Entamoeba histolytica Schaudinn, 1903
(Figures 1-38 and 1-39)
ETYMOLOGY: (Ent=internal + amoeba; histo=tissue + lytica=lysis)
SYNONYMS:Amoeba coli Lösch, 1878; Amoeba dysenteriae Councilman and Lafleur, 1891; Entamoeba dysenteriae (Councilman and Lafleur, 1891) Craig, 1905; Entamoeba tetragena Hartmann, 1908; Endamoeba histolytica (Schaudinn, 1903) Hickson, 1909; Endamoeba dysenteria Kofoid, 1920; Entamoeba dispar Brumpt, 1925.
HISTORY: Disease due to Entamoeba histolytica was first observed by Lösch in 1875 in Leningrad. Lösch observed amoebas in ulcers of the colon at necropsy and induced disease in a dog by a rectal inoculation with human feces. Work by others, including Councilman and Lafleur, showed that the amoeba was the cause of the disease. Entamoeba histolytica was distinguished from the nonpathogenic commensal of humans, Entamoeba coli, by Schaudinn in 1903.
GEOGRAPHIC DISTRIBUTION: These organisms are found throughout the world, but are more common in the tropics. There is only a single report in which amoebae specifically identified as Entamoeba histolytica have been found in naturally infected cats.
LOCATION IN THE HOST:Entamoeba histolytica is a parasite of the mucosa of the large intestine. Some strains are more pathogenic than others, and are capable of causing ulcers within the mucosa and being carried by the blood stream to other organs, e.g., the liver, lung, and brain, where abscesses develop. In experimentally infected cats, abscesses have been observed to develop in the liver.
DIAGNOSIS: The parasite is diagnosed in formed feces by the identification of the cyst in the feces (Fig. 1-38). In loose or dysenteric stools, a diagnosis requires the identification of the motile trophozoite stage (Fig. 1-39). The only diagnosis made in naturally infected cats has been based on the identification of trophozoites in feces and in histologic sections of the wall of the colon (Kessel, 1928). Typically, cats do not appear to shed cysts, however, Quincke and Roos (1893), who were the first to observe cysts in the feces of humans, observed cysts in the feces of cats that they had infected with cysts from humans. Also, Jungmann et al. (1986) reported 1 of 13 cats in East Berlin to be shedding cysts of an unidentified Entamoeba spp. It would appear that cats are refractory to infections with the other Entamoeba spp. that infect humans, i.e., Entamoeba coli and Entamoeba hartmanni (Wenyon, 1912; Dale and Dobell, 1917); this simplifies the identification of the trophozoite and cyst in cat feces.
IDENTIFICATION OF THE PARASITE: The 8 to 30 m trophozoite in a fecal smear prepared from fresh feces in physiologic saline will continue to be motile and finger-shaped, rapidly extended pseudopodia can be observed. The tropho zoites of Entamoeba histolytica are often seen to contain ingested red blood cells. If the fecal material is stained with a trichrome stain or iron hematoxylin, the characteristic morphology of the nucleus with its small central karyosome and peripheral chromatin granules.
The spherical cyst, 10 to 20 m in diameter, is more likely to be observed in formed feces. A fully developed cyst will contain 4 nuclei, although maturing cysts can contain anywhere from 1 to 4 nuclei. The cyst may contain elongate rod-shaped structures, chromatoidal bodies, that will have blunt ends.
LIFE CYCLE: In humans, the typical life cycle includes the feeding, trophozoite stage that is found on or in the mucosa of the large bowel. The trophozoite is the stage that causes disease, and is the stage passed in the feces of patients with dysentery. The cyst stage is passed into the environment with the formed feces of individuals that serve as carriers of the infection. The cyst is a relatively resistant form that serves to transport the ameba from host to host in fecal contaminated water.
It is difficult to infect kittens with a per os inoculation of cysts of Entamoeba histolytica, although it has been done (Dale and Dobell, 1917). More typically, kittens have been experimentally infected by the intrarectal inoculation of cysts or trophozoites obtained from human cases or other experimentally infected cats. In cats that are experimentally infected, amebas can first be detected in dysenteric stools as early as 3 days after infection (Sanders, 1928) with the average prepatent period being about 6 days (Kessel, 1928). As noted above (under DIAGNOSIS), cysts are rarely seen in cats following experimental infection.
CLINICAL PRESENTATION AND PATHOGENESIS: Diamond & Clark (1993) proposed that there were two morphologically indistinguishable species of Entamoeba. One of these species, Entamoebahistolytica Schaudinn, 1903 (Walker, 1911) is pathogenic in cats, while a second species, Entamoebadispar Brumpt, 1925 is nonpathogenic in cats. This was a concept originally proposed by Brumpt in 1925 based on pathogenicity of isolates in humans and in experimentally infected kittens. These two isolates of pathogenic and nonpathogenic strains can be differentiated on the basis of electrophoretic enzyme analysis, by using monoclonal antibodies, and various DNA probes that hybridize selectively to the DNA of the different amoeba isolates. Thus, it would appear that cats that are passing cysts without signs of disease are probably infected with the noninvasive Entamoebadispar while cats or kittens that develop amebiasis are probably infected with the invasive species Entamoebahistolytica.
