Entamoeba histolytica is a eukaryotic microorganism; that is, the nuclear genetic material is enclosed within a specialized membrane. Furthermore, the microbe is a protozoan parasite. It requires a host for the completion of its life cycle, and its survival comes at the expense of the host organism. Entamoeba histolytica causes disease in humans. Indeed, after malaria and schistosomiasis, the dysentery caused by the amoeba is the third leading cause of death in the world. One-tenth of the world's population, some 500 million people, are infected by Entamoeba histolytica, with between 50,000 and 100,000 people dying of the infection each year.
The bulk of these deaths occurs in underdeveloped areas of the world, where sanitation and personal hygiene is lacking. In developed regions, where sanitation is established and where water treatment systems are in routine use, the dysentery caused by Entamoeba histolytica is almost nonexistent.
A characteristic feature of Entamoeba histolytica is the invasion of host tissue. Another species, Entamoeba dispar does not invade tissue and so does not cause disease. This non-pathogenic species does appear similar to the disease-causing species, however, which can complicate the diagnosis of the dysentery caused by Entamoeba histolytica.
Both microorganisms have been known for a long time, having been originally described in 1903. Even at that time the existence of two forms of the microorganisms were known. The two forms are called the cyst and the trophozoite. A cyst is an environmentally hardy form, designed to protect the genetic material when conditions are harsh and unfavorable for the growth of the organism. For example, cysts are found in food and water, and are the means whereby the organism is transmitted to humans. Often, the cysts are ingested in water or food that has been contaminated with the fecal material of an infected human. Within the small intestine, the cyst undergoes division of the nuclear material and then resuscitation and division of the remaining material to form eight trophozoites.
Some of the trophozoites go on to adhere to the intestinal wall and reproduce, so as to colonize the intestinal surface. The adherent trophozoites can feed on bacteria and cell debris that are present in the area. Some of the trophozoites are able to break down the membrane barrier of the intestinal cells and kill these cells. The resulting abdominal pain and tenderness, with sudden and explosive bloody diarrhea, is called dysentery. Other symptoms of the dysentery include dehydration, fever, and sometimes the establishment of a bowel malfunction that can become chronic. The damage can be so extensive that a complete perforation of the intestinal wall can occur. Leakage of intestinal contents into the abdominal cavity can be a result, as can a thickening of the abdominal wall.
Other trophozoites form cysts and are shed into the external environment via the feces. These can spread the infection to another human.
Drugs are available to treat the symptomatic and asymptomatic forms of the infection.
In about 10 percent of people who are infected, some of the trophozoites can enter the circulatory system and invade other parts of the body, such as the liver, colon, and infrequently the brain. The reasons for the ability of the trophozoites to establish infections in widespread areas of the body are still not understood. The current consensus is that these trophozoites must somehow be better equipped to evade the immune responses of the host, and have more potent virulence factors capable of damaging host tissue.
Infection can occur with no obvious symptoms being shown by the infected person. However, these people will still excrete the cysts in their feces and so can spread the infection to others. In others, infection could produce no symptoms, or symptoms ranging from mild to fatal.
Although the molecular mechanisms of infection of Entamoeba histolytica are still unclear, it is clear that infection is a multi-stage process. In the first step the amoeba recognizes the presence of a number of surface receptors on host cells. This likely involves a reaction between the particular host receptor and a complimentary molecule on the surface of the amoeba that is known as an adhesion. Once the association between the parasite and the host intestinal cell is firm, other molecules of the parasite, which may already be present or which may be produced after adhesion, are responsible for the damage to the intestinal wall. These virulence factors include a protein that can form a hole in the intestinal wall of the host, a protein-dissolving enzyme (protease), a glycocalyx that covers the surface of the protozoan, and a toxin.
Comparison of pathogenic strains of Entamoeba histolytica with strains that look the same but which do not cause disease has revealed some differences. For example, the non-pathogenic forms have much less of two so-called glycolipids that are anchored in the microbe membrane and protrude out from the surface. Their function is not known, although they must be important to the establishment of an infection.
Completion of the sequencing of the genome of Entamoeba histolytica, expected by 2005, should help identify the function of the suspected virulence factors, and other, yet unknown, virulence factors. Currently, little is known of the genetic organization and regulation of expression of the genetic material in the protozoan. For example, the reasons for the variation in the infection and the symptoms are unclear.
See also Amebic dysentery; Parasites