do not invade the membrane, and do not form ulcers or abscesses. After feeding, they round up and form cysts, as in the pathogenic phase.
From Haque, R. et al.2003 (see citation below)
· How does transmission occur?
Transmission occurs in several ways:
1) By ingesting cysts in fecally contaminated food/drinks
2) By directly inoculating trophozoites in colon or other sites (ex. Anal sex).
3) By fecal-oral self-inoculation (hand to mouth)
· What are the clinical symptoms?
Many carriers of Amebiasis have no symptoms, and eventually clear the infection without disease. However, 4-10% of asymptomatic carriers develop symptomatic infections within 1 year. For this reason, it is strongly suggested these asymptomatic individuals obtain treatment.
Symptoms occur 1-4 weeks after ingestion. These include vague and nonspecific abdominal symptoms, such as watery and bloody diarrhea, abdominal pain, cramping, flatulence, weight loss, and chronic fatigue. Fever occurs occasionally, and megacolon is present very rarely (0.5%patients).
a) Liver: Liver abscess (can present months to years after travel). 10 times more common in men than women, and rare in children. Symptoms include: fever, cough, dull abdominal pain, nausea, diarrhea, ulcers, constipation, gas, hepatomegaly, cough, and weight loss. Symptoms can last for less than 10 days, although others may be chronic(e.g. weight loss).
b) Respiratory tract: Symptoms include cough and chest pain
c) Brain: This is very rare. Symptoms are headache, vomiting, and seizures. 50% of patients with cerebral abscesses die.
d) Other: This can include areas such as urinary tract problems, genital disease, perianal disease, and cutaneous lesions.
· How is Amebiasis diagnosed?
In prior years, fecal smears and visual identification were used to detect Amebiasis. However, upon the realization that the morphologies of E. dispar and E. histolytica were identical, better methods needed to be used. Current methods are:
1) Antigen detection (ELISA assays)
2) Antibody detection (Indirect hemagglutination):
· Is there an effective treatment or prophylaxis?
There is NO effective prophylaxis. Enterovioform is NOT an effective prophylaxis; do not take it, as it also has the potential of causing serious eye disease.
Treatment varies widely depending on the stage of the infection. Noninvasive infections can be treated with luminal agents (paromomycin, iodoquinol, or diloxanide furoate).Invasive infections usually require the use of metronidazole or tinidazole. See the chart below:
From Haque, R., et al. 2003 (see citation below)
· How can Amebiasis be prevented?
1) Boiling drinking water or passing it through a .22 micron filter
2) Cleaning of uncooked fruits or vegetables with boiled or filtered water
3) Proper handling of food
4) Public services: adequate sewage disposal and clean water supply
5) Education about proper food handling and sanitation
6) Health regulations: monitoring of food handlers/vendors, and prevention of cockroaches and flies around food.
Linksto other Amebiasis sites:
This web page was created with information used from these sources:
Haque,R., Huston, C., Hughes, M., Houpt, E. Petri, W. A.
2003. Amebiasis. N Eng J Med. 348: 1565-1573.
Markell,E. K., John, D.T., Krotoski, W. A. 1999. Markell
and VogeÕs Medical Parasitology. Philadelphia: Saunders.
StanleyJr., Samuel L. Amoebiasis. The Lancet. 361:
Copyright 2003by Natasha Li. Questions/comments? Email firstname.lastname@example.org