The experimental inoculation of adult cats with Entamoebahistolytica seldom results in infection or disease, although a carrier state has developed in a small number of adult animals (Baetjer and Sellards, 1914), of course, it has not always been clear whether the authors were working with pathogenic or nonpathogenic isolates. Disease occurs mainly in kittens. In the three naturally infected kittens that have been observed to have a pathogenic form of the organism (Kessel, 1928), trophozoites were noted in fecal samples taken soon after the kittens were purchased on the streets of Peking, China. These three kittens developed dysentery and succumbed to the infections within a few days after purchase. Histologic examination of the large bowel revealed lesions similar to those seen in experimentally infected kittens with ulcers containing amebae extending to the level of the muscularis mucosa. Lesions in experimentally infected kittens are typically restricted to the distal fourth of the large bowel, although in some older animals, lesions have been noted anterior to the ileo-cecal valve. It is difficult to judge whether the obsreved localization approximates the natural state of disease in the cat, because the amoebas were often inoculated intrarectally which may have some effect on where the lesions are produced.
In the experimentally infected kittens, the amebae enter the bottom of the glands in the large intestine and then pass into the connective tissue beneath. This is followed by the degeneration of epithelial cells. As the lesions grow in size and severity, the kitten develops the typical bloody and mucoid stools. A common occurrence in infected cats appears to be a generalized septicemia. Cats typically die within 8 days after infection (Kessel, 1928), but ranges from 4 to 39 days have been reported in cats with dysentery. A few cats have become "carriers" and been observed apparently healthy 62 days after infection. These carrier cats were without signs of dysentery and without amebae in their stools, but on necropsy they did have lesions (in one an 8 cm bloody patch) containing motile amoebae.
Liver abscesses are capable of developing in experimentally infected cats (Wenyon, 1912; Baetjer and Sellards 1914; Dale and Dobell, 1917). The amebae are first carried to the mesenteric lymph nodes which become enlarged and in which the amebae multiply. The amebae are then carried to the liver where amebic abscesses typical of those of human amebiasis develop. In some cats, the observed abscesses have remained less than a centimeter in size, and cause superficial bulges of the liver surface. In one case, an extensive internalized abscess developed that ocupied about one-quarter of the entire liver (Baetjer and Sellards, 1914). Examination of the abscesses has revealed them to contain numerous amebae. The typical abscess appears to remain free for the most part of contaminating bacterial although there is extensive necrosis and caseation.
TREATMENT: Kittens were used in a series of trials on the therapeutic effects of a number of ipecacuanha alkaloids (Dale and Dobell, 1917) without any being found to be of significant therapeutic value. There have been no recent reports of attempts to treat infected cats.
EPIZOOTIOLOGY: Cats do not appear to be regular hosts of this human pathogen even though cysts have been reported in the feces of cats on several occasions (Baetjer and Sellards, 1914; Jungmann, 1986). It would thus appear that kittens are at risk when around water that has been contaminated with human sewage. This parasite has been found in humans throughout the world, it is more common in the warmer climates, but it is present in human populations who live in situations where human feces is not properly disposed of with respect to water and foodstuffs.
HAZARDS TO OTHER ANIMALS: This is unlikely due to cats seldom shedding the transmission stage, the cyst, in their feces even when infected.
HAZARDS TO HUMANS: This is a situation where cats are probably mainly at risk of being infected from a human source rather than vice versa.
CONTROL/PREVENTION: Control and prevention of the disease in cats would be directed at improving the sanitary disposal of human excrement around the world and by providing all people and animals sources of clean drinking water.
Baetjer WA, Sellards AW. 1914. The behavior of amoebic dysentery in lower animals and its bearing upon the interpretation of the clinical symptoms of the disease in man. Johs Hopkins Hosp Bull 282:237-241
Brumpt E. 1925. Étude sommaire de l’ “Entamoebadispar” n.sp amibe à kystes quadrinucléés, parasite de l’homme. Bull Acad Méd (Paris) 94:943-952.
Diamond LS, Clark CG. 1993. A redescription of Entamoebahistolytica Schaudinn, 1903 (Emended Walker, 1911) separating it from Entamoebadispar Brumpt, 1925. J Euk Microbiol 40:340-344.
Dale HH, Dobell C. 1917. Experiments on the therapeutics of amoebic dysentery. 1917. J Pharm Exp Therap 10:399-459.
Jungmann R, Hiepe T, Scheffler C. 1986. Zur parasitären Intestinalfauna bei Hund und Katze mit einem spziellen Beitrag zur Giardia-Infektion. Nh Vet Med 41:309-311.
Kessel JH. 1928. Amoebiasis in kitterns infected with amoebae from acute and “carrier” human cases and with the tetranucleate amoebae of the monkey and of the pig. Am J Hyg 8:311-355.
Lösch F. 1875. Massenhafte Entwickelung von Amöben im Dickdarm. Arch Path Anat 65:196-211.
Quincke H, Roos E. 1893. Ueber Amöben-Enteritis. Berl Klin Wocheschr 45:1089-1094.
Sanders EP. 1928. Changes in the blood cells of kittens resulting from infections with Endamoebahistolytica. Am J Hyg 8:963-989.
Schaudinn F. 1903. Untersuchungen über die Fontpflauzung einigen Rhizopoden (Vorlaufige Mittheilung). Arb K Gsudhtsamte 19:547-576.
Wenyon CM. 1912. Experimental amoebic dysentery and liver-abscess in cats. J Lond Sch Trop Med 2:27-34.
Figure 1-38. Cyst of Entamoebahistolytica in human feces that was fixed and then stained with iron hematoxylin. Note the characteristic nucleus and kinetoplast and the rounded, dark chromatoidal bodies. In this cyst only one of the four nuclei is visible in the focal plane of the photomicrograph.
Figure 1-39. Trophozoite of Entamoebahistolytic in human feces that was fixed, then stained with iron hematoxylin., and photographed using phase microscopy. The trophozoite has the characteristic nucleus tht is surrounded by chromatin and has a central nucleolus.