Amebiasis is an infectious disease caused by the protozoan parasite, Entamoeba histolytica. The disease occurs in two forms: intestinal and extra-intestinal amebiasis.
Amebiasis arises due to the following process: infectious.
Persons with amebiasis may or may not manifest the disease. Symptoms, if any, include flatulence, alternating diarrhea and constipation, and abdominal cramps. In advanced cases, the patient may complain of fever, abdominal tenderness and passage of bloody, mucoid stools (frank dysentery). Dehydration is imminent. The patient is emaciated and possibly anemic from chronic infection and malnutrion. A large mass (ameboma) may obliterate the intestines.
Colonies of trophozoites can cause ulcers and perforate the intestinal wall, resulting in severe abdominal pain and peritonitis needing urgent medical intervention.
Extraintestinal amebiasis can cause suppurative infection of the liver parenchyma (abscess), fever, chills, sweating, general debility, nausea, vomiting, and pain in the upper right quadrant. Amebas may spread to other organs, including the lungs or brain, the skin, especially around the buttocks, genitals, or wounds from abdominal surgery or injury.
Complications of amebic colitis include ameboma, toxic megacolon, fulminant or necrotizing colitis, and rectovaginal fistula. Hepatic amebiasis or liver abscess may lead to intrapericardial, intrathoracic, or intraperitoneal rupture, with or without secondary bacterial infection; invasion of the pleural or pericardial cavity; and migration to the brain via blood route and development of brain abscess. Other complications include GI bleeding, bowel perforation, peritonitis, stricture formation, empysema and intussusception [11] [12].
The diagnosis of amebiasis requires collection of fecal sample from the patient for subsequent tests [13]. Microscopic examination may not always reveal the presence of the amebas (trophozoites and/or cysts). Two methods are currently available:
Molecular diagnostic technique to identify ameba's genetic material. PCR amplifies the ameba's genetic material when present and makes detection possible even with minute quantities of reagents. Both tests are sensitive and specific. Routine microscopy examination may require three to six repeat ed stool examinations and differential diagnosis of ameba species is difficult based on gross morphology.
Colonoscopy can reveal the presence of ulcers or other signs of infection in the large intestine. Tissue samples may be obtained for further evaluation.
Parasites may not be found in the stool in extraintestinal amebiasis. Appropriate diagnostic methods are ultrasonography, CT scan, or MRI, with serological test for anti-ameba antibodies to confirm liver abscess or infection in other sites. Given a strong index of suspicion, the physician may initiate treatment with an amebicidal drug and if the patient responds well, the disease is presumed to be amebiasis.
The current drug of choice for amebiasis is metronidazole or tinidazole [14], which kills the trophozoites in the intestine and other organs. Metronidazole is taken daily for several days, whereas tinidazole is given as a single large dose, with fewer side effects. Dehydrated patients are given fluids. Alcoholic drink is contraindicated since it may cause nausea, vomiting, flushing and headaches. These drugs are not to be taken by pregnant women.
Metronidazole and tinidazole do not kill ameba cysts that are in the large intestine. A second drug (such as diloxanide, paromomycin, or iodoquinol) is prescribed to eliminate the cysts, thus prevent a relapse. These drugs may be taken by asymptomatic individuals who are positive for cysts both for prophylaxis and for eliminating the source of contamination of the environment with the infective stage of the parasite.
Amebiasis is among the leading causes of morbidity in developing countries. Susceptibility to infection and fatality rates vary with age, nutritional status, immune status , and involvement of extraintestinal foci. Severity of amebiasis is more pronounced in young children, especially neonates; malnourished individuals; pregnant and postpartum women; those on corticosteroids and those with immune deficiencies and/or malignancies.
Treatment of intestinal amebiasis with appropriate drugs is straightforward but there is no immunity following previous infections nor guarantee against reinfections. Complete elimination of the intestinal forms can prevent the occurrence of extraintestinal amebiasis. Ninety percent (90%) of persons with intestinal amebiasis are asymptomatic and only 4-10% of them developed colitis or extraintestinal amebiasis after a one year follow-up period.
