The Organism E. histolytica cysts are present only in the lumen of the colon and in mushy or formed feces and range in size from 10 to 20 μm (Figure 1A). The cyst may contain a glycogen vacuole and chromatoid bodies (masses of ribonucleoprotein) with characteristic rounded ends (in contrast to splinter chromatoidals in developing cysts of Entamoeba coli). Nuclear division occurs within the cyst, resulting in a quadrinucleated cyst, and the chromatoid bodies and glycogen vacuoles disappear. Diagnosis in most cases rests on the characteristics of the cyst, as trophozoites usually appear only in diarrheic feces in active cases and survive for only a few hours.
Fig1. Entamoeba histolytica. A: Cyst (12–15 μm) with two (of four) nuclei and a chromatoid body. B: Trophozoite (10–20 μm). (Used with permission from Sullivan J: A Color Atlas of Parasitology, 8th ed. 2009.)
The ameboid trophozoite is the only form present in tis sues (Figure 1B). The cytoplasm has two zones, a hyaline outer margin and a granular inner region that may contain red blood cells (pathognomonic) but ordinarily contains no bacteria. The nuclear membrane is lined by fine, regular granules of chromatin with a small central body (endosome or karyosome).
Pathology and Pathogenesis of Invasive Amebiasis
It is estimated that approximately 50 million cases occur each year, with up to 100,000 deaths (Marie and Petri, 2014). Disease results when the trophozoites of E. histolytica invade the intestinal epithelium and form discrete ulcers with a pinhead-sized center and raised edges, from which mucus, necrotic cells, and amebae pass. The trophozoites multi ply and accumulate above the muscularis mucosae, often spreading laterally. Rapid lateral spread of the multiplying amebae follows, undermining the mucosa and producing the characteristic “flask-shaped” ulcer of primary amebiasis: a small point of entry, leading via a narrow neck through the mucosa into an expanded necrotic area in the submucosa. Bacterial invasion usually does not occur at this time, cellular reaction is limited, and damage is by lytic necrosis.
Subsequent spread may coalesce colonies of amebae, undermining large areas of the mucosal surface. Trophozoites may penetrate the muscle layers and occasionally the serosa, leading to perforation into the peritoneal cavity. Subsequent enlargement of the necrotic area produces gross changes in the ulcer, which may develop shaggy overhanging edges, secondary bacterial invasion, and accumulation of neutrophilic leukocytes. Secondary intestinal lesions may develop as extensions from the primary lesion (usually in the cecum, appendix, or nearby portion of the ascending colon). The organisms may travel to the ileocecal valve and terminal ileum, producing a chronic infection. The sigmoid colon and rectum are favored sites for later lesions. An amebic inflammatory or granulomatous tumorlike mass (ameboma) may form on the intestinal wall, sometimes growing sufficiently large to block the lumen.
Factors that determine invasion of amebae include the following: the number of amebae ingested, the pathogenic capacity of the parasite strain, host factors such as gut motility and immune competence, and the presence of suitable enteric bacteria that enhance amebic growth. Correct and prompt identification of the Entamoeba species remains a critical problem. Trophozoites, especially with red blood cells in the cytoplasm, found in liquid or semi-formed stools are pathognomonic.
Symptoms vary greatly depending on the site and intensity of lesions. Extreme abdominal tenderness, fulminating dysentery, dehydration, and incapacitation occur in serious disease. In less acute disease, onset of symptoms is usually gradual and often includes episodes of diarrhea, abdominal cramps, nausea and vomiting, and an urgent desire to defecate. More frequently, there will be weeks of cramps and general discomfort, loss of appetite, and weight loss, with general malaise. Symptoms may develop within 4 days of exposure, may occur up to a year later, or may never occur.
Extraintestinal infection is metastatic and rarely occurs by direct extension from the bowel. By far the most common form is amebic hepatitis or liver abscess (4% or more of clinical infections), which is assumed to be due to micro emboli, including trophozoites carried through the portal circulation. It is assumed that hepatic microembolism with trophozoites is a common accompaniment of bowel lesions but that these diffuse focal lesions rarely progress. A true amebic abscess is progressive, nonsuppurative (unless secondarily infected), and destructive without compression and formation of a wall. The contents are necrotic and bacteriologically sterile, active amebae being confined to the walls. A characteristic “anchovy paste” is produced in the abscess and seen on surgical drainage. More than half of patients with amebic liver abscess give no history of intestinal infection, and rarely, amebic abscesses occur elsewhere (eg, lung, brain, and spleen). Any organ or tissue in contact with active trophozoites may become a site of invasion and abscess. Hepatic abscess, usually showing as an elevation of the right dome of the diaphragm, can be observed by ultrasonography, computerized tomography, magnetic resonance imaging, or radio isotope scanning. Serologic tests in these cases are usually strongly positive.
