All amoebae presented in this class are parasitic. There are many others that are free-living. The typical life cycle involves infection of the host with the trophozoite multiplying by binary fission and in some cases, producing cysts. Diagnosis in all species requires microscopic evaluation of either trophozoites or cysts. (Not all species of amoebae have a cyst stage).
Entamoeba histolytica- Agent of intestinal amebiasis. This is a pathogenic organism commonly recovered from man but has also been reported from lower primates, dogs, and cats. The typical location is the cecum, colon or rectum with extra-intestinal locations common. E. hostolytica trophozoites damage the intestine by attaching to and lysing host cells and secreting enzymes that disrupt intercellular connections. The presence of some bacteria and deficient protein intake may contribute to parasite virulence. Erosion or ulceration of the colon mucosa is common with classical "flask-shaped" ulcers. These are the result of trophozoite undermining the mucosa and submucosa. Clinically, diarrhea with dysentery (diarrhea with abdominal pain, straining and blood in the stool) is the main problem in intestinal infections. Clinical problems associated with extraintestinal lesions depend on the organs involved (above right). Although a problem in humans, E. histolytica rarely causes clinical problems in other non-primate animals. Although dogs and cats are susceptible to infection, it is not likely that they contribute to the epidemiology of human infections and are most likely infected themselves from exposure to infected human feces. Treatment should be used to destroy trophozoites, relieve symptoms and control secondary infection. The drug(s) of choice are metronidizole and diiodohydroxyquin. Tetracycline therapy is used in combination with both drugs to combat secondary bacterial infections. Hepatic amoebiasis (above right) usually responds to metronidazole therapy but may not be totally effective. Chloroquine therapy is often used when contraindications occur but has no effect on intestinal trophozoites. Both trophozoite (above left) and cyst (above middle) stages occur. Man is also infected with a variety of other non-pathogenic amoebae that require differentiation from E. histolytica.
Acanthamoeba spp infections are becoming more common in both humans an canines. This organisms are ubiquitous free-living amoebae that under specific circumstances can cause infection and disease in some animals. Acanthamoeba infections in canines are rare but reported. Young dogs appear to be the most susceptible and infections in greyhounds, German shepherds and an Akita are recorded. Clinical signs include mild oculonasal discharge, anorexia and lethargy. Increased body temperature, respiratory distress and occasional neuralgic signs. Laboratory findings are generally nonspecific. Premortum diagnosis is rare. New cases of Acanthamoeba respond to sulfonamides while established cases are generally treated with amphotericin B. Corneal ulcers resulting from infections with Acanthamoeba infections in contact lens wearers appear refractory to treatment. The life cycle of Acanthamoeba spp appears similar to that of Naegleria fowleri (below) and several cases of chronic PAM have been attributed to this organism.
Entamoeba coli - This amoebae is similar to E. histolytica but is not considered a true tissue invader and thus is non-pathogenic. Differentiation from E. histolytica is based on morphologic differences and the number of nuclei (4 in E. histolytica, 8 in E coli) in the cysts and nuclear morphology in the trophozoites.
Naegleria fowleri -Agent of primary amoebic meningoencephalitis (PAM). This is a free-living amoebae that occasionally infects humans with a high case fatality ratio. It was first identified as a problem in 1965 and over 150 cases have now been recorded. Most human victims have a history of exposure to warm, fresh or brackish water, such as swimming pools, ponds, lakes or streams. Transmission to humans appears to occur when the nasopharyngeal mucosa is invaded by the flagellated trophozoite form of the organism. These trophozoites migrate through the nervous system to the brain where inflammation occurs followed by death. Most cases are diagnosed at autopsy by microscopic identification of the motile amoebic trophozoite form in cerebrospinal fluid. The clinical course of the disease is generally 5 to 7 days after exposure. No effective treatment exists but favorable response to intravenous administration of amphotericin B has been reported. Although a variety of animals are known to be susceptible to infection, little is known about the prevalence of this organism in domestic or wild animals.