Effective treatment with amebicidal drugs has kept mortality rates below 1% for patients with uncomplicated liver abscess. On the other hand, hepatic amebiasis can be complicated by intraperitoneal rupture in 2-7% of patients and higher mortality rates can result from this [2].
Amebiasis is infection with the protozoan parasite, Entamoeba histolytica, which has two clinical manifestations i.e., intestinal amebiasis (colitis. diarrhea, dysentery) and extraintestinal amebiasis (liver abscess, pleuropulmonary, cardiac, and cerebral involvement).
Other species of Entamoeba are: E coli, E dispar, E moshkovskii, E polecki, E coli, and E hartmanni. These too reside in the human intestinal lumen as commensals (non-pathogenic) and should be differentiated from E histolytica as the only potentially pathogenic species. E dispar and E moshkovskii have been recovered from patients with gastrointestinal (GI) symptoms; however, their role in the pathogenesis of amebiasis remains to be verified.
E dispar and E histolytica are indistinguishable from each other by light microscopy. Molecular techniques have shown them as two different species, with E dispar being the commensal (as in patients with HIV infection) and E histolytica, the pathogenic species.
Co-infections with E histolytica and E dispar have been reported in many individuals, with E dispar being 10 times more common than E histolytica. In Brazil and Egypt, E dispar and E histolytica infections are equally prevalent [2]. In Western countries, E dispar has been isolated from 20%-30% of MSM (men having sex with other men).
Transmission of E histolytica is primarily through the ingestion of fecally contaminated food and water containing cysts, or through the hands of food handlers. Sexual transmission occurs via oral-anal practices (anilingus). Malnutrition, resulting in immune deficiency , is a risk factor in amebiasis [3].
Amebiasis in the United States is approximately 4% of the total population. Of these, only 10% of E histolytica infections are invasive, and only 1% of those positive for E histolytica by stool examination actually develop symptomatic amebiasis. Asymptomatic E dispar infection is 10 times more prevalent than E histolytica.
About 50 million cases of amebiasis due to E histolytica are reported each year, with 100,000 deaths worldwide. This is presumed to be an underestimation, representing as it is, the so-called tip of the iceberg, since only 10%-20% of infected individuals become symptomatic [4] [5]. Amebiasis is among the leading causes of morbidity in developing countries [6].
Infection with the protozoan parasite E histolytica is associated with proteolysis, tissue damage and host-cell apoptosis in humans and presumably nonhuman primates. Ingested E histolytica cysts from contaminated food and water or oral-anal sex undergo excystation in the terminal ileum or colon. Each mature cyst can give rise to four highly motile trophozoites which will colonize the intestinal mucosa, causing tissue lysis and ulcerations. Meanwhile, trophozoites may find their way in the bloodstream and migrate to the liver, lung, and other sites, causing further damage thereat. With physiological changes in conditions in the intestinal lumen, the amebas may transform into cysts that are excreted in the feces. Excreted cysts when ingested by the next susceptible host will initiate a new infectious cycle.
The trophozoite's ability to invade the colonic epithelium is facilitated by a 260-kd surface protein, galactose/N -acetylgalactosamine (GAL/GalNAc)–specific lectin, containing a 170-kd subunit and a 35-kd subunit [7] [8]. IgA antibody binds to this lectin receptor, killing the ameba thus, preventing reinfection [9].
Amebapores, which are peptides capable of forming pores in bimolecular lipid layers of cell membranes are responsible for cytolysis and apoptosis of the parasite. Trophozoite-induced apoptosis in liver abscess was observed with a non-Fas and non–tumor necrosis factor (TNF)-α1 receptor pathway in experimental animal models [10]. Amebapores can also induce apoptosis at sublytic concentrations.
Cysteine proteinases are involved in colonization of the gut and may amplify interleukin (IL)-1–mediated inflammation just as human IL-1–converting enzyme would cleave IL-1 precursor to its active form [11]. The anaphylatoxins C3a and C5a and immunoglobulins, IgA and IgG are likewise cleaved and inactivated by cysteine proteinases [12].
E histolytica is equipped with 100 putative transmembrane kinases (TMKs), of which there are 9 subgroups. EhTMKB1-9 is found in proliferating trophozoites and is induced by serum. This was shown to be involved in phagocytosis and virulence of E histolytica in amebic colitis. Thus, TMKs such as EhTMKB1-9 may serve as potential targets for future drug development.
Amebiasis is an infectious disease of the large intestine, liver and other organs that is caused by the protozoan parasite, Entamoeba histolytica [1]. The parasite undergoes two developmental stages, namely:
The infective stage or cyst is transmitted directly from one person to another, or through food and water. The trophozoite or vegetative stage invades the intestinal mucosa, causing diarrhea or fulminant dysentery in intestinal amebiasis. Involvement of the liver and other organs such as the skin or brain is called extra-intestinal amebiasis.
Affected persons may be asymptomatic or may experience a variety of clinical manifestations such as alternate diarrhea and constipation, abdominal tenderness, cramps, malaise, and fever. Asymptomatic persons may be cyst-passers that is, cysts are found in their stools. Cyst is the infective stage to man. Trophozoites are found in the stools of patients with diarrhea or dysentery. These are motile amebas, usually seen with ingested red blood cells under the microscope.
Diagnosis is by routine microscopic examination of fecal smears or liver aspirate, and if needed, colonoscopy or ultrasonography, and blood tests. Oral anti-trophozoite drugs are taken by patients with diarrhea or dysentery, with another amebicide to eliminate the cysts.
Amebiasis is common in areas where fecal contamination of food and water is rampant due to poor sanitation. These are in Africa, the Indian subcontinent, parts of Central and South America, and Asia. In the United States, there are cases among immigrants and sometimes in travelers who might have acquired the infection from developing countries.
Amebiasis is an infectious disease primarily of the intestines caused by the protozoan parasite, Entamoeba histolytica. The ameba can reside in the large intestine (colon) with other species of amebas as commensals without causing disease. When conditions permit as when the innate immunity of the human host is impaired, the parasite may invade the intestinal wall, cause ulcers or perforations, and manifest clinically as colitis, chronic diarrhea, or at its worst, acute dysentery.
From the intestines the amebas can migrate via the blood route to the liver, causing liver abscess. In severe cases the lungs, brain, skin and other organs may become involved.
Infection with Entamoeba histolytica cysts is acquired from ingestion of ameba cysts from contaminated food or water, through the unwashed hands of food handlers, through oral-anal sex, or in some places, when human waste is used as fertilizer.
Symptoms
The symptoms of amebiasis range from mild to severe. Mild symptoms are:
Severe symptoms include:
Diagnosis
Treatment
Valenzuela O, Morán P, Gómez A, et al. Epidemiology of amoebic liver abscess in Mexico: the case of Sonora. Ann Trop Med Parasitol. 2007 Sep; 101(6):533-8.
Van Hal SJ, Stark DJ, Fotedar R, et al. Amoebiasis: current status in Australia. Med J Aust. 2007 Apr 16; 186(8):412-6.
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.
Ravdin JI, Stanley P, Murphy CF, et al. Characterization of cell surface carbohydrate receptors for Entamoeba histolytica adherence lectin. Infect Immun. 1989 Jul; 57(7):2179-86.
Ximénez C, Cerritos R, Rojas L, et al. Human amebiasis: breaking the paradigm?. Int J Environ Res Public Health. 2010 Mar; 7(3):1105-20.
Haque R, Mondal D, Duggal P, et al. Entamoeba histolytica infection in children and protection from subsequent amebiasis. Infect Immun. 2006 Feb; 74(2):904-9.
Rao S, Solaymani-Mohammadi S, Petri WA Jr, et al. Hepatic amebiasis: a reminder of the complications. Curr Opin Pediatr. 2009 Feb; 21(1):145-